p15 |
colorectal cancer |
We demonstrate that neither of these colorectal cancer cells undergo growth arrest in response to TGF-beta, which can be explained, at least in part, by their inability to up-regulate cyclin-dependent kinase inhibitors p21 (CIP1 ) or p15 ( INK4b) after TG |
14715079 |
Human |
ink4b |
colorectal cancer |
We demonstrate that neither of these colorectal cancer cells undergo growth arrest in response to TGF-beta, which can be explained, at least in part, by their inability to up-regulate cyclin-dependent kinase inhibitors p21 (CIP1 ) or p15 ( INK4b) after TG |
14715079 |
Human |
p15 |
head and neck squamous cell carcinoma |
Smoking and drinking can induce p15 methylation in the upper aerodigestive tract of healthy individuals and patients with head and neck squamous cell carcinoma. |
15221997 |
Human |
p15 |
tumor |
Among 31 patients with HNSCC, 20 patients (65%) had methylated p15 gene in their tumor biopsies. |
15221997 |
Human |
p15 |
tumor |
The methylation index of tumor cells with p15 methylation ranged from 0% to 65%. |
15221997 |
Human |
p15 |
carcinoma in situ |
EXPERIMENTAL DESIGN: The methylation status of 7 genes (RARbeta, DAPK, E-cadherin, p16, p15, GSTP1, and MGMT) in 98 cases of bladder transitional cell carcinoma and 4 cases of carcinoma in situ was analyzed by methylation-specific PCR. |
11839665 |
Human |
p15 |
bladder transitional cell carcinoma |
EXPERIMENTAL DESIGN: The methylation status of 7 genes (RARbeta, DAPK, E-cadherin, p16, p15, GSTP1, and MGMT) in 98 cases of bladder transitional cell carcinoma and 4 cases of carcinoma in situ was analyzed by methylation-specific PCR. |
11839665 |
Human |
p15 |
transitional cell carcinoma |
RESULTS: In transitional cell carcinoma tumor tissues, aberrant methylation was frequently detected in RARbeta (87.8%), DAPK (58.2%), E-cadherin (63.3%), and p16 (26.5%), whereas methylation of p15 (13.3%), GSTP1 (5.1%), and MGMT (5.1%) is not common. |
11839665 |
Human |
p15 |
tumor |
RESULTS: In transitional cell carcinoma tumor tissues, aberrant methylation was frequently detected in RARbeta (87.8%), DAPK (58.2%), E-cadherin (63.3%), and p16 (26.5%), whereas methylation of p15 (13.3%), GSTP1 (5.1%), and MGMT (5.1%) is not common. |
11839665 |
Human |
p15 |
idiopathic myelofibrosis |
Hypermethylation of p15 and p16 genes was determined in 32 patients with agnogenic myeloid metaplasia(AMM), also known as idiopathic myelofibrosis (MF). |
11849214 |
Human |
p15 |
mycosis fungoides and sezary syndrome |
Frequent abnormalities of the p15 and p16 genes in mycosis fungoides and sezary syndrome. |
11874489 |
Human |
p15 |
melanoma |
The P15 and P16 genes are intricately linked on 9p21 and can be inactivated in melanoma and non-Hodgkin's lymphoma. |
11874489 |
Human |
p15 |
non-hodgkins lymphoma |
The P15 and P16 genes are intricately linked on 9p21 and can be inactivated in melanoma and non-Hodgkin's lymphoma. |
11874489 |
Human |
p15 |
mycosis fungoides and sezary syndrome |
This study suggests that abnormalities of the P15 and P16 genes are common in both early and advanced stages of mycosis fungoides and Sezary syndrome and that these genes may be inactivated by allelic loss and aberrant promoter methylation. |
11874489 |
Human |
ink4b |
human tumors |
This pathway is deregulated in the vast majority of human tumors by genetic and epigenetic alterations that target at least some of its key members such as Cyclin D1, Cdk4, INK4a and INK4b, pRb etc. |
11960696 |
Human |
cdkn2b |
tumour |
In addition, we screened the CDKN2B (p15 INK4b), CDKN2C (p18 INK4c), CDK4 and p53R2 genes for mutations in the tumour tissues. |
11960918 |
Human |
p15 ink4b |
tumour |
In addition, we screened the CDKN2B (p15 INK4b), CDKN2C (p18 INK4c), CDK4 and p53R2 genes for mutations in the tumour tissues. |
11960918 |
Human |
p15 |
leukemia |
The potential for leukemia evolution is compounded by epigenetic events including methylation silencing of the p15 proto-oncogene or activating ras point mutations. |
11961208 |
Human |
p15 |
ovarian cancer |
Inactivation of p16/CDKN2 and p15/MTS2 is associated with prognosis and response to chemotherapy in ovarian cancer. |
11992549 |
Human |
mts2 |
ovarian cancer |
Inactivation of p16/CDKN2 and p15/MTS2 is associated with prognosis and response to chemotherapy in ovarian cancer. |
11992549 |
Human |
p15 |
primary epithelial ovarian cancer |
To define the involvement of p16/CDKN2 and p15/MTS2 tumor-suppressor genes for response to chemotherapy in primary epithelial ovarian cancer, we analyzed alterations of the gene in 45 patients who were treated with primary cytoreductive surgery followed b |
11992549 |
Human |
mts2 |
primary epithelial ovarian cancer |
To define the involvement of p16/CDKN2 and p15/MTS2 tumor-suppressor genes for response to chemotherapy in primary epithelial ovarian cancer, we analyzed alterations of the gene in 45 patients who were treated with primary cytoreductive surgery followed b |
11992549 |
Human |
p15 |
ovarian cancer |
These results suggest that deletion of p16/CDKN2 and/or p15/MTS2 is a potential indicator for poor chemotherapy response and adverse prognosis in ovarian cancer patients. |
11992549 |
Human |
mts2 |
ovarian cancer |
These results suggest that deletion of p16/CDKN2 and/or p15/MTS2 is a potential indicator for poor chemotherapy response and adverse prognosis in ovarian cancer patients. |
11992549 |
Human |
p15 |
b-cell acute lymphoblastic leukaemia |
We examined deletion and methylation of the p15INK4B (p15) and p16INK4A (p16) genes, using Southern blotting and methylation-specific polymerase chain reaction (PCR), in 70 untreated adult patients with precursor B-cell acute lymphoblastic leukaemia (PBC- |
12028019 |
Human |
p15 |
tumor |
The tumor and the paired serum were examined for aberrant methylation in DAP-kinase, E-cadherin, GSTP1, p15, and p16 by methylation-specific PCR. |
12060614 |
Human |
p15 |
primary tumor |
RESULTS: Promoter methylation in DAP-kinase, E-cadherin, GSTP1, p15, and p16 were detected in 70.3, 75.9, 18.5, 68.5, and 66.7% of primary tumor. |
12060614 |
Human |
p15 |
gastric cancer |
In serum of gastric cancer patients, methylation in DAP-kinase, E-cadherin, GSTP1, p15, and p16 were detected in 48.1, 57.4, 14.8, 55.6, and 51.9%, respectively. |
12060614 |
Human |
p15 |
b-cell lymphomas |
We analyzed DNA from 36 cases of primary cutaneous B cell lymphomas, four systemic B cell lymphomas, and six benign B cell lymphoproliferative infiltrates for abnormalities of p15 and p16 using microsatellite markers for 9p21, methylation specific polymer |
12060387 |
Human |
p15 |
primary cutaneous b-cell lymphomas |
We analyzed DNA from 36 cases of primary cutaneous B cell lymphomas, four systemic B cell lymphomas, and six benign B cell lymphoproliferative infiltrates for abnormalities of p15 and p16 using microsatellite markers for 9p21, methylation specific polymer |
12060387 |
Human |
p15 |
primary cutaneous b-cell lymphomas |
In primary cutaneous B cell lymphomas with allelic loss or promotor hypermethylation of either p15 or p16, loss of expression in tumor cells was identified in 5 of 8 and 9 of 10 cases, respectively. |
12060387 |
Human |
p15 |
tumor |
In primary cutaneous B cell lymphomas with allelic loss or promotor hypermethylation of either p15 or p16, loss of expression in tumor cells was identified in 5 of 8 and 9 of 10 cases, respectively. |
12060387 |
Human |
cdkn2b |
neuroblastoma |
In previous work, we showed that CDKN2A and CDKN2B genes, mapped at 9p21, were not deleted in neuroblastoma cells. |
12072202 |
Human |
p15 |
astrocytoma |
For example, in astrocytoma the frequency of gains culminated at 7p12, 8q24.1, and 12q13-q15 (the loci of EGF-R, C-MYC and CDK4, respectively) and losses at 9p21 (the locus of p15 and p16) and 10q23.3 where PTEN resides. |
12127399 |
Human |
ink4b |
tumors |
None of the juvenile tumors demonstrated altered expression, but 7/12 (58%) adult GCTs lacked expression of INK4A, INK4B, or both. |
12203782 |
Human |
p15 |
anaplastic large-cell lymphomas |
The p16 and p15 promoter regions were studied using methylation-specific polymerase chain reaction in 53 CD30 non-Hodgkin's lymphomas (25 anaplastic large-cell, 13 peripheral T cell, and 15 anaplastic diffuse large B cell) and 26 Hodgkin's lymph |
12213729 |
Human |
p15 |
non-hodgkins lymphomas |
The p16 and p15 promoter regions were studied using methylation-specific polymerase chain reaction in 53 CD30 non-Hodgkin's lymphomas (25 anaplastic large-cell, 13 peripheral T cell, and 15 anaplastic diffuse large B cell) and 26 Hodgkin's lymph |
12213729 |
Human |
p15 |
tumor |
The p16 and p15 promoter regions were studied using methylation-specific polymerase chain reaction in 53 CD30 non-Hodgkin's lymphomas (25 anaplastic large-cell, 13 peripheral T cell, and 15 anaplastic diffuse large B cell) and 26 Hodgkin's lymph |
12213729 |
Human |
p15 |
hodgkins lymphomas |
The p16 and p15 promoter regions were studied using methylation-specific polymerase chain reaction in 53 CD30 non-Hodgkin's lymphomas (25 anaplastic large-cell, 13 peripheral T cell, and 15 anaplastic diffuse large B cell) and 26 Hodgkin's lymph |
12213729 |
Human |
p15 |
neoplasms |
The p16 and p15 promoter regions were studied using methylation-specific polymerase chain reaction in 53 CD30 non-Hodgkin's lymphomas (25 anaplastic large-cell, 13 peripheral T cell, and 15 anaplastic diffuse large B cell) and 26 Hodgkin's lymph |
12213729 |
Human |
p15 |
lymphoma |
This confirms the p16-methylated status in Hodgkin's cases described in a single previous study and adds information concerning the p15 gene that was also found to be methylated in this lymphoma subtype. |
12213729 |
Human |
p15 |
tumors |
Our results show that although p16 and/or p15 methylation is involved in non-Hodgkin's and Hodgkin's tumors that share morphological and phenotypic features, differences in incidence, pattern of methylation, and implication in tumor progression |
12213729 |
Human |
p15 |
tumor |
Our results show that although p16 and/or p15 methylation is involved in non-Hodgkin's and Hodgkin's tumors that share morphological and phenotypic features, differences in incidence, pattern of methylation, and implication in tumor progression |
12213729 |
Human |
p15 |
tumors |
Aberrant hypermethylation was observed in 7 (32%) and 5 (23%) cases accompanied, by immunohistochemical loss of expression for p16 and p15 genes respectively, in both high stage and grade tumors from patients living in radiocontaminated areas, this being |
12218456 |
Human |
p15 |
therapy-related leukemia |
Methylation profile was analyzed in eleven cases of therapy-related leukemia (t-leukemia) for p14, p15, p16, Rb, hMLH1, hMSH2, MGMT, APC, RAR beta, DAPK, RIZ1, FHIT, and SOCS-1 genes by using methylation specific polymerase chain reaction (MSP) analysis. |
12888905 |
Human |
p15 ink4b |
myelodysplastic syndrome |
Demethylation of a hypermethylated P15/INK4B gene in patients with myelodysplastic syndrome by 5-Aza-2'-deoxycytidine (decitabine) treatment. p16 and p15, 2 inhibitors of cyclin-dependent kinases, are frequently hypermethylated in hematologic neoplas |
12351408 |
Human |
p15 |
lung adenocarcinoma |
The presence of genes coding for TGF-beta receptors I and II at these loci suggests that the TGF-beta/CDK inhibitor P16/P15 signaling pathway might be involved in lung adenocarcinoma development. |
12356584 |
Human |
ink4b |
carcinomas |
We analyzed 22 patients with CIS of the bladder (15 patients with isolated CIS, 7 patients combined with synchronous pTa or pT1 carcinomas) for gains and losses of chromosome (peri)centromere loci 1q12, 7p11-q11, 9p11-q12, and 9p21 harboring the INK4A/ARF |
12368185 |
Human |
p15 |
cancer |
By examining the methylation patterns of these genes, 3 differential methylation patterns were recognized: hypermethylation was more frequent in cancer than in IM (DAP-kinase, p14, p15 and p16); comparable frequencies of methylation in cancer and IM (E-ca |
12448005 |
Human |
cdkn2b |
tumour |
Germline deletions of the region on 9p21 containing the CDKN2A and CDKN2B genes and CDKN2A exon 1beta have been reported in kindreds, implicating contiguous tumour suppressor gene deletion as a cause of this syndrome. |
11136714 |
Human |
p15 |
acute promyelocytic leukemia |
Methylation of p15 and p16 genes in acute promyelocytic leukemia: potential diagnostic and prognostic significance. |
11283136 |
Human |
p15 |
acute promyelocytic leukemia (apl) |
PURPOSE: To investigate the frequency of p15 and p16 gene promoter methylation in acute promyelocytic leukemia (APL), and to define its value in the detection of minimal residual disease (MRD) and treatment prognostication. |
11283136 |
Human |
ink4b |
primary carcinomas |
Molecular analysis of the INK4A and INK4B gene loci in human breast cancer cell lines and primary carcinomas. |
11369056 |
Human |
ink4b |
human breast cancer |
Molecular analysis of the INK4A and INK4B gene loci in human breast cancer cell lines and primary carcinomas. |
11369056 |
Human |
ink4b |
breast carcinoma |
Our results show that these structurally and functionally related genes are not invariably affected together, and the most frequently observed alteration at the INK4A and INK4B loci in breast carcinoma appears to be p16(INK4A) hypomethylation. |
11369056 |
Human |
p15 |
childhood acute lymphoblastic leukaemia |
Relationship of p15 and p16 gene alterations to elevated dihydrofolate reductase in childhood acute lymphoblastic leukaemia. |
11380466 |
Human |
p15 |
acute lymphoblastic leukaemia (all) |
The downstream effects of p15 and p16 gene deletions and loss of transcripts on dihydrofolate reductase (DHFR) were examined in 63 B-precursor (BP) acute lymphoblastic leukaemia (ALL) samples. p15 and/or p16 gene deletions were seen in 6% and 8%, respecti |
11380466 |
Human |
p15 |
retinoblastoma |
In p15- and p16-null K562 cells transfected with a tetracycline-inducible p15 cDNA construct, induction of p15 transcripts and protein was accompanied by decreased growth rates, decreased S-phase fraction, decreased retinoblastoma protein phosphorylation, |
11380466 |
Human |
p15 |
adult acute leukemia |
Methylation of p15 and p16 genes in adult acute leukemia: lack of prognostic significance. |
11413509 |
Human |
p15 |
adult acute leukemia |
In this study, the authors investigated the frequency and prognostic significance of p15 and p16 gene methylation in adult acute leukemia. |
11413509 |
Human |
p15 |
acute lymphoblastic leukemia (all) |
METHOD: The methylation-specific polymerase chain reaction (MS-PCR) was used to analyze p15 and p16 gene methylation in 49 cases of acute lymphoblastic leukemia (ALL) and 29 cases of acute myelogenous leukemia (AML). |
11413509 |
Human |
p15 |
acute myelogenous leukemia (aml) |
METHOD: The methylation-specific polymerase chain reaction (MS-PCR) was used to analyze p15 and p16 gene methylation in 49 cases of acute lymphoblastic leukemia (ALL) and 29 cases of acute myelogenous leukemia (AML). |
11413509 |
Human |
p15 |
adult acute leukemias |
CONCLUSION: Gene methylation of p15, but not p16, is frequent in adult acute leukemias. |
11413509 |
Human |
p15 |
gastric carcinoma |
METHODS: The authors examined 5 gastric carcinoma cell lines, 26 frozen gastric carcinoma tissues and their adjacent nontumor area for concurrent CpG-island hypermethylation in 6 tumor-related genes (p15, p16, E-cadherin, GST-pi, hMLH1, and VHL) by methyl |
11413518 |
Human |
p15 |
myelodysplastic syndrome |
In myelodysplastic syndrome (MDS), the expression of the cyclin-dependent kinase inhibitor p15(ink4B) (p15) is frequently decreased because of the aberrant methylation of the gene promoter; p15 is normally up-regulated during megakaryocytic differentiatio |
11435325 |
Human |
cdkn2b |
cancer |
We found that CpG islands at GSTP1, APC, RASSF1a, PTGS2, and MDR1 were hypermethylated in >85% of prostate cancers and cancer cell lines but not in normal prostate cells and tissues; CpG islands at EDNRB, ESR1, CDKN2a, and hMLH1 exhibited low to moderate |
15026333 |
Human |
cdkn2b |
prostate cancer |
We found that CpG islands at GSTP1, APC, RASSF1a, PTGS2, and MDR1 were hypermethylated in >85% of prostate cancers and cancer cell lines but not in normal prostate cells and tissues; CpG islands at EDNRB, ESR1, CDKN2a, and hMLH1 exhibited low to moderate |
15026333 |
Human |
cdkn2b |
prostate cancers |
We found that CpG islands at GSTP1, APC, RASSF1a, PTGS2, and MDR1 were hypermethylated in >85% of prostate cancers and cancer cell lines but not in normal prostate cells and tissues; CpG islands at EDNRB, ESR1, CDKN2a, and hMLH1 exhibited low to moderate |
15026333 |
Human |
p15 |
bladder cancer |
Three genes known to be aberrantly methylated in bladder cancer (p16, p15, and PAX6) were studied in detail by methylation-sensitive single nucleotide primer extension and showed increased methylation in culture at preexisting methylated sites for all of |
11479229 |
Human |
p15 |
insulinomas |
RT-PCR analysis revealed loss of expression of at least one of the tumor suppressor genes CDKN2A/p16, CDKN2B/p15, and CDKN2D/p14 with distinct genetic profiles, most frequently in nonfunctional pancreatic tumors (57%) and small intestinal carcinoids (44%) |
11479232 |
Human |
cdkn2b |
insulinomas |
RT-PCR analysis revealed loss of expression of at least one of the tumor suppressor genes CDKN2A/p16, CDKN2B/p15, and CDKN2D/p14 with distinct genetic profiles, most frequently in nonfunctional pancreatic tumors (57%) and small intestinal carcinoids (44%) |
11479232 |
Human |
p15 |
pancreatic tumors |
RT-PCR analysis revealed loss of expression of at least one of the tumor suppressor genes CDKN2A/p16, CDKN2B/p15, and CDKN2D/p14 with distinct genetic profiles, most frequently in nonfunctional pancreatic tumors (57%) and small intestinal carcinoids (44%) |
11479232 |
Human |
cdkn2b |
pancreatic tumors |
RT-PCR analysis revealed loss of expression of at least one of the tumor suppressor genes CDKN2A/p16, CDKN2B/p15, and CDKN2D/p14 with distinct genetic profiles, most frequently in nonfunctional pancreatic tumors (57%) and small intestinal carcinoids (44%) |
11479232 |
Human |
p15 |
tumor |
RT-PCR analysis revealed loss of expression of at least one of the tumor suppressor genes CDKN2A/p16, CDKN2B/p15, and CDKN2D/p14 with distinct genetic profiles, most frequently in nonfunctional pancreatic tumors (57%) and small intestinal carcinoids (44%) |
11479232 |
Human |
cdkn2b |
tumor |
RT-PCR analysis revealed loss of expression of at least one of the tumor suppressor genes CDKN2A/p16, CDKN2B/p15, and CDKN2D/p14 with distinct genetic profiles, most frequently in nonfunctional pancreatic tumors (57%) and small intestinal carcinoids (44%) |
11479232 |
Human |
cdkn2b |
meningiomas |
Alterations of the tumor suppressor genes CDKN2A (p16(INK4a)), p14(ARF), CDKN2B (p15(INK4b)), and CDKN2C (p18(INK4c)) in atypical and anaplastic meningiomas. |
11485924 |
Human |
cdkn2b |
tumor |
Alterations of the tumor suppressor genes CDKN2A (p16(INK4a)), p14(ARF), CDKN2B (p15(INK4b)), and CDKN2C (p18(INK4c)) in atypical and anaplastic meningiomas. |
11485924 |
Human |
cdkn2b |
meningiomas |
We investigated 67 meningothelial tumors (20 benign meningiomas, 34 atypical meningiomas, and 13 anaplastic meningiomas) for losses of genetic information from chromosome arms 1p and 9p, as well as for deletion, mutation, and expression of the tumor suppr |
11485924 |
Human |
cdkn2b |
tumors |
We investigated 67 meningothelial tumors (20 benign meningiomas, 34 atypical meningiomas, and 13 anaplastic meningiomas) for losses of genetic information from chromosome arms 1p and 9p, as well as for deletion, mutation, and expression of the tumor suppr |
11485924 |
Human |
cdkn2b |
atypical meningiomas |
We investigated 67 meningothelial tumors (20 benign meningiomas, 34 atypical meningiomas, and 13 anaplastic meningiomas) for losses of genetic information from chromosome arms 1p and 9p, as well as for deletion, mutation, and expression of the tumor suppr |
11485924 |
Human |
cdkn2b |
tumor |
We investigated 67 meningothelial tumors (20 benign meningiomas, 34 atypical meningiomas, and 13 anaplastic meningiomas) for losses of genetic information from chromosome arms 1p and 9p, as well as for deletion, mutation, and expression of the tumor suppr |
11485924 |
Human |
cdkn2b |
benign meningiomas |
We investigated 67 meningothelial tumors (20 benign meningiomas, 34 atypical meningiomas, and 13 anaplastic meningiomas) for losses of genetic information from chromosome arms 1p and 9p, as well as for deletion, mutation, and expression of the tumor suppr |
11485924 |
Human |
cdkn2b |
meningiomas |
Six anaplastic meningiomas (46%) and one atypical meningioma (3%) showed homozygous deletions of the CDKN2A, p14(ARF), and CDKN2B genes. |
11485924 |
Human |
cdkn2b |
atypical meningioma |
Six anaplastic meningiomas (46%) and one atypical meningioma (3%) showed homozygous deletions of the CDKN2A, p14(ARF), and CDKN2B genes. |
11485924 |
Human |
cdkn2b |
meningioma |
One anaplastic meningioma, three atypical meningiomas, and one benign meningioma without a demonstrated homozygous deletion or mutation of CDKN2A, p14(ARF), or CDKN2B lacked detectable transcripts from at least one of these genes. |
11485924 |
Human |
cdkn2b |
benign meningioma |
One anaplastic meningioma, three atypical meningiomas, and one benign meningioma without a demonstrated homozygous deletion or mutation of CDKN2A, p14(ARF), or CDKN2B lacked detectable transcripts from at least one of these genes. |
11485924 |
Human |
cdkn2b |
atypical meningiomas |
One anaplastic meningioma, three atypical meningiomas, and one benign meningioma without a demonstrated homozygous deletion or mutation of CDKN2A, p14(ARF), or CDKN2B lacked detectable transcripts from at least one of these genes. |
11485924 |
Human |
cdkn2b |
meningiomas |
However, the majority of anaplastic meningiomas either show homozygous deletions of CDKN2A, p14(ARF), and CDKN2B, mutations in CDKN2A and p14(ARF), or lack of expression of one or more of these genes. |
11485924 |
Human |
p15 |
acute myeloid leukemia |
KG-1 and KG-1a model the p15 CpG island methylation observed in acute myeloid leukemia patients. p15 and p16 are tumor suppressor genes that have 5' CpG islands and both are subject to hypermethylation associated with their transcriptional inactivati |
11532526 |
Human |
p15 |
hematological malignancies |
KG-1 and KG-1a model the p15 CpG island methylation observed in acute myeloid leukemia patients. p15 and p16 are tumor suppressor genes that have 5' CpG islands and both are subject to hypermethylation associated with their transcriptional inactivati |
11532526 |
Human |
p15 |
adult acute myeloid leukemia |
In this study, we used sodium bisulfite sequencing to obtain a complete map of the 5-methylcytosine status of 80 CpGs covering approximately 900 bp in the 5' p15 CpG island, and 53 CpGs covering approximately 700 bp in the 5' p16 CpG island in t |
11532526 |
Human |
p15 |
tumors |
Although no alterations in TGF-beta, TbetaR-I, or Smad7 were found in tumors, a significant increase in c-myc expression (2.5-fold, P < 0.05 ) and a significant decrease in p15 expression (4.5-fold, P < 0.05 ) were noted. |
11536370 |
Mouse |
p15 |
tumors |
The significant decrease in p15 expression in tumors provides additional evidence that TGF-beta signaling may be markedly attenuated during colon tumorigenesis. |
11536370 |
Mouse |
p15 cdk inhibitor |
glioblastoma multiforme |
Alternative splicing of the p15 cdk inhibitor in glioblastoma multiforme. |
11563632 |
Human |
p15 |
glioblastoma |
Both, wild-type p15 and p10 were detected in three of nine glioblastoma cell lines. |
11563632 |
Human |
ink4b |
glioblastoma |
Sixteen of twenty-nine (55%) glioblastoma tumor samples contained INK4b transcripts, but only nine (31%) tumors expressed p15 protein. |
11563632 |
Human |
p15 |
glioblastoma |
Sixteen of twenty-nine (55%) glioblastoma tumor samples contained INK4b transcripts, but only nine (31%) tumors expressed p15 protein. |
11563632 |
Human |
ink4b |
tumors |
Sixteen of twenty-nine (55%) glioblastoma tumor samples contained INK4b transcripts, but only nine (31%) tumors expressed p15 protein. |
11563632 |
Human |
p15 |
tumors |
Sixteen of twenty-nine (55%) glioblastoma tumor samples contained INK4b transcripts, but only nine (31%) tumors expressed p15 protein. |
11563632 |
Human |
ink4b |
tumor |
Sixteen of twenty-nine (55%) glioblastoma tumor samples contained INK4b transcripts, but only nine (31%) tumors expressed p15 protein. |
11563632 |
Human |
p15 |
tumor |
Sixteen of twenty-nine (55%) glioblastoma tumor samples contained INK4b transcripts, but only nine (31%) tumors expressed p15 protein. |
11563632 |
Human |
p15 |
tumors |
Three p15 protein-negative tumors expressed only p10 mRNA. |
11563632 |
Human |
p15 |
glioblastoma |
Strong suppression of tumorigenicity was seen in four glioblastoma cell lines after transfection with p15 but not with p10. |
11563632 |
Human |
p15 |
leukemias |
Moreover, two different patterns of promoter methylation distinguished the leukemias from colorectal cancer: p15 promoter hypermethylation was found only in the leukemias, and p16 promoter hypermethylation occurred only in colon tumors. |
11584062 |
Human |
p15 |
colorectal cancer |
Moreover, two different patterns of promoter methylation distinguished the leukemias from colorectal cancer: p15 promoter hypermethylation was found only in the leukemias, and p16 promoter hypermethylation occurred only in colon tumors. |
11584062 |
Human |
p15 |
colon tumors |
Moreover, two different patterns of promoter methylation distinguished the leukemias from colorectal cancer: p15 promoter hypermethylation was found only in the leukemias, and p16 promoter hypermethylation occurred only in colon tumors. |
11584062 |
Human |
cdkn2b |
acute myeloid leukemia |
Specifically, we were interested in the expression of the tumor suppressor gene Cdkn2b (p15(INK4b)) in MML because this gene is expressed during myeloid differentiation and its inactivation by methylation has been shown to be important for the development |
11593429 |
Human |
cdkn2b |
tumors |
Although Cdkn2b (p15(INK4b)) mRNA was expressed in the Myc tumors, many transcripts were aberrant in size and contained only exon 1. |
11593429 |
Human |
p15 |
tumours |
Expression of p15 and p15.5 products in neuroendocrine lung tumours: relationship with p15(INK4b) methylation status. |
11641784 |
Human |
p15 |
tumours |
Expressions of p15 and p15.5 protein isoforms were analysed in a series of eight control normal lung, 12 tumour-associated normal lung, five low grade and 15 high grade neuroendocrine (NE) lung tumours and relationship with a specific p15(INK4b) methylati |
11641784 |
Human |
p15 |
tumour |
Using Western blot analysis, we showed that p15 and p15.5 isoforms displayed a high heterogeneous pattern of expression in both normal and tumour tissues. |
11641784 |
Human |
p15 |
tumours |
P15 and p15.5 expressions were correlated in control normal lung (P<0.04) whereas they were not in tumours and associated normal lung. |
11641784 |
Human |
p15 |
tumours |
Levels of p15 and p15.5 were distinct (up- or downregulated) from those observed in paired normal lung in 4/12 (33%) and 10/12 (83%) tumours respectively. |
11641784 |
Human |
cdkn2b |
melanomas |
A single nucleotide polymorphism in the 3'untranslated region of the CDKN2A gene is common in sporadic primary melanomas but mutations in the CDKN2B, CDKN2C, CDK4 and p53 genes are rare. |
11668523 |
Human |
cdkn2b |
melanomas |
In this report we present the results of mutational analysis of the CDKN2B, CDKN2C, CDK4, p53 genes and 5'UTR of the CDKN2A gene in a set of 44 sporadic primary melanomas, which had been earlier analysed for mutations in the CDKN2A (p16/p14(ARF)) gen |
11668523 |
Human |
cdkn2b |
melanomas |
The 500 C>G polymorphism, however, was in linkage disequilibrium with approximately 50 kb apart the C>A intronic polymorphism in the CDKN2B gene (determined in 44 melanomas and 90 controls; Fisher exact test, p<0.0001). |
11668523 |
Human |
p15 |
blastic nk-cell lymphoma |
In addition, homozygous deletions of p15, p16 and p14 genes in 5 out of 31 samples were detected; 3 were from nasal NK cell lymphoma and 2 from blastic NK cell lymphoma / leukemia. |
11676855 |
Human |
p15 |
leukemia |
In addition, homozygous deletions of p15, p16 and p14 genes in 5 out of 31 samples were detected; 3 were from nasal NK cell lymphoma and 2 from blastic NK cell lymphoma / leukemia. |
11676855 |
Human |
p15 |
cell lymphoma |
In addition, homozygous deletions of p15, p16 and p14 genes in 5 out of 31 samples were detected; 3 were from nasal NK cell lymphoma and 2 from blastic NK cell lymphoma / leukemia. |
11676855 |
Human |
p15 |
neoplasms |
Although the number of cases we analyzed was not large, alterations identified in the Rb, p53, p16, p15 and p14 genes are of significance and might be associated with tumorigenesis in NK cell neoplasms. |
11676855 |
Human |
p15 |
bladder transitional cell carcinomas |
The p15 gene which encodes a cyclin-dependent kinase inhibitor, is located in the 9p21 chromosomal region that is frequently deleted in human bladder transitional cell carcinomas (TCCs). |
11720438 |
Human |
p15 |
tumours |
Lower p15 expression in superficial tumours did not reflect a switch from quiescence to proliferative activity as normal proliferative urothelial controls did not present decreased p15 mRNA levels relative to quiescent normal urothelia. |
11720438 |
Human |
mts2 |
oligodendroglial tumors |
Oligodendroglial tumors frequently demonstrate hypermethylation of the CDKN2A (MTS1, p16INK4a), p14ARF, and CDKN2B (MTS2, p15INK4b) tumor suppressor genes. |
11764089 |
Human |
cdkn2b |
oligodendroglial tumors |
Oligodendroglial tumors frequently demonstrate hypermethylation of the CDKN2A (MTS1, p16INK4a), p14ARF, and CDKN2B (MTS2, p15INK4b) tumor suppressor genes. |
11764089 |
Human |
mts2 |
oligodendroglial tumors |
We investigated 34 oligodendroglial tumors (7 oligodendrogliomas, 11 anaplastic oligodendrogliomas, 8 oligoastrocytomas, and 8 anaplastic oligoastrocytomas) for deletion, mutation, hypermethylation, and expression of the CDKN2A (MTS1, p16INK4a), p14ARF, a |
11764089 |
Human |
cdkn2b |
oligodendroglial tumors |
We investigated 34 oligodendroglial tumors (7 oligodendrogliomas, 11 anaplastic oligodendrogliomas, 8 oligoastrocytomas, and 8 anaplastic oligoastrocytomas) for deletion, mutation, hypermethylation, and expression of the CDKN2A (MTS1, p16INK4a), p14ARF, a |
11764089 |
Human |
cdkn2b |
tumors |
Most tumors with CDKN2A, p14ARF, and/or CDKN2B hypermethylation either lacked detectable transcripts from these genes or had lower mRNA levels than those determined for non-neoplastic brain tissue. |
11764089 |
Human |
cdkn2b |
oligodendroglial tumors |
Taken together, our results indicate that hypermethylation of CDKN2A, p14ARF, and CDKN2B is an important epigenetic mechanism by which oligodendroglial tumors may escape from p53- and pRb-dependent growth control. |
11764089 |
Human |
p15 |
cancer |
Cell proliferation regulatory pathways including genes involved in the GIS checkpoint (p53, pRb, p15, p16, and cyclins A, D, E, and cdk 2,4) have been associated with plaque progression, stenosis and restenosis after angioplasty as well as in cancer progr |
11795276 |
Human |
p15 |
anaplastic tumors |
7/26 (27%) benign, 3/12 (25%) atypical but 4/7 (57%) anaplastic tumors lacked both, p16 and p15 protein expression. |
11859969 |
Human |
ink4b |
meningiomas |
Exclusive expression of the alternative INK4b transcript p10 possibly at the expense of p15 and therefore resulting in loss of p15 tumor suppressor activity was noted in two meningiomas. |
11859969 |
Human |
p15 |
meningiomas |
Exclusive expression of the alternative INK4b transcript p10 possibly at the expense of p15 and therefore resulting in loss of p15 tumor suppressor activity was noted in two meningiomas. |
11859969 |
Human |
ink4b |
meningioma |
In conclusion, our results suggest a greater role for losses of INK4a/INK4b gene products in meningioma formation and malignant progression than previously thought. |
11859969 |
Human |
p15 |
acute leukemia |
Hypermethylation of p16 and p15 genes and RB protein expression in acute leukemia. |
10634644 |
Human |
p15 |
neoplasms |
Both p16 and p15, encoded by genes located on chromosome 9p21, are inhibitors of cyclin-dependent kinases 4/6 (CDK4/6) and upstream regulators of RB function, and set up the RB/p16 tumor suppressive pathway, which is abrogated frequently in human neoplasm |
10634644 |
Human |
p15 |
t-cell acute lymphoblastic leukemia (t-all) |
In hematological malignancies, deletion of p16/p15 locus has been shown to be highly specific to lymphoid malignancies, and more particularly to T-cell acute lymphoblastic leukemia (T-ALL). |
10634644 |
Human |
p15 |
hematological malignancies |
In hematological malignancies, deletion of p16/p15 locus has been shown to be highly specific to lymphoid malignancies, and more particularly to T-cell acute lymphoblastic leukemia (T-ALL). |
10634644 |
Human |
p15 |
lymphoid malignancies |
In hematological malignancies, deletion of p16/p15 locus has been shown to be highly specific to lymphoid malignancies, and more particularly to T-cell acute lymphoblastic leukemia (T-ALL). |
10634644 |
Human |
p15 |
leukemias |
These results revealed the frequent methylation of p16 and p15 genes in B-ALL and AML despite a low frequency of p16 and p15 deletions and mutations in these leukemias. |
10634644 |
Human |
p15 |
acute leukemia |
These results suggest that inactivation of p16 and p15 genes is one of the most common genetic events in acute leukemia, and plays an important role for the RB/p16 pathway in the pathogenesis of acute leukemia. |
10634644 |
Human |
p15 |
rhabdomyosarcoma |
Expression of the p16INK4A (p16), p15INK4B (p15), and p14ARF genes, located at 9p21, was examined in pediatric neuroblastoma (NB), Ewing's sarcoma (ES), and rhabdomyosarcoma (RMS). p16 expression was absent in 4 of 5 ESs, and 2 of these 4 cases died. |
12963998 |
Human |
p15 |
ewings sarcoma |
Expression of the p16INK4A (p16), p15INK4B (p15), and p14ARF genes, located at 9p21, was examined in pediatric neuroblastoma (NB), Ewing's sarcoma (ES), and rhabdomyosarcoma (RMS). p16 expression was absent in 4 of 5 ESs, and 2 of these 4 cases died. |
12963998 |
Human |
p15 |
neuroblastoma |
Expression of the p16INK4A (p16), p15INK4B (p15), and p14ARF genes, located at 9p21, was examined in pediatric neuroblastoma (NB), Ewing's sarcoma (ES), and rhabdomyosarcoma (RMS). p16 expression was absent in 4 of 5 ESs, and 2 of these 4 cases died. |
12963998 |
Human |
p15 |
tumors |
The different incidence of expression of the p16, p15, and p14ARF genes in these 3 tumor types may reflect differences of the molecular process through which the 3 tumors develop. |
12963998 |
Human |
p15 |
tumor |
The different incidence of expression of the p16, p15, and p14ARF genes in these 3 tumor types may reflect differences of the molecular process through which the 3 tumors develop. |
12963998 |
Human |
p15 |
acute leukemias |
Aberrant p15 promoter methylation in adult and childhood acute leukemias of nearly all morphologic subtypes: potential prognostic implications. |
10706859 |
Human |
p15 |
acute leukemias |
We prospectively analyzed p15 and p16 promoter methylation patterns using methylation-specific polymerase chain reaction (PCR) in patients with adult and childhood acute leukemias and studied the association of methylation patterns with chromosomal abnorm |
10706859 |
Human |
p15 |
acute biphenotypic leukemia (abl) |
In nearly all French-American-British leukemia subtypes, we found p15 methylation in bone marrow or peripheral blood cells from 58% (46/79) of patients with acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), or acute biphenotypic leukemia ( |
10706859 |
Human |
p15 |
acute myeloid leukemia (aml) |
In nearly all French-American-British leukemia subtypes, we found p15 methylation in bone marrow or peripheral blood cells from 58% (46/79) of patients with acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), or acute biphenotypic leukemia ( |
10706859 |
Human |
p15 |
acute lymphoblastic leukemia (all) |
In nearly all French-American-British leukemia subtypes, we found p15 methylation in bone marrow or peripheral blood cells from 58% (46/79) of patients with acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), or acute biphenotypic leukemia ( |
10706859 |
Human |
p15 |
leukemia |
In nearly all French-American-British leukemia subtypes, we found p15 methylation in bone marrow or peripheral blood cells from 58% (46/79) of patients with acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), or acute biphenotypic leukemia ( |
10706859 |
Human |
ink4b |
primary lymphomas |
Although hypermethylation of the INK4a and INK4b promoters is frequently involved in murine lymphomas, the p19(ARF) CpG island is infrequently methylated in the murine primary lymphomas studied in this work. |
10753221 |
others |
ink4b |
lymphomas |
Although hypermethylation of the INK4a and INK4b promoters is frequently involved in murine lymphomas, the p19(ARF) CpG island is infrequently methylated in the murine primary lymphomas studied in this work. |
10753221 |
others |
p15 |
human tumors |
Aberrations of various components of the pRb pathway, such as retinoblastoma protein and its upstream actors including cyclin D1, cyclin dependence kinase-4 and p16/p15 cyclin dependent kinase inhibitors, have been reported in a variety of human tumors. |
10773403 |
Human |
p15 |
mouse lymphomas |
Previously, we have reported frequent inactivation of the Cdkn2a/Cdkn2b loci encoding p16/p15 cyclin dependent kinase inhibitors in a subset of 2',3'-dideoxycytidine- and 1, 3-butadiene-induced mouse lymphomas (S.-M. Zhuang, A. Schippert, A. Hau |
10773403 |
Mouse |
cdkn2b |
mouse lymphomas |
Previously, we have reported frequent inactivation of the Cdkn2a/Cdkn2b loci encoding p16/p15 cyclin dependent kinase inhibitors in a subset of 2',3'-dideoxycytidine- and 1, 3-butadiene-induced mouse lymphomas (S.-M. Zhuang, A. Schippert, A. Hau |
10773403 |
Mouse |
p15 |
lymphomas |
These results indicate that the mechanisms underlying the development of 2', 3'-dideoxycytidine- and 1,3-butadiene-induced lymphomas involve inactivation of p16/p15 cyclin-dependent kinase inhibitors but not genomic alterations of the Rb1, Ccnd1 |
10773403 |
Human |
p15 |
t-cell acute lymphoblastic leukemia |
Universal inactivation of both p16 and p15 but not downstream components is an essential event in the pathogenesis of T-cell acute lymphoblastic leukemia. p16/p15 regulate the cell cycle pathway by inhibiting the cyclin Ds-CDK4/6 mediated phosphorylation |
10778944 |
Human |
p15 |
t-cell acute lymphoblastic leukemia (t-all) |
We reported previously that in T-cell acute lymphoblastic leukemia (T-ALL), p16 and p15 were frequently (approximately 70%) inactivated at the DNA level by deletion, mutation, or hypermethylation. |
10778944 |
Human |
p15 |
chronic myelogenous leukemia |
Quantitative measure of c-abl and p15 methylation in chronic myelogenous leukemia: biological implications. |
10779450 |
Human |
p15 |
chronic myelogenous leukemia (cml) |
We used a sensitive, quantitative bisulfite PCR assay, methylation sensitive single nucleotide primer extension (Ms-SNuPE), to measure methylation of the 5' CpG islands of c-abl and p15 in chronic myelogenous leukemia (CML) patients during progressio |
10779450 |
Human |
p15 |
human prostate cancer |
We examined the expression levels of the p16, p15, p14, and retinoblastoma-susceptibility (RB) genes in primary prostate cancers and human prostate cancer cell lines, and correlated this with the DNA methylation levels of two loci in p16. |
10797499 |
Human |
p15 |
primary prostate cancers |
We examined the expression levels of the p16, p15, p14, and retinoblastoma-susceptibility (RB) genes in primary prostate cancers and human prostate cancer cell lines, and correlated this with the DNA methylation levels of two loci in p16. |
10797499 |
Human |
p15 |
tumors |
RESULTS: Overexpression of p16 mRNA was found in 6/9 (67) of prostate tumors compared to the adjacent normal prostate, whereas elevated p14 and p15 levels were only observed in 2/9 (22) and 1/6 (17) of prostate cases, respectively. |
10797499 |
Human |
p15 |
prostate cancers |
CONCLUSIONS: Our studies show that although the levels of the cell cycle regulators p16, p15, p14, and Rb are altered in prostate cancers, there is no apparent correlation to grade, stage, or any pattern of regulation between the related genes. |
10797499 |
Human |
p15 |
multiple myeloma |
Methylation of p16 and p15 genes in multiple myeloma. |
12906163 |
Human |
p15 |
multiple myeloma (mm) |
OBJECTIVE: To investigate the frequency of p16 and p15 gene methylation in multiple myeloma (MM), and its relationship with bone marrow cell apoptosis and clinical outcome. |
12906163 |
Human |
cdkn2b |
esophageal squamous-cell carcinoma (escc) |
Because previous studies have shown that loss of heterozygosity (LOH) is common on chromosome arm 9p in esophageal squamous cell carcinoma (ESCC) and that genetic alterations in CDKN2A and CDKN2B on 9p are also common, we sought to determine whether LOH a |
14732922 |
Human |
cdkn2b |
cancer |
Cyclin-dependent kinase (CDK) inhibitors represented by the INK4 family (including p16(INK4a, CDKN2A), p15(INK4b, CDKN2B), p18(INK4c, CDKN2C), and p19(INK4d, CDKN2D)) are regulators of the cell cycle shown to be aberrant in many types of human cancer. |
10918395 |
Human |
p15 ink4b |
lymphomas |
Deletions at chromosome 9p21, which harbours the tumour suppressor genes p14/ARF, p15/INK4b, and p16/INK4a, and 17p13, where p53 is located, are associated with the development and progression of lymphomas. |
14743509 |
Human |
p15 |
human gastric cancer |
Introduction of Smad3 into human gastric cancer cells that did not express Smad3, restored TGF-beta responsiveness: induction of p21 and p15 gene expression, and growth inhibition in response to TGF-beta. |
14647420 |
Human |
cdkn2b |
primary tumors |
The genes encoding the cyclin-dependent kinase inhibitors p16INK4A (CDKN2A) and p15INK4B (CDKN2B) are frequently homozygously deleted in a variety of tumor cell lines and primary tumors, including glioblastomas in which 40-50% of primary tumors display ho |
10939591 |
Human |
cdkn2b |
tumor |
The genes encoding the cyclin-dependent kinase inhibitors p16INK4A (CDKN2A) and p15INK4B (CDKN2B) are frequently homozygously deleted in a variety of tumor cell lines and primary tumors, including glioblastomas in which 40-50% of primary tumors display ho |
10939591 |
Human |
p15 |
glioma |
Here, we have used replication-defective recombinant adenoviruses to compare the effects of expressing wild-type p16 and p15 in glioma cell lines. |
10939591 |
Human |
p15 |
glioma |
After infection, high levels of p16 and p15 were observed in two human glioma cell lines (U251 MG and U373 MG). |
10939591 |
Human |
p15 |
glioma |
Thus, we conclude that overexpression of p15 has a similar ability to inhibit cell proliferation, to cause replicative senescence, and to inhibit telomerase activity as p16 in glioma cells with an intact RB protein pathway. |
10939591 |
Human |
p15 |
osteosarcoma |
Analysis of the p16INK4, p14ARF, p15, TP53, and MDM2 genes and their prognostic implications in osteosarcoma and Ewing sarcoma. |
10942797 |
Human |
p15 |
ewing sarcoma |
Analysis of the p16INK4, p14ARF, p15, TP53, and MDM2 genes and their prognostic implications in osteosarcoma and Ewing sarcoma. |
10942797 |
Human |
p15 |
ewing sarcomas |
We examined alterations of the p16INK4, p14ARF, p15, TP53, and MDM2 genes in 30 osteosarcomas and 24 Ewing sarcomas. |
10942797 |
Human |
p15 |
ewing sarcomas |
Among 21 osteosarcomas and 24 Ewing sarcomas, p16INK4, p14ARF, and p15 abnormalities were found in 4 (19%), 2 (9%), and 3 (14%) osteosarcomas, respectively, and in 4 (17%), 3 (13%), and 4 (17%) Ewing sarcomas, respectively. |
10942797 |
Human |
p15 |
osteosarcoma |
While TP53 abnormalities were far more frequent in osteosarcoma than in Ewing sarcoma, alterations of p16INK4, p14ARF, and p15 were present at similar frequencies in the two types of sarcoma. |
10942797 |
Human |
p15 |
sarcoma |
While TP53 abnormalities were far more frequent in osteosarcoma than in Ewing sarcoma, alterations of p16INK4, p14ARF, and p15 were present at similar frequencies in the two types of sarcoma. |
10942797 |
Human |
p15 |
ewing sarcoma |
While TP53 abnormalities were far more frequent in osteosarcoma than in Ewing sarcoma, alterations of p16INK4, p14ARF, and p15 were present at similar frequencies in the two types of sarcoma. |
10942797 |
Human |
ink4b |
papillomas |
Consistent with a perturbed cell cycle, deltabetaRII papillomas and SCC showed reduced expression of the TGFbeta target genes p15 (INK4b), p21 (WAF-1) and p27 (Kip1), inhibitors of cyclin-dependent kinases (cdks). |
10951568 |
Mouse |
p15 |
papillomas |
Consistent with a perturbed cell cycle, deltabetaRII papillomas and SCC showed reduced expression of the TGFbeta target genes p15 (INK4b), p21 (WAF-1) and p27 (Kip1), inhibitors of cyclin-dependent kinases (cdks). |
10951568 |
Mouse |
p15 |
bladder cancer |
Deletion of p16 and p15 genes In schistosomiasis-associated bladder cancer (SABC). |
10958872 |
Human |
p15 |
cancer |
Alterations of p16 and p15 genes have been reported in cancer cell lines and in certain malignant neoplasm. |
10958872 |
Human |
p15 |
malignant neoplasm |
Alterations of p16 and p15 genes have been reported in cancer cell lines and in certain malignant neoplasm. |
10958872 |
Human |
p15 |
bladder tumors |
Deletion of both p16 and p15 genes was observed in 72 and 36 bladder tumors, respectively. |
10958872 |
Human |
p15 |
bladder tumors |
The expression of p16 and p15 proteins was undetectable in 75 and 38 bladder tumors, respectively, by Western blot analysis. |
10958872 |
Human |
p15 |
bladder cancer |
Alteration of the p16 and p15 genes appears to be an early event in bladder cancer which occurs more frequently in SABC and SCC, and may play an important role in the development of schistosomal bladder cancer. |
10958872 |
Human |
p15 |
schistosomal bladder cancer |
Alteration of the p16 and p15 genes appears to be an early event in bladder cancer which occurs more frequently in SABC and SCC, and may play an important role in the development of schistosomal bladder cancer. |
10958872 |
Human |
p15 |
acute myeloblastic leukemia |
Anticorresponding p15 promoter methylation and microsatellite instability in acute myeloblastic leukemia. |
11041632 |
Human |
p15 |
hepatocellular carcinoma |
Frequent p15 promoter methylation in tumor and peripheral blood from hepatocellular carcinoma patients. |
10999738 |
Human |
p15 |
tumor |
Frequent p15 promoter methylation in tumor and peripheral blood from hepatocellular carcinoma patients. |
10999738 |
Human |
p15 |
tumors |
We prospectively analyzed p15 methylation patterns in 25 surgically resected tumors and 130 plasma, serum, and buffy coat samples from hepatocellular carcinoma (HCC) patients, controls with chronic hepatitis/cirrhosis, and healthy subjects. |
10999738 |
Human |
p15 |
hepatocellular carcinoma (hcc) |
We prospectively analyzed p15 methylation patterns in 25 surgically resected tumors and 130 plasma, serum, and buffy coat samples from hepatocellular carcinoma (HCC) patients, controls with chronic hepatitis/cirrhosis, and healthy subjects. |
10999738 |
Human |
p15 |
tumors |
Using methylation-specific PCR, we demonstrated for the first time p15 promoter methylation in 64% of tumors and 25% (4 of 16) of patients' plasma and serum samples. |
10999738 |
Human |
p15 |
tumors |
Concurrent p15 and p16 methylation was shown in 48% of tumors, and p15/p16 methylation was detected in the plasma/serum of 92% (11 of 12) of patients. |
10999738 |
Human |
p15 |
tumor |
In buffy coat samples, p15 methylation was detected in all eight patients with tumor p15 methylation, suggesting the presence of circulating tumor cells. |
10999738 |
Human |
p15 |
tumor |
Our data underscore the important role(s) of p15 and p16 methylation in hepatocarcinogenesis and tumor progression. |
10999738 |
Human |
p15 |
tumor |
Among 92% (23 of 25) of patients with tumor p15/p16 methylation, circulating tumor DNA and HCC cells were detected in the peripheral blood of 87% (20 of 23) of patients. |
10999738 |
Human |
p15 |
prostate carcinomas |
As PCR based approaches analyzing for homozygous deletions could be confounded by unavoidable contributions of normal cells in microdissected tissue, we performed in situ hybridization (ISH) on primary prostate carcinomas to accurately evaluate p16 and p1 |
11025389 |
Human |
p15 |
prostate cancer |
MATERIAL AND METHODS: p16 and p15 loci were evaluated in 28 pT3N0M0 prostate cancer specimens. |
11025389 |
Human |
p15 |
melanoma |
In addition to the CDKN genes (p16/CDKN2A, p15/CDKN2B and p19(ARF), frequently inactivated in familial MM), widely reported data suggested the presence within this region of other melanoma susceptibility gene(s). |
11104570 |
Human |
cdkn2b |
melanoma |
In addition to the CDKN genes (p16/CDKN2A, p15/CDKN2B and p19(ARF), frequently inactivated in familial MM), widely reported data suggested the presence within this region of other melanoma susceptibility gene(s). |
11104570 |
Human |
p15 |
hepatocellular carcinoma |
[The expression of P21 and P15 proteins in liver tissue of chronic viral hepatitis and hepatocellular carcinoma and their relation to cell apoptosis] OBJECTIVE: To study the expression of P21 and P15 proteins in liver tissue of chronic viral hepatitis (CH |
11503050 |
Human |
p15 |
hepatocellular carcinoma (hcc) |
[The expression of P21 and P15 proteins in liver tissue of chronic viral hepatitis and hepatocellular carcinoma and their relation to cell apoptosis] OBJECTIVE: To study the expression of P21 and P15 proteins in liver tissue of chronic viral hepatitis (CH |
11503050 |
Human |
mts2 |
hepatocellular carcinomas |
Deletion of chromosomes 9p and 17 associated with abnormal expression of p53, p16/MTS1 and p15/MTS2 gene protein in hepatocellular carcinomas. |
11776078 |
Human |
p15 |
hepatocellular carcinomas |
Deletion of chromosomes 9p and 17 associated with abnormal expression of p53, p16/MTS1 and p15/MTS2 gene protein in hepatocellular carcinomas. |
11776078 |
Human |
p15 |
malignant gliomas |
Functional evidence for a role of combined CDKN2A (p16-p14(ARF))/CDKN2B (p15) gene inactivation in malignant gliomas. |
10541865 |
Human |
p15 |
glioblastoma |
Concerted inactivation of p16, p15 and p14(ARF) could be demonstrated in seven of nine glioblastoma cell lines. |
10541865 |
Human |
p15 |
tumors |
Significantly weaker growth suppression was observed in tumors either retaining expression of both p16 and p15 or p15 only. p14(ARF) proved to be a potent tumor suppressor in the presence of wild-type p53, while mutant p53 substantially reduced growth inh |
10541865 |
Human |
p15 |
malignant gliomas |
Combined inactivation of CDKN2A and CDKN2B, i.e., loss of both p16 and p15 as well as p14(ARF), results in disruption of two major growth control pathways involving pRB and p53 in malignant gliomas. |
10541865 |
Human |
cdkn2b |
malignant gliomas |
Combined inactivation of CDKN2A and CDKN2B, i.e., loss of both p16 and p15 as well as p14(ARF), results in disruption of two major growth control pathways involving pRB and p53 in malignant gliomas. |
10541865 |
Human |
cdkn2b |
tumors |
Therefore, homozygous co-deletions of CDKN2A and CDKN2B rather than mutations targeting individual transcripts are frequently selected for in these tumors. |
10541865 |
Human |
cdkn2b |
neoplasms |
Yeast artificial chromosome (YAC) mapping localized PLAA proximal to the CDKN2A/CDKN2B genes and to a region flanked by D9S171 and INFA commonly deleted in many neoplasms. |
10644453 |
Human |
p15 |
cancer |
Both p16 and p15 are an inhibitor of cyclin D-cdk4,cyclin D-cdk6 complex and have been implicated in a wide variety of cancer types, including the germline of patients with familial melanoma. |
12894891 |
Human |
p15 |
melanoma |
Both p16 and p15 are an inhibitor of cyclin D-cdk4,cyclin D-cdk6 complex and have been implicated in a wide variety of cancer types, including the germline of patients with familial melanoma. |
12894891 |
Human |
p15 |
tumors |
The data showed the following: 1) Homozygous deletions of p16,p15 were comparatively rare and far less common than previously reported, although hemizygous deletions were observed in a significant fraction of many tumor types; 2) the incidence of p16,p15 |
12894891 |
Human |
p15 |
tumor |
The data showed the following: 1) Homozygous deletions of p16,p15 were comparatively rare and far less common than previously reported, although hemizygous deletions were observed in a significant fraction of many tumor types; 2) the incidence of p16,p15 |
12894891 |
Human |
p15 |
pancreatic carcinoma |
Here, we found that several pancreatic carcinoma cell lines exert TGFbeta-induced negative growth control in spite of the loss of p15 and p16 expression. |
9863014 |
Human |
ink4b |
adult soft tissue sarcomas |
Alterations of INK4A and INK4B genes in adult soft tissue sarcomas: effect on survival. |
9890173 |
Human |
ink4b |
primary malignant neoplasms |
Alterations of the INK4A and INK4B genes occur frequently in certain primary malignant neoplasms. |
9890173 |
Human |
ink4b |
adult soft tissue sarcomas |
This study was undertaken to evaluate the frequency of INK4A and INK4B gene alterations in a cohort of adult soft tissue sarcomas. |
9890173 |
Human |
ink4b |
soft-tissue sarcomas |
METHODS: The status of the INK4A and INK4B genes was determined in 46 soft tissue sarcomas by use of the following methods: Southern blotting, polymerase chain reaction (PCR), single-strand conformation polymorphism analysis, comparative multiplex PCR, an |
9890173 |
Human |
ink4b |
tumor |
Alteration of the INK4A and INK4B genes was the only statistically significant predictor for poor survival when controlling for tumor grade and size (P = .03). |
9890173 |
Human |
ink4b |
adult soft tissue sarcomas |
CONCLUSION/IMPLICATIONS: Coincident homozygous deletion of the INK4A and INK4B genes occurs frequently in adult soft tissue sarcomas. |
9890173 |
Human |
ink4b |
tumour |
We show here that the hypermethylated genes MLH1, TIMP3 (TIMP3), CDKN2B (INK4B, p15) and CDKN2A (INK4, p16) cannot be transcriptionally reactivated with TSA alone in tumour cells in which we have shown that TSA alone can upregulate the expression of non-m |
9916800 |
Human |
p15 |
tumour |
We show here that the hypermethylated genes MLH1, TIMP3 (TIMP3), CDKN2B (INK4B, p15) and CDKN2A (INK4, p16) cannot be transcriptionally reactivated with TSA alone in tumour cells in which we have shown that TSA alone can upregulate the expression of non-m |
9916800 |
Human |
cdkn2b |
tumour |
We show here that the hypermethylated genes MLH1, TIMP3 (TIMP3), CDKN2B (INK4B, p15) and CDKN2A (INK4, p16) cannot be transcriptionally reactivated with TSA alone in tumour cells in which we have shown that TSA alone can upregulate the expression of non-m |
9916800 |
Human |
p15 |
tumors |
Hybrid cell lines yielded tumors upon s.c. injection into athymic nude mice regardless of p16/p15 status. |
9950215 |
Mouse |
p15 |
tumors |
Tumors derived from six p16/p15-positive hybrid cells, however, revealed deletions of both p16 and p15. |
9950215 |
Human |
p15 |
melanoma |
These data define a TSG or TSGs that function independently of p15/p16 on chromosome 9 and provide evidence for a TSG (or TSGs) on chromosome 10 that may be important in melanoma development. |
9973191 |
Human |
p15 |
t-cell acute lymphoblastic leukemia |
Alterations of the p53, p21, p16, p15 and RAS genes in childhood T-cell acute lymphoblastic leukemia. |
10071127 |
Human |
p15 |
t-cell acute lymphoblastic leukemia (t-all) |
We investigated the alterations of the p53, p21, p16, p15 and RAS genes in childhood T-cell acute lymphoblastic leukemia (T-ALL) and T-ALL cell lines by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis and direct seque |
10071127 |
Human |
p15 |
acute leukemias |
Reports on homozygous deletion of p16 and p15 genes suggest the value of larger, prospective studies with standardized treatment protocols to definitively establish the prognostic utility of p15/p16 deletions in acute leukemias. |
10073286 |
Human |
p15 |
relapsed childhood all |
These findings indicate that loss of function of proteins encoded by p16 and/or p15 plays an important role in the biology of relapsed childhood ALL, and is associated with disease progression in a subset of cases. |
10090949 |
Human |
cdkn2b |
tumour |
Components of the pRb pathway which are often altered in tumour progression include the INK4 cyclin-dependent kinase (CDK) inhibitors p16INK4a/ CDKN2A and p15INK4b/CDKN2B, CDK4, D-type cyclins and pRb. |
10338330 |
Human |
cdkn2b |
melanoma |
CDK4 was mutated or overexpressed in two melanoma cell lines with homozygously deleted CDKN2A and CDKN2B genes. |
10338330 |
Human |
ink4b |
bladder tumors |
Evaluation of alterations in the tumor suppressor genes INK4A and INK4B in human bladder tumors. |
11692873 |
Human |
cdk inhibitory protein |
cancer |
Activation of the cdk inhibitory protein p21 by ellagic acid suggests a role for ellagic acid in cell cycle regulation of cancer cells. |
10355751 |
Human |
p15 |
primary tumors |
In this article, we describe the characteristics of 12 human colorectal-carcinoma cell lines established from 6 primary tumors and 6 metastatic sites of 11 Korean colorectal-carcinoma patients, including the morphology in vivo and in vitro and mutations o |
10362137 |
Human |
p15 |
adult t-cell leukemia |
Because tumorigenesis frequently involves the dysfunction of cell cycle-related proteins, we examined the effect of mutations in CDK inhibitor p16 and its linked genomic loci p15, cl.B, and 1063.7 on the growth of primary adult T-cell leukemia (ATL) cells |
10378889 |
Human |
ink4b |
neoplasms |
Many neoplasms in which INK4A and INK4B genes are altered show deletions involving both genes. |
10375589 |
Human |
ink4b |
tumors |
In the present study we examined the genetic alterations affecting the remaining Ink4a allele and the Ink4b gene in tumors arising in heterozygous Ink4a mice. |
10375589 |
Human |
p15 |
tumours |
Alteration of p16 and p15 genes in human uterine tumours. |
10408854 |
Human |
p15 |
tumour |
The roles of the p16 and p15 inhibitor of cyclin-dependent kinase tumour suppressor genes were examined in human uterine cervical and endometrial cancers. p16 mRNA, examined by reverse transcription polymerase chain reaction (RT-PCR), was significantly re |
10408854 |
Human |
p15 |
endometrial cancers |
The roles of the p16 and p15 inhibitor of cyclin-dependent kinase tumour suppressor genes were examined in human uterine cervical and endometrial cancers. p16 mRNA, examined by reverse transcription polymerase chain reaction (RT-PCR), was significantly re |
10408854 |
Human |
p15 |
tumours |
Homozygous deletion of p15 was found in three of 40 (8%) cervical tumours and one of 38 (3%) endometrial tumours. |
10408854 |
Human |
ink4b |
bladder neoplasms |
Association with recurrence. The INK4A and the INK4B genes map to chromosome 9p21, an area frequently deleted in bladder neoplasms. |
10393843 |
Human |
p15 |
tumors |
On the other hand, advanced passages of tumors acquire additional alterations in the p15 and Smad4 genes. |
10415855 |
Human |
p15 |
pancreatic tumor |
Mutations in K-ras, p53, p15 and Smad4 genes can be acquired, in this model system, in the more advanced stages of pancreatic tumor dissemination. |
10415855 |
Human |
p15 |
maxillofacial squamous cell carcinomas |
Abnormalities of tumor suppressor genes P16 and P15 in primary maxillofacial squamous cell carcinomas. |
10432931 |
Human |
p15 |
maxillofacial squamous cell carcinomas (mscc) |
However, the status of P16 and P15 genes in primary maxillofacial squamous cell carcinomas (MSCC) has not been reported. |
10432931 |
Human |
p15 |
tumors |
The P15 gene appeared to play a lesser role in tumorigenesis of these tumors. |
10432931 |
Human |
p15 |
acute myeloid leukaemia (aml) |
We used bisulfite genomic sequencing to characterize the methylation pattern of the CpG islands associated with the calcitonin, estrogen receptor, E-cadherin, p15, p16, Rb, GST-Pi, and HIC1 genes in the bone marrow from 9 normal and 20 patients with acute |
10446989 |
Human |
mts2 |
t-cell lymphomas |
Frequent methylation silencing of p15(INK4b) (MTS2) and p16(INK4a) (MTS1) in B-cell and T-cell lymphomas. |
10477703 |
Human |
mts2 |
lymphomas |
The methylation status of p15(INK4b) (MTS2), p16(INK4a) (MTS1) and p14(ARF) (p16beta) was analyzed in 56 lymphomas by restriction-enzyme related polymerase chain reaction (PCR) (REP), methylation-specific PCR (MSP), and bisulfite genomic sequencing (BGS). |
10477703 |
Human |
p15 |
b-cell lymphomas |
Methylation of the p15 and p16 genes was detected, respectively, in 64% and 32% of the B-cell lymphomas, in 44% and 22% of the T-cell lymphomas, and in none of the 5 reactive lymph nodes analyzed. |
10477703 |
Human |
p15 |
t-cell lymphomas |
Methylation of the p15 and p16 genes was detected, respectively, in 64% and 32% of the B-cell lymphomas, in 44% and 22% of the T-cell lymphomas, and in none of the 5 reactive lymph nodes analyzed. |
10477703 |
Human |
p15 |
b-cell lymphomas |
Both p15 and p16 genes were methylated more often in the high-grade (78% and 50%, respectively) than in the low-grade B-cell lymphomas (55% and 21%, respectively). |
10477703 |
Human |
p15 |
lymphomas |
We found no mutations of p15, p16, or p14 in any of the 56 lymphomas. |
10477703 |
Human |
p15 |
t-cell lymphomas |
Our results suggest a role for p15 and p16 gene methylation during lymphomagenesis and a possible association between p15 and p16 inactivation and aggressive transformation in B-cell and T-cell lymphomas. |
10477703 |
Human |
p15 |
multiple myeloma (mm) |
Recently, alteration of p16 and p15 solely by hypermethylation has been detected in high frequencies hitherto unreported in multiple myeloma (MM). |
10492069 |
Human |
p15 |
cancer |
The reversibility of this epigenetic inactivation of the p16 and p15 genes in MM may also provide a broad clinical application in the development of new therapeutic interventions in this uniformly fatal form of cancer. |
10492069 |
Human |
p15 |
acute leukemia |
The entire CpG island region of p15 was largely devoid of methylation in normal lymphocytes, but methylation of varying density was found in primary acute leukemia. |
10498617 |
Human |
cdkn2b |
neuroblastoma |
Structural and functional analysis of cyclin-dependent kinase inhibitor genes (CDKN2A, CDKN2B, and CDKN2C) in neuroblastoma. |
9432125 |
Human |
cdkn2b |
neuroblastoma |
The status of the CDKN2A gene family, including CDKN2A, CDKN2B, and CDKN2C, was investigated in 24 cases of neuroblastoma. |
9432125 |
Human |
cdkn2b |
tumors |
Finally, expression of the CDKN2B gene was demonstrated in all stage IV neuroblastomas, whereas none of stage I tumors expressed this gene. |
9432125 |
Human |
cdkn2b |
tumor |
This finding suggests the occurrence of a correlation between CDKN2B transcription and tumor phenotype. |
9432125 |
Human |
cdkn2b |
malignant mesothelioma |
Malignant mesothelioma expresses pRb, which, together with the cytogenetic data, suggests the involvement of CDKN2A and/or CDKN2B in its tumorigenesis. |
9466670 |
Human |
cdkn2b |
malignant mesothelioma |
Our data show that deletions of a critical region of chromosome 9, including the CDKN2A but not the CDKN2B locus, are common among malignant mesothelioma. |
9466670 |
Human |
p15 ink4b |
burkitts lymphoma |
p16/INK4a and p15/INK4b gene methylation and absence of p16/INK4a mRNA and protein expression in Burkitt's lymphoma. |
9473234 |
Human |
p15 ink4b |
b-cell lymphomas |
The fact that the p16/INK4a and p15/INK4b genes are frequently inactivated in human malignancies and that p16/INK4a null mice spontaneously develop B-cell lymphomas prompted us to examine the status of both genes in Burkitt's Lymphoma (BL). |
9473234 |
Mouse |
p15 ink4b |
burkitts lymphoma |
The fact that the p16/INK4a and p15/INK4b genes are frequently inactivated in human malignancies and that p16/INK4a null mice spontaneously develop B-cell lymphomas prompted us to examine the status of both genes in Burkitt's Lymphoma (BL). |
9473234 |
Human |
cdkn2b |
thymic lymphomas |
We used this microsatellite to detect loss of heterozygosity of the Cdkn2A and Cdkn2B loci in gamma-irradiation-induced thymic lymphomas of C57BL/6J x RF/J F1 hybrids. |
9501299 |
Human |
cdkn2b |
hepatoblastoma |
Analysis of CDKN2A, CDKN2B, CDKN2C, and cyclin Ds gene status in hepatoblastoma. |
9537438 |
Human |
cdkn2b |
tumors |
These genes were selected because: 1) CDKN2A and CDKN2B are very frequently inactivated in human cancers; 2) cyclin Ds are overexpressed in several tumors and 3) CDKN2A is posttranscriptionally silenced in hepatocellular carcinomas. |
9537438 |
Human |
cdkn2b |
hepatocellular carcinomas |
These genes were selected because: 1) CDKN2A and CDKN2B are very frequently inactivated in human cancers; 2) cyclin Ds are overexpressed in several tumors and 3) CDKN2A is posttranscriptionally silenced in hepatocellular carcinomas. |
9537438 |
Human |
cdkn2b |
cancers |
These genes were selected because: 1) CDKN2A and CDKN2B are very frequently inactivated in human cancers; 2) cyclin Ds are overexpressed in several tumors and 3) CDKN2A is posttranscriptionally silenced in hepatocellular carcinomas. |
9537438 |
Human |
cdkn2b |
hepatoblastoma |
Structural analysis of the CDKN2A, CDKN2B, and CDKN2C genes in hepatoblastoma cases showed the absence of deletions and/or point mutations. |
9537438 |
Human |
cdkn2b |
cancer |
Messenger RNA (mRNA) analysis showed that CDKN2C is expressed in all hepatoblastoma samples studied, while both CDKN2A and CDKN2B genes are not transcribed in the cancer specimens as well as in the matched normal liver tissues. |
9537438 |
Human |
cdkn2b |
hepatoblastoma |
Messenger RNA (mRNA) analysis showed that CDKN2C is expressed in all hepatoblastoma samples studied, while both CDKN2A and CDKN2B genes are not transcribed in the cancer specimens as well as in the matched normal liver tissues. |
9537438 |
Human |
cdkn2b |
human hepatoblastoma |
Our findings demonstrated the following: 1) CDKN2A, CDKN2B, and CDKN2C genes are structurally unmodified in human hepatoblastoma, and 2) CDKN2A (alpha-transcript) and CDKN2B are transcriptionally silenced in normal liver whereas CDKN2A (beta-transcript) a |
9537438 |
Human |
p15 |
acute lymphoblastic leukemia |
Inactivation of the p15 gene in children with acute lymphoblastic leukemia. |
14666292 |
Human |
p15 |
acute lymphoblastic leukemia |
OBJECTIVE: To study the inactivation of the p15 gene in children with acute lymphoblastic leukemia. |
14666292 |
Human |
p15 |
acute lymphoblastic leukemia |
CONCLUSION: According to the literature, inactivation of the p15 gene by deletion of exon 2 in acute lymphoblastic leukemia found in the population studied would be considered to be a molecular marker for diagnosis or relapse. |
14666292 |
Human |
ink4b |
leukemia |
Hypermethylation of the Ink4b locus in murine myeloid leukemia and increased susceptibility to leukemia in p15(Ink4b)-deficient mice. |
14681685 |
Mouse |
ink4b |
myeloid leukemia |
Hypermethylation of the Ink4b locus in murine myeloid leukemia and increased susceptibility to leukemia in p15(Ink4b)-deficient mice. |
14681685 |
Mouse |
ink4b |
myeloid leukemias |
The evidence is twofold: (1) retrovirus-induced myeloid leukemias of the myelomonocytic phenotype were found to have hypermethylation of the 5' CpG island of the Ink4b gene, and this could be correlated with reduced mRNA expression, as demonstrated b |
14681685 |
Mouse |
ink4b |
leukemia |
The evidence is twofold: (1) retrovirus-induced myeloid leukemias of the myelomonocytic phenotype were found to have hypermethylation of the 5' CpG island of the Ink4b gene, and this could be correlated with reduced mRNA expression, as demonstrated b |
14681685 |
Mouse |
ink4b |
myeloid leukemia |
Mice deficient in both alleles were not more susceptible to myeloid disease than those deficient in one allele, raising the possibility that there are opposing forces related to the development of myeloid leukemia in Ink4b null mice. |
14681685 |
Mouse |
p15 |
cancer |
Both p15 and p16 are located on chromosome 9p21 and alterations have been demonstrated in a variety of human malignancies and human cancer cell lines. |
9554401 |
Human |
p15 |
testicular cancer |
The aim of our study was to examine TGCT and testicular cancer cell lines for deletions and mutations of the p15 and p16 genes. |
9554401 |
Human |
p15 |
testicular cancer |
For p15 no band shifts were observed for exons 1 to 2 in TGCT or testicular cancer cell lines; none of benign testicular tumors or normal control tissues demonstrated any band shifts for p15 or p16. |
9554401 |
Human |
p15 |
testicular tumors |
For p15 no band shifts were observed for exons 1 to 2 in TGCT or testicular cancer cell lines; none of benign testicular tumors or normal control tissues demonstrated any band shifts for p15 or p16. |
9554401 |
Human |
p15 |
testicular germ-cell tumors |
The absence of mutations in p15 gene in TGCT specimens suggests that p15 might not play an important role in the pathogenesis of testicular germ cell tumors. |
9554401 |
Human |
p15 |
human gastric carcinoma |
Overexpression of mutant p53 and c-erbB-2 proteins and mutations of the p15 and p16 genes in human gastric carcinoma: with respect to histological subtypes and stages. |
9570245 |
Human |
p15 |
tumour |
Mutations of the p15 and p16 tumour suppressor genes were assessed by polymerase chain reaction, Southern blotting, and direct DNA sequencing. |
9570245 |
Human |
p15 |
tumour |
Our preliminary results indicate alterations in the p15 gene were not important in gastric tumorigenesis, while infrequent homozygous deletions in the p16 gene play a limited role in tumour progression of intestinal-type GC. |
9570245 |
Human |
p15 |
myeloma |
To determine whether the differential effects of IFN-alpha on myeloma cell cycle progression could also result from differences in the expression of cyclin-dependent kinase inhibitors, we examined the effects of IFN-alpha on the induction of cyclin-depend |
9565604 |
Human |
cdkn2b |
tumor |
Recently, we and others have defined a tumor suppressor region on the short arm of chromosome 9 harboring a cluster of genes, including MTAP, CDKN2A (p16INK4a), and CDKN2B (p15INK4B), which is frequently deleted in a variety of tumor types. |
9591637 |
Human |
cdkn2b |
melanoma |
Virtually 100% of melanoma cell lines harbor alterations at the DNA level within CDKN2A, CDKN2B, or one of their downstream targets. |
9598804 |
Human |
cdkn2b |
melanoma |
Surprisingly, at the DNA level alone, 96% (43/45) of melanoma cell lines examined were found to be deleted/mutated/methylated for CDKN2A (34/45), homozygously deleted for CDKN2A's neighbor and homolog CDKN2B (6/45), and/or mutated/amplified for CDK4 |
9598804 |
Human |
p15 |
sporadic malignant melanoma |
Mutations of p16 and p15 tumor suppressor genes and replication errors contribute independently to the pathogenesis of sporadic malignant melanoma. |
9617435 |
Human |
p15 |
sporadic malignant melanomas |
Mutations of p16 and p15 suppressor oncogenes and the replication errors in six microsatellite loci in sporadic malignant melanomas were analyzed. |
9617435 |
Human |
p15 |
melanoma |
Four (9.1%) homozygous deletions of both p16 and p15 genes and one point mutation (2.3%) in the p15 gene were detected among 44 primary melanoma samples. |
9617435 |
Human |
p15 |
sporadic malignant melanomas |
These results suggest that (1) the homozygous deletions of p16/p15 genes and the replication errors may occur in rather early stages of melanoma tumorigenesis, while the p16/p15 gene mutation may occur in later stages, and (2) the p16 and p15 gene mutatio |
9617435 |
Human |
p15 |
melanoma |
These results suggest that (1) the homozygous deletions of p16/p15 genes and the replication errors may occur in rather early stages of melanoma tumorigenesis, while the p16/p15 gene mutation may occur in later stages, and (2) the p16 and p15 gene mutatio |
9617435 |
Human |
p15 |
melanoma |
In the family segregating the melanoma/NST syndrome, a large germ-line deletion ablated the whole p16, p19, and p15 gene cluster (or INK4 locus), whereas a more circumscribed molecular lesion disrupting p16 and p19 but leaving p15 unaltered segregated wit |
9622062 |
Human |
p15 |
human leukemia-lymphoma |
Review of alterations of the cyclin-dependent kinase inhibitor INK4 family genes p15, p16, p18 and p19 in human leukemia-lymphoma cells. |
9639410 |
Human |
p15 |
multiple myeloma |
Here, p15 is most often inactivated, at particularly high frequencies in the disorders lacking any p15/p16 deletions: 40-80% p15met in AML, MDS and multiple myeloma. |
9639410 |
Human |
p15 |
t-cell lymphomas |
There is controversy concerning the prognostic impact of p15 and p16 aberrations with some studies describing a significant correlation between inactivation of these genes and poor prognosis, while most others did not detect any prognostic relevance, at l |
9639410 |
Human |
p15 |
tumors |
Deletions at the 9p21 region frequently affect both p16 and p15 genes, however, mutations in the coding sequence of the p15 gene have not been found in the majority of tumors analyzed, including non-Hodgkin's lymphomas. |
9639423 |
Human |
p15 |
non-hodgkins lymphomas |
Deletions at the 9p21 region frequently affect both p16 and p15 genes, however, mutations in the coding sequence of the p15 gene have not been found in the majority of tumors analyzed, including non-Hodgkin's lymphomas. |
9639423 |
Human |
p15 |
non-hodgkins lymphomas |
We analyzed 72 non-Hodgkin's lymphomas (NHL) for methylation at p15 exon 1 by PCR and Southern blot techniques using methylation-sensitive restriction enzymes. |
9639423 |
Human |
cdkn2b |
tumours |
CDKN2A, CDKN2B and p14ARF are frequently and differentially methylated in ependymal tumours. |
14636164 |
Human |
cdkn2b |
tumour |
Nevertheless, the three important tumour suppressor genes located in this chromosome, CDKN2A, CDKN2B and p14 ARF, have not been reported to be commonly altered in them. |
14636164 |
Human |
cdkn2b |
tumours |
We observed promoter methylation for CDKN2A in 21% (26/123) of tumours, for CDKN2B in 32% (23/71) and p14 ARF in 21% (23/108). |
14636164 |
Human |
cdkn2b |
tumours |
For CDKN2B, extracranial tumours were more frequently methylated than intracranial ones. |
14636164 |
Human |
cdkn2b |
tumours |
For CDKN2B and p14 ARF, methylation was more frequent in low-grade tumours; the reverse was observed for CDKN2A. |
14636164 |
Human |
cdkn2b |
tumours |
CDKN2A, CDKN2B and p14 ARF promoters were methylated in 21-32% of the tumours. |
14636164 |
Human |
p15 |
mantle-cell lymphoma |
Concurrent disruption of cell cycle associated genes in mantle cell lymphoma: a genotypic and phenotypic study of cyclin D1, p16, p15, p53 and pRb. |
9697882 |
Human |
mts2 |
head and neck squamous cell carcinomas |
Deletion of P15 (MTS2) in head and neck squamous cell carcinomas. |
9698532 |
Human |
p15 |
head and neck squamous cell carcinomas |
Deletion of P15 (MTS2) in head and neck squamous cell carcinomas. |
9698532 |
Human |
multiple tumor suppressor 2 |
head and neck squamous cell carcinomas |
INTRODUCTION: The purpose of this study was to determine whether the multiple tumor suppressor 2 (MTS2) gene, encoding an inhibitor (p15) of cyclin D-dependent kinases 4 and 6 (cdk4, cdk6), is deleted in head and neck squamous cell carcinomas (HNSCC). |
9698532 |
Human |
mts2 |
head and neck squamous cell carcinomas |
INTRODUCTION: The purpose of this study was to determine whether the multiple tumor suppressor 2 (MTS2) gene, encoding an inhibitor (p15) of cyclin D-dependent kinases 4 and 6 (cdk4, cdk6), is deleted in head and neck squamous cell carcinomas (HNSCC). |
9698532 |
Human |
p15 |
head and neck squamous cell carcinomas |
INTRODUCTION: The purpose of this study was to determine whether the multiple tumor suppressor 2 (MTS2) gene, encoding an inhibitor (p15) of cyclin D-dependent kinases 4 and 6 (cdk4, cdk6), is deleted in head and neck squamous cell carcinomas (HNSCC). |
9698532 |
Human |
p15 |
tumors |
Of 21 HNSCC tumors, 9 showed no amplification of the p15 gene; none of these 9 neoplasms had visible PCR products. |
9698532 |
Human |
p15 |
neoplasms |
Of 21 HNSCC tumors, 9 showed no amplification of the p15 gene; none of these 9 neoplasms had visible PCR products. |
9698532 |
Human |
p15 |
tumor |
CONCLUSIONS: Although PCR is not a quantitative technique, densitometric analysis of PCR products showed it was unlikely that the p15 gene was present in more than a small fraction of the tumor cells. |
9698532 |
Human |
p15 |
t-cell childhood acute lymphoblastic leukaemias |
As a high proportion of T-cell childhood acute lymphoblastic leukaemias have deletions of both p15 and p16, our data suggest that inactivation of these genes makes it possible for leukemic cells to avoid senescence. |
9704925 |
Human |
p15 |
childhood acute lymphoblastic leukemias |
The p16INK4A (p16) and p15INK4B (p15) tumor suppressor genes are inactivated by homozygous gene deletion and p15 promoter hypermethylation in a significant proportion of childhood acute lymphoblastic leukemias (ALLs). |
9737691 |
Human |
p15 |
tumor |
The p16INK4A (p16) and p15INK4B (p15) tumor suppressor genes are inactivated by homozygous gene deletion and p15 promoter hypermethylation in a significant proportion of childhood acute lymphoblastic leukemias (ALLs). |
9737691 |
Human |
p15 |
haematological malignancies |
Recently, p16 and p15 have been identified as commonly inactivated tumour suppressor genes in haematological malignancies. |
9792305 |
Human |
p15 |
hematological malignancies |
Several studies report deletion or transcriptional loss of the p15 gene in myeloid and lymphoid hematological malignancies, and a possible role as a tumor suppressor gene has been proposed for this CDKI. |
9808052 |
Human |
mts2 |
human thyroid cancer |
Rare loss of heterozygosity of the MTS1 and MTS2 tumor suppressor genes in differentiated human thyroid cancer. |
9808321 |
Human |
p15 |
acute myeloid leukemia |
Selective variegated methylation of the p15 CpG island in acute myeloid leukemia. |
9808523 |
Human |
p15 |
acute myeloid leukemia (aml) |
In our study, we used sodium bisulfite sequencing to generate high resolution maps of 5-methylcytosine in the CpG islands associated with p15, p16 and dCK in normal human bone marrow (BM), peripheral blood lymphocytes (PBL) and cytosine arabinoside (ara-C |
9808523 |
Human |
p15 |
tumor |
In our study, we used sodium bisulfite sequencing to generate high resolution maps of 5-methylcytosine in the CpG islands associated with p15, p16 and dCK in normal human bone marrow (BM), peripheral blood lymphocytes (PBL) and cytosine arabinoside (ara-C |
9808523 |
Human |
p15 |
follicular carcinoma |
In follicular carcinoma (WRO) cells, both the p15 and p16 genes were homozygously deleted. |
9827724 |
Human |
p15 |
pancreatic cancers |
Eighty-two % of these pancreatic cancers had genetic inactivation of the DPC4, p15, ALK-5, or TGFBR2 genes. |
9850059 |
Human |
mts2 |
hepatocellular carcinoma |
Infrequent mutations and no methylation of CDKN2A (P16/MTS1) and CDKN2B (p15/MTS2) in hepatocellular carcinoma in Taiwan. |
9893670 |
Human |
p15 |
hepatocellular carcinoma |
Infrequent mutations and no methylation of CDKN2A (P16/MTS1) and CDKN2B (p15/MTS2) in hepatocellular carcinoma in Taiwan. |
9893670 |
Human |
cdkn2b |
hepatocellular carcinoma |
Infrequent mutations and no methylation of CDKN2A (P16/MTS1) and CDKN2B (p15/MTS2) in hepatocellular carcinoma in Taiwan. |
9893670 |
Human |
mts2 |
cancers |
More recently, another reported pathway of inactivation involves loss of transcription associated with de novo methylation of the 5' CpG island of p16/MTS1 and p15/MTS2 in human cancers. |
9893670 |
Human |
p15 |
cancers |
More recently, another reported pathway of inactivation involves loss of transcription associated with de novo methylation of the 5' CpG island of p16/MTS1 and p15/MTS2 in human cancers. |
9893670 |
Human |
p15 |
primary tumours |
No aberrant 5' CpG island hypermethylation of p16 or p15 was found in any of the primary tumours by Southern blot. |
9893670 |
Human |
p15 |
human breast cancer |
The TSG101 tumor susceptibility gene is located in chromosome 11 band p15 and is mutated in human breast cancer. |
9019400 |
Human |
cdkn2b |
tumours |
In a series of 46 glioblastomas, 16 anaplastic astrocytomas and eight astrocytomas, all tumours retaining one or both alleles of CDKN2A (48 tumours) and CDKN2B (49 tumours) were subjected to sequence analysis (entire coding region and splice acceptor and |
9000591 |
Human |
cdkn2b |
tumours |
None of the tumours retaining alleles of CDKN2B showed mutations of this gene. |
9000591 |
Human |
cdkn2b |
tumours |
Glioblastomas with retention of both alleles of CDKN2A (14 tumours) and CDKN2B (16 tumours) expressed transcripts for these genes. |
9000591 |
Human |
p15 |
lymphoblastic leukemias |
The commonly deleted region at 9p21-22 in lymphoblastic leukemias spans at least 400 kb and includes p16 but not p15 or the IFN gene cluster. |
9009086 |
Human |
p15 |
lymphoblastic leukemias |
To define the smallest region of overlap of deletions at chromosome band 9p21-22 and to clarify the involvement of p16, p15 and the IFN cluster gene in lymphoblastic leukemias, we used a multiplex polymerase chain reaction to construct a detailed map of d |
9009086 |
Human |
ink4b |
plasma-cell leukaemia |
To study the structural integrity of the cyclin-dependent kinase inhibitors known as INK4A (p16), INK4B (p15) and INK4C (p18) in multiple myeloma, we examined 20 primary myeloma samples (including one case of plasma cell leukaemia) using polymerase chain |
9012694 |
Human |
p15 |
plasma-cell leukaemia |
To study the structural integrity of the cyclin-dependent kinase inhibitors known as INK4A (p16), INK4B (p15) and INK4C (p18) in multiple myeloma, we examined 20 primary myeloma samples (including one case of plasma cell leukaemia) using polymerase chain |
9012694 |
Human |
ink4b |
myeloma |
To study the structural integrity of the cyclin-dependent kinase inhibitors known as INK4A (p16), INK4B (p15) and INK4C (p18) in multiple myeloma, we examined 20 primary myeloma samples (including one case of plasma cell leukaemia) using polymerase chain |
9012694 |
Human |
p15 |
myeloma |
To study the structural integrity of the cyclin-dependent kinase inhibitors known as INK4A (p16), INK4B (p15) and INK4C (p18) in multiple myeloma, we examined 20 primary myeloma samples (including one case of plasma cell leukaemia) using polymerase chain |
9012694 |
Human |
ink4b |
multiple myeloma |
To study the structural integrity of the cyclin-dependent kinase inhibitors known as INK4A (p16), INK4B (p15) and INK4C (p18) in multiple myeloma, we examined 20 primary myeloma samples (including one case of plasma cell leukaemia) using polymerase chain |
9012694 |
Human |
p15 |
multiple myeloma |
To study the structural integrity of the cyclin-dependent kinase inhibitors known as INK4A (p16), INK4B (p15) and INK4C (p18) in multiple myeloma, we examined 20 primary myeloma samples (including one case of plasma cell leukaemia) using polymerase chain |
9012694 |
Human |
p15 |
plasma-cell leukaemia |
The plasma cell leukaemia sample had homozygous deletions of the p15 and p16 genes (6%). |
9012694 |
Human |
p15 |
myeloma |
One myeloma case had a p15 gene homozygous deletion (6%) with an intact p16 gene. |
9012694 |
Human |
p15 |
multiple myeloma |
This is the first report that indicates that deletions of p15, p16 and p18 genes occur in some individuals with multiple myeloma (2/17 cases). |
9012694 |
Human |
p15 |
tumor |
Studies on the expression of these inhibitors in normal versus tumor human breast cancer cells revealed that although p27 and p16 are expressed at higher levels in tumor cells, p21 and p15 expression were higher in normal cells. |
9044834 |
Human |
p15 |
human breast cancer |
Studies on the expression of these inhibitors in normal versus tumor human breast cancer cells revealed that although p27 and p16 are expressed at higher levels in tumor cells, p21 and p15 expression were higher in normal cells. |
9044834 |
Human |
p15 |
tumor |
Levels of p15, p16, and p27 remained relatively constant throughout the cell cycle of normal and tumor cells. |
9044834 |
Human |
p15 |
esophageal tumors |
To determine the role and mode of inactivation of the p16 and p15 genes in human esophageal tumors, we examined alterations and expression of the alpha and beta forms of the p16 gene, 5' CpG island methylation of p16 exon 1 alpha, and alterations of |
9033652 |
Human |
p15 |
tumor |
Increases in specific cyclin-dependent kinase inhibitor steady-state mRNA levels were detected in p15, p18, p27, and p57 during tumor progression. |
9040936 |
Human |
p15 |
t-cell acute lymphoblastic leukemia |
Frequent and selective methylation of p15 and deletion of both p15 and p16 in T-cell acute lymphoblastic leukemia. |
9041181 |
Human |
p15 |
t-cell acute lymphoblastic leukemia (t-all) |
We recently found that in T-cell acute lymphoblastic leukemia (T-ALL), both the p15 and p16 genes are deleted at a high frequency, with p16 gene deletion occurring slightly more frequently than p15 gene deletion. |
9041181 |
Human |
p15 |
tumor |
These results lend strong support for a role of both p15 and p16 as tumor suppressors in T-ALL. |
9041181 |
Human |
p15 |
tumors |
Loss of heterozygosity (LOH) analysis was performed using eight polymorphic markers immediately surrounding CDKN2A, and showed a contiguous region of loss, with the two most commonly deleted markers being D9S1604, located between the p16 and p15 genes, at |
9049204 |
Human |
p15 |
oral cancer |
Epigenetic changes of tumor suppressor genes, P15, P16, VHL and P53 in oral cancer. |
12684640 |
Human |
p15 |
oral cancer |
Altogether, over 50% of the samples showed the CpG-island methylation modification in at least one of the three tumor suppressor genes, indicating that the frequent inactivation of these genes may be an important step during oral cancer development, and t |
12684640 |
Human |
p15 |
tumors |
Recent allelotyping of chemical-induced lung tumors in hybrid mice has detected loss of heterozygosity on chromosome 4 in a region involving the interferon-alpha (IFN-alpha gene cluster that is syntenic to human chromosome 9p21-22, the location of the p16 |
9054597 |
Mouse |
p15 |
tumors |
The purpose of the current investigation was to characterize the expression of p16 and p15 in lung tumors and tumor-derived cell lines induced in A/J mice by exposure to the tobacco-specific nitrosamine, 4-methylnitrosamino-1-(3-pyridyl)-1-butanone (NNK). |
9054597 |
Human |
p15 |
tumors |
Expression of p16 and p15 was detected in all primary lung tumors; however, levels of expression of p16 differed by up to 15-fold between tumors. |
9054597 |
Human |
p15 |
primary lung tumors |
Expression of p16 and p15 was detected in all primary lung tumors; however, levels of expression of p16 differed by up to 15-fold between tumors. |
9054597 |
Human |
mts2 |
hepatoma |
Alterations in the tumor suppressor genes p53, RB, p16/MTS1, and p15/MTS2 in human pancreatic cancer and hepatoma cell lines. |
9058294 |
Human |
p15 |
hepatoma |
Alterations in the tumor suppressor genes p53, RB, p16/MTS1, and p15/MTS2 in human pancreatic cancer and hepatoma cell lines. |
9058294 |
Human |
mts2 |
human pancreatic cancer |
Alterations in the tumor suppressor genes p53, RB, p16/MTS1, and p15/MTS2 in human pancreatic cancer and hepatoma cell lines. |
9058294 |
Human |
p15 |
human pancreatic cancer |
Alterations in the tumor suppressor genes p53, RB, p16/MTS1, and p15/MTS2 in human pancreatic cancer and hepatoma cell lines. |
9058294 |
Human |
p15 |
hepatoma |
There were no deletions of p16 and p15 in any of the hepatoma cell lines. |
9058294 |
Human |
p15 |
hepatoma |
These findings suggest that alterations in the p53, p16, and p15 genes are common in human pancreatic cancer cell lines, while p53 or RB mutations are common in hepatoma cell lines. |
9058294 |
Human |
p15 |
human pancreatic cancer |
These findings suggest that alterations in the p53, p16, and p15 genes are common in human pancreatic cancer cell lines, while p53 or RB mutations are common in hepatoma cell lines. |
9058294 |
Human |
p15 |
multiple myeloma |
Frequent hypermethylation of p16 and p15 genes in multiple myeloma. |
9116295 |
Human |
p15 |
hematopoietic malignancies |
In hematopoietic malignancies, deletion of p16/p15 locus has been shown to be highly specific to lymphoid, and more particularly from B-lineage malignancies except multiple myeloma (MM). |
9116295 |
Human |
p15 |
multiple myeloma (mm) |
In hematopoietic malignancies, deletion of p16/p15 locus has been shown to be highly specific to lymphoid, and more particularly from B-lineage malignancies except multiple myeloma (MM). |
9116295 |
Human |
p15 |
plasmacytoma |
Moreover, hypermethylation of p16/p15 was associated with blastic disease and concomitant hypermethylation of both genes may be pathogenetically related to plasmacytoma development. |
9116295 |
Human |
mts2 |
childhood acute lymphoblastic leukemia |
Incidence and clinical significance of CDKN2/MTS1/P16ink4A and MTS2/P15ink4B gene deletions in childhood acute lymphoblastic leukemia. |
9089742 |
Human |
mts2 |
pediatric acute lymphoblastic leukemia |
We have examined the incidence and clinical significance of deletions of two candidate tumor suppressor genes, CDKN2/MTS1/p16ink4A and MTS2/p15ink4B, in pediatric acute lymphoblastic leukemia (ALL). |
9089742 |
Human |
mts2 |
tumor |
We have examined the incidence and clinical significance of deletions of two candidate tumor suppressor genes, CDKN2/MTS1/p16ink4A and MTS2/p15ink4B, in pediatric acute lymphoblastic leukemia (ALL). |
9089742 |
Human |
ink4b |
tumor |
A group of cyclin-dependent kinase inhibitors, p15 (INK4B), p16 (INK4A), p18 (INK4C) and p19 (INK4D), are candidate tumor suppressor genes. |
9111168 |
Human |
p15 |
tumor |
A group of cyclin-dependent kinase inhibitors, p15 (INK4B), p16 (INK4A), p18 (INK4C) and p19 (INK4D), are candidate tumor suppressor genes. |
9111168 |
Human |
p15 |
prostate cancer |
MATERIALS AND METHODS: Thirty-two primary prostate cancer samples and two prostate cancer cell lines were examined for alterations of the p16, p15, p18, and p19 genes by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and Sout |
9112579 |
Human |
p15 |
primary prostate cancer |
MATERIALS AND METHODS: Thirty-two primary prostate cancer samples and two prostate cancer cell lines were examined for alterations of the p16, p15, p18, and p19 genes by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and Sout |
9112579 |
Human |
p15 |
leukemias |
Hypermethylation within the promoters of some genes appear to be an early event in the pathogenesis of neoplasia (ER, P15), while other genes seem to become methylated during the progression of leukemias (HIC1, c-abl). |
9130685 |
Human |
p15 |
epithelial ovarian tumors |
Alteration of p16 and p15 genes in common epithelial ovarian tumors. |
9133447 |
Human |
p15 |
tumors |
Homozygous gene deletion, evaluated by differential PCR analysis, was found in 2 tumors for the p16 gene and in 1 tumor for the p15 gene among 70 ovarian tumors examined. |
9133447 |
Human |
p15 |
ovarian tumors |
Homozygous gene deletion, evaluated by differential PCR analysis, was found in 2 tumors for the p16 gene and in 1 tumor for the p15 gene among 70 ovarian tumors examined. |
9133447 |
Human |
p15 |
tumor |
Homozygous gene deletion, evaluated by differential PCR analysis, was found in 2 tumors for the p16 gene and in 1 tumor for the p15 gene among 70 ovarian tumors examined. |
9133447 |
Human |
p15 |
tumors |
PCR-SSCP analysis detected point mutations in p16 in 4 tumors and in p15 in 1 tumor. |
9133447 |
Human |
p15 |
tumor |
PCR-SSCP analysis detected point mutations in p16 in 4 tumors and in p15 in 1 tumor. |
9133447 |
Human |
cdkn2b |
melanoma |
In this study, we examined whether two other potential tumor suppressors, CDKN2B and p19ARF, which also map within the 9p21 region, play a role in the development of familial melanoma. |
9135995 |
Human |
cdkn2b |
tumor |
In this study, we examined whether two other potential tumor suppressors, CDKN2B and p19ARF, which also map within the 9p21 region, play a role in the development of familial melanoma. |
9135995 |
Human |
cdkn2b |
melanoma |
We conclude either that another melanoma susceptibility gene exists within this chromosomal area or that mutations in noncoding regions of CDKN2A, CDKN2B, or p19ARF predispose to melanoma. |
9135995 |
Human |
p15 |
adult t-cell leukemia |
Deletions of p15 and/or p16 genes as a poor-prognosis factor in adult T-cell leukemia. |
9164185 |
Human |
p15 |
adult t-cell leukemia |
PURPOSE: To determine the frequency of the deletions of p15/p16 genes in adult T-cell leukemia (ATL) cells and to evaluate their value in the diagnosis of clinical subtypes of ATL patients and the prediction of their clinical outcome. |
9164185 |
Human |
cdkn2b |
cutaneous melanoma |
Screening of germline mutations in the CDKN2A and CDKN2B genes in Swedish families with hereditary cutaneous melanoma. |
9168184 |
Human |
cdkn2b |
melanoma |
The tumor suppressor genes CDKN2A and CDKN2B have been mapped to the 9p21 region, and genetic analyses have revealed the presence of germline CDKN2A alterations in melanoma families. |
9168184 |
Human |
cdkn2b |
melanoma |
PURPOSE: The present investigation was carried out to determine the frequencies of CDKN2A and CDKN2B germline gene mutations among members in a population-based cohort of Swedish melanoma families (i.e., melanoma kindreds). |
9168184 |
Human |
mts2 |
pituitary adenomas |
Chromosome 9p deletions in invasive and noninvasive nonfunctional pituitary adenomas: the deleted region involves markers outside of the MTS1 and MTS2 genes. |
9205080 |
Human |
mts2 |
tumor |
However, multiplex PCR analysis (MTS1 and MTS2) and the presence of a 3' untranslated region polymorphism in MTS1 suggested that neither of these tumor suppressor genes was homozygously deleted. |
9205080 |
Human |
p15 |
tumors |
In order to clarify the significance of p16 gene (CDKN2) inactivation and its disease specificity among hematopoietic tumors, configurations of the p16 gene as well as those of the adjacent p15 and interferon alpha (IFN alpha) genes were examined in prima |
9209389 |
Human |
p15 |
other tumor |
This result suggests the presence of at least one other tumor suppressor gene at 9p21, apart from the p16 and p15 genes, which may be of importance to the development of neuroblastoma. |
9216721 |
Human |
p15 |
neuroblastoma |
This result suggests the presence of at least one other tumor suppressor gene at 9p21, apart from the p16 and p15 genes, which may be of importance to the development of neuroblastoma. |
9216721 |
Human |
p15 |
t-cell acute lymphoblastic leukemia |
Shortened survival after relapse in T-cell acute lymphoblastic leukemia patients with p16/p15 deletions. p16 Alterations were detected in > 60% of 103 primary T-ALL samples. |
9279366 |
Human |
ink4b |
tumors |
Recently two cyclin-dependent kinase inhibitors, known as P16 (INK4A/MTS1) and P15 (INK4B/MTS2), which map to 9p21, have been found deleted in a wide range of tumors and particularly in leukemic cells. |
9324291 |
Human |
mts2 |
tumors |
Recently two cyclin-dependent kinase inhibitors, known as P16 (INK4A/MTS1) and P15 (INK4B/MTS2), which map to 9p21, have been found deleted in a wide range of tumors and particularly in leukemic cells. |
9324291 |
Human |
p15 |
tumors |
Recently two cyclin-dependent kinase inhibitors, known as P16 (INK4A/MTS1) and P15 (INK4B/MTS2), which map to 9p21, have been found deleted in a wide range of tumors and particularly in leukemic cells. |
9324291 |
Human |
p15 |
b-chronic lymphocytic leukemias |
We report here Southern blot analyses of cyclin-dependent kinase inhibitors (P16, P15, P21, and P27) status in primary tumoral cells of 121 patients with acute lymphoblastic leukemias, 85 patients with acute myeloid leukemias and 42 patients with B-chroni |
9324291 |
Human |
p15 |
acute myeloid leukemias |
We report here Southern blot analyses of cyclin-dependent kinase inhibitors (P16, P15, P21, and P27) status in primary tumoral cells of 121 patients with acute lymphoblastic leukemias, 85 patients with acute myeloid leukemias and 42 patients with B-chroni |
9324291 |
Human |
p15 |
acute lymphoblastic leukemias |
We report here Southern blot analyses of cyclin-dependent kinase inhibitors (P16, P15, P21, and P27) status in primary tumoral cells of 121 patients with acute lymphoblastic leukemias, 85 patients with acute myeloid leukemias and 42 patients with B-chroni |
9324291 |
Human |
p15 |
head and neck squamous cell carcinomas |
AIMS: To study the homozygous deletion and methylation status of the 5' CpG island of the p16 and p15 genes (9p21) in a set of primary advanced head and neck squamous cell carcinomas (SCC) and to test whether inactivation of these genes by these mech |
9378820 |
Human |
p15 |
tumours |
RESULTS: The p16 and p15 genes were homozygously deleted in 20% and 10% of the tumours, respectively. |
9378820 |
Human |
p15 |
tumor |
BACKGROUND: It has been suggested that cyclin-dependent kinase inhibitors (CDKIs), including p16 and p15, are tumor suppressor genes. |
9366289 |
Human |
p15 |
gastric carcinoma |
However, little is known about the status of p16 and p15 genes, including methylation of the promoter region, in gastric carcinoma. |
9366289 |
Human |
p15 |
tumors |
METHODS: Thirty-six primary gastric tumors and 9 gastric carcinoma cell lines were examined for alterations of the p16 and p15 genes. |
9366289 |
Human |
p15 |
gastric carcinoma |
METHODS: Thirty-six primary gastric tumors and 9 gastric carcinoma cell lines were examined for alterations of the p16 and p15 genes. |
9366289 |
Human |
p15 |
primary tumor |
In contrast, no deletions were detected in 36 primary gastric tumors, and one primary tumor showed rearrangements of the p16 and p15 genes. |
9366289 |
Human |
p15 |
tumors |
In contrast, no deletions were detected in 36 primary gastric tumors, and one primary tumor showed rearrangements of the p16 and p15 genes. |
9366289 |
Human |
p15 |
tumors |
Two gastric carcinoma cell lines showed a point mutation and an insertional mutation of the p16 gene, respectively; however, no point mutations were noted for the p16 and p15 genes in any of the primary gastric tumors. |
9366289 |
Human |
p15 |
gastric carcinoma |
Two gastric carcinoma cell lines showed a point mutation and an insertional mutation of the p16 gene, respectively; however, no point mutations were noted for the p16 and p15 genes in any of the primary gastric tumors. |
9366289 |
Human |
p15 |
gastric carcinoma |
Constitutive levels of p16 mRNA expression in gastric carcinoma cell lines were quite heterogeneous; four gastric carcinoma cell lines had no detectable p16 mRNA and 6 gastric carcinoma cell lines had negligible expression of p15 mRNA. |
9366289 |
Human |
p15 |
gastric carcinomas |
CONCLUSIONS: Deletions or mutations of the p16 and p15 genes are uncommon in primary gastric carcinomas. |
9366289 |
Human |
cdkn2b |
b-cell chronic lymphocytic leukaemia |
De novo methylation of tumour suppressor genes CDKN2A and CDKN2B is a rare finding in B-cell chronic lymphocytic leukaemia. |
9375748 |
Human |
cdkn2b |
b-cell chronic lymphocytic leukaemia |
We examined CDKN2A methylation status at diagnosis in 42 B-cell chronic lymphocytic leukaemia (CLL) patients, in 19 cases the CDKN2B methylation status was also analysed. |
9375748 |
Human |
p15 |
tumors |
We investigated the status and expression of p16, p15, CCND1, CDK4 and RB genes in the Ewing family of tumors. |
9393981 |
Human |
mts2 |
childhood acute lymphoblastic leukemia |
Methylation of the multi tumor suppressor gene-2 (MTS2, CDKN1, p15INK4B) in childhood acute lymphoblastic leukemia. |
9399648 |
Human |
mts2 |
cancers |
The multi tumor suppressor genes MTS1 (CDKN2 p16INK4A) and MTS2 (CDKN1, p15INK4B) located at 9p21-22 are inactivated in some human cancers via several mechanisms including deletion and hypermethylation. |
9399648 |
Human |
mts2 |
childhood acute lymphoblastic leukemia |
We have investigated the deletion and methylation status of MTS1 and MTS2 in childhood acute lymphoblastic leukemia (ALL) of both T-cell (17 cases) and B-cell phenotypes (29 cases), and p16INK4A and p15INK4B mRNA expression in 36 of these cases. |
9399648 |
Human |
cdkn2b |
melanoma |
Analysis of the CDKN2A, CDKN2B and CDK4 genes in 48 Australian melanoma kindreds. |
9416844 |
Human |
cdkn2b |
melanoma |
In none of the 'CDKN2A-negative' families was melanoma found to segregate with either an untranscribed CDKN2A allele, an R24C CDK4 mutation, a CDKN2B mutation, or an E1beta mutation. |
9416844 |
Human |
p15 |
acute leukemia |
Alterations of p16 and p15 genes in acute leukemia with MLL gene rearrangements and their correlation with clinical features. p16 and p15 genes are putative tumor suppressor genes located on chromosome 9p21. |
9447829 |
Human |
p15 |
acute leukemias |
In acute leukemias, alterations of p16 and p15 genes have been reported to occur exclusively in lymphoid lineage. |
9447829 |
Human |
p15 |
acute leukemias |
We analyzed alterations of p16 and p15 genes in 46 acute leukemias with MLL gene rearrangements by Southern blot analysis, and investigated the association with clinical characteristics. |
9447829 |
Human |
p15 |
acute lymphoblastic leukemias (alls) |
We identified homozygous deletion of p16 and p15 genes in five (19%) of 27 acute lymphoblastic leukemias (ALLs) and in two (11%) of 19 acute myeloid leukemias (AMLs). |
9447829 |
Human |
p15 |
acute myeloid leukemias (amls) |
We identified homozygous deletion of p16 and p15 genes in five (19%) of 27 acute lymphoblastic leukemias (ALLs) and in two (11%) of 19 acute myeloid leukemias (AMLs). |
9447829 |
Human |
p15 |
acute leukemias |
Our results suggest that alterations of p16 and p15 genes are involved in a subset of acute leukemias with MLL gene rearrangement not only of lymphoid but also of myeloid phenotype. |
9447829 |
Human |
p15 |
tumor |
New light may be shed on the role of the p16 locus in tumor development by the recent finding that an alternative transcript from the p16INK4a gene encodes p19ARF, a negative regulator of cell cycle progression which is unrelated to p16 and p15 and does n |
9552410 |
Human |
p15 |
primary breast cancers |
We have examined the genomic status of two recently isolated p16-related CDK inhibitors, p15 and p18, in 15 normal and 73 tumor-derived cell lines established from 23 different tissues, as well as 26 invasive primary breast cancers and 20 acute myelogenou |
8570224 |
Human |
p15 |
acute myelogenous leukemias |
We have examined the genomic status of two recently isolated p16-related CDK inhibitors, p15 and p18, in 15 normal and 73 tumor-derived cell lines established from 23 different tissues, as well as 26 invasive primary breast cancers and 20 acute myelogenou |
8570224 |
Human |
p15 |
primary tumors |
We have examined the genomic status of two recently isolated p16-related CDK inhibitors, p15 and p18, in 15 normal and 73 tumor-derived cell lines established from 23 different tissues, as well as 26 invasive primary breast cancers and 20 acute myelogenou |
8570224 |
Human |
p15 |
tumor |
We have examined the genomic status of two recently isolated p16-related CDK inhibitors, p15 and p18, in 15 normal and 73 tumor-derived cell lines established from 23 different tissues, as well as 26 invasive primary breast cancers and 20 acute myelogenou |
8570224 |
Human |
cdkn2b |
tumours |
Subsequently, presence of deletions in the other studied regions, (epi)genetic changes in p14ARF, CDKN2A and CDKN2B, as well as histological features, were associated to these tumours. |
14507338 |
Human |
mts2 |
pancreatic tumors |
Frequent codeletion of p16/MTS1 and p15/MTS2 and genetic alterations in p16/MTS1 in pancreatic tumors. |
8613012 |
Human |
p15 |
pancreatic tumors |
Frequent codeletion of p16/MTS1 and p15/MTS2 and genetic alterations in p16/MTS1 in pancreatic tumors. |
8613012 |
Human |
mts2 |
pancreatic tumors |
To directly investigate genetic alterations and expression of p16/MTS1 and p15/MTS2, this study surveyed pancreatic tumors. |
8613012 |
Human |
p15 |
pancreatic tumors |
To directly investigate genetic alterations and expression of p16/MTS1 and p15/MTS2, this study surveyed pancreatic tumors. |
8613012 |
Human |
mts2 |
pancreatic adenocarcinoma |
RESULTS: The analysis of pancreatic adenocarcinoma (19 cell lines and 3 xenografts) for p16/MTS1 and p15/MTS2 revealed homozygous deletions in 10 of 22 cases (46%) (7 cell lines and 3 xenografts) involving both genes. |
8613012 |
Human |
p15 |
pancreatic adenocarcinoma |
RESULTS: The analysis of pancreatic adenocarcinoma (19 cell lines and 3 xenografts) for p16/MTS1 and p15/MTS2 revealed homozygous deletions in 10 of 22 cases (46%) (7 cell lines and 3 xenografts) involving both genes. |
8613012 |
Human |
p15 |
acute leukaemias |
Mutational analysis of the p15 and p16 genes in acute leukaemias. |
8616035 |
Human |
p15 |
tumour |
Recently the p16 and related p15 genes have been described as candidate tumour suppressors at chromosome 9p21. |
8616035 |
Human |
p15 |
acute myeloid leukaemia |
In order to determine whether these genes are more widely involved in haematological malignancies, we have investigated a total of 84 samples that did not have homozygous p16 or p15 deletions from patients with acute lymphoid leukaemia (n=13), acute myelo |
8616035 |
Human |
p15 |
chronic myeloid leukaemia |
In order to determine whether these genes are more widely involved in haematological malignancies, we have investigated a total of 84 samples that did not have homozygous p16 or p15 deletions from patients with acute lymphoid leukaemia (n=13), acute myelo |
8616035 |
Human |
p15 |
blast crisis |
In order to determine whether these genes are more widely involved in haematological malignancies, we have investigated a total of 84 samples that did not have homozygous p16 or p15 deletions from patients with acute lymphoid leukaemia (n=13), acute myelo |
8616035 |
Human |
p15 |
acute lymphoid leukaemia |
In order to determine whether these genes are more widely involved in haematological malignancies, we have investigated a total of 84 samples that did not have homozygous p16 or p15 deletions from patients with acute lymphoid leukaemia (n=13), acute myelo |
8616035 |
Human |
p15 |
haematological malignancies |
In order to determine whether these genes are more widely involved in haematological malignancies, we have investigated a total of 84 samples that did not have homozygous p16 or p15 deletions from patients with acute lymphoid leukaemia (n=13), acute myelo |
8616035 |
Human |
p15 |
acute leukaemias |
These data show that inactivation of either the p15 or p16 gene by point mutation is a very uncommon event in acute leukaemias. |
8616035 |
Human |
p15 |
osteosarcoma |
Alterations of the p15, p16,and p18 genes in osteosarcoma. |
8603340 |
Human |
p15 |
brain tumors |
Infrequent alterations of the p15, p16, CDK4 and cyclin D1 genes in non-astrocytic human brain tumors. |
8621248 |
Human |
p15 |
meningiomas |
In this study, p15, p16, CDK4 and cyclin D1 genes were analyzed in 69 nonastrocytic human brain tumors, including 17 oligodendrogliomas, 16 medulloblastomas/primitive neuroectodermal tumors (PNETs), 14 ependymomas and 22 meningiomas. |
8621248 |
Human |
p15 |
primitive neuroectodermal tumors (pnets) |
In this study, p15, p16, CDK4 and cyclin D1 genes were analyzed in 69 nonastrocytic human brain tumors, including 17 oligodendrogliomas, 16 medulloblastomas/primitive neuroectodermal tumors (PNETs), 14 ependymomas and 22 meningiomas. |
8621248 |
Human |
p15 |
tumors |
Southern blot analysis of DNA from frozen samples showed no homozygous deletions in p15 or p16 genes in any of these tumors. |
8621248 |
Human |
p15 |
oligodendroglioma |
No mobility shift was found by PCR-single-strand conformation polymorphism (PCR-SSCP) analysis in exons 1 and 2 of the p15 gene and exons 1 and 2 of the p16 genes, except for one oligodendroglioma. |
8621248 |
Human |
p15 |
lymphoid malignancies |
Because of p18's structural and functional homology to p16 and p15, we hypothesized that it may also function as a tumor suppressor gene in some lymphoid malignancies. |
8637248 |
Human |
p15 |
lymphoblastic lymphomas |
None of the lymphoid tumors studied possessed deletions of p18, including a group of lymphoblastic lymphomas which we previously reported to have deletions of p16 and p15. |
8637248 |
Human |
p15 |
lymphoid tumors |
None of the lymphoid tumors studied possessed deletions of p18, including a group of lymphoblastic lymphomas which we previously reported to have deletions of p16 and p15. |
8637248 |
Human |
ink4b |
leukemia |
Deletion or lack of expression of CDKN2 (CDK4I/MTS1/INK4A) and MTS2 (INK4B) in acute lymphoblastic leukemia cell lines reflects the phenotype of the uncultured primary leukemia cells. |
8618438 |
Human |
mts2 |
leukemia |
Deletion or lack of expression of CDKN2 (CDK4I/MTS1/INK4A) and MTS2 (INK4B) in acute lymphoblastic leukemia cell lines reflects the phenotype of the uncultured primary leukemia cells. |
8618438 |
Human |
ink4b |
acute lymphoblastic leukemia |
Deletion or lack of expression of CDKN2 (CDK4I/MTS1/INK4A) and MTS2 (INK4B) in acute lymphoblastic leukemia cell lines reflects the phenotype of the uncultured primary leukemia cells. |
8618438 |
Human |
mts2 |
acute lymphoblastic leukemia |
Deletion or lack of expression of CDKN2 (CDK4I/MTS1/INK4A) and MTS2 (INK4B) in acute lymphoblastic leukemia cell lines reflects the phenotype of the uncultured primary leukemia cells. |
8618438 |
Human |
p15 |
leukemias |
We report that in gliomas and, to a striking degree, in leukemias, the p15 gene is commonly inactivated in association with promoter region hypermethylation involving multiple sites in a 5'-CpG island. |
8631003 |
Human |
p15 |
leukemia |
In selected leukemia cell lines, p15 inactivation correlates with known resistance to the growth-suppressive effects of transforming growth factor-beta. |
8631003 |
Human |
p15 |
cancer |
However, the order of the MTAP, p16, p15, and IFNA genes on chromosome 9p is uncertain, and the molecular basis for MTAP deficiency in cancer is unknown. |
8650244 |
Human |
mts2 |
hematological malignancies |
The genes for the CDK4/6-inhibitors p16INK4A/MTS1 and p15INK4B/MTS2 are frequently deleted in hematological malignancies. |
8628020 |
Human |
mts2 |
lymphoid malignancies |
Inactivation of multiple tumor-suppressor genes involved in negative regulation of the cell cycle, MTS1/p16INK4A/CDKN2, MTS2/p15INK4B, p53, and Rb genes in primary lymphoid malignancies. |
8652807 |
Human |
mts2 |
cancers |
However, among these negative regulators in cell cycle control, only 4 have been shown to be consistently involved in the development of human cancers as tumor suppressors: Rb (Retinoblastoma susceptibility protein), p53, and two recently identified cycli |
8652807 |
Human |
mts2 |
tumor |
However, among these negative regulators in cell cycle control, only 4 have been shown to be consistently involved in the development of human cancers as tumor suppressors: Rb (Retinoblastoma susceptibility protein), p53, and two recently identified cycli |
8652807 |
Human |
cdkn2b |
childhood rhabdomyosarcoma |
Analysis of cyclin-dependent kinase inhibitor genes (CDKN2A, CDKN2B, and CDKN2C) in childhood rhabdomyosarcoma. p16INK4A, p15INK4B, and p18 proteins are highly specific inhibitors of cyclin-dependent serine/threonine kinase (CDK) activities required for G |
8703847 |
Human |
cdkn2b |
cancer |
We looked for homozygous deletions of CDKN2A, CDKN2B (p15INK4B), and CDKN2C (p18) in 12 primary rhabdomyosarcoma (RMS) specimens and in five cell lines established from this cancer type. |
8703847 |
Human |
cdkn2b |
rhabdomyosarcoma |
We looked for homozygous deletions of CDKN2A, CDKN2B (p15INK4B), and CDKN2C (p18) in 12 primary rhabdomyosarcoma (RMS) specimens and in five cell lines established from this cancer type. |
8703847 |
Human |
mts2 |
acute lymphoblastic leukemia |
Homozygous deletions of p16/MTS1 and p15/MTS2 genes are frequent in t(1;19)-negative but not in t(1;19)-positive B precursor acute lymphoblastic leukemia in childhood. |
8683987 |
Human |
p15 |
acute lymphoblastic leukemia |
Homozygous deletions of p16/MTS1 and p15/MTS2 genes are frequent in t(1;19)-negative but not in t(1;19)-positive B precursor acute lymphoblastic leukemia in childhood. |
8683987 |
Human |
p15 |
acute lymphoblastic leukemia (all) |
We analyzed 60 B precursor acute lymphoblastic leukemia (ALL) primary samples and 15 cell lines for homozygous deletions of p16 and p15 genes and mutations of p16 gene. |
8683987 |
Human |
mts2 |
myxoid chondrosarcoma |
Partial deletions of the CDKN2 and MTS2 putative tumor suppressor genes in a myxoid chondrosarcoma. |
8689636 |
Human |
mts2 |
chondrosarcoma |
In addition, we have also shown the presence of deletions involving the CDKN2 and the MTS2 putative tumor suppressor genes in these chondrosarcoma cell lines. |
8689636 |
Human |
mts2 |
chondrosarcoma |
The above studies were extended to other chondrosarcoma cell lines and primary tumors, where similar deletions of the CDKN2 and MTS2 genes were found to be present (unpublished data). |
8689636 |
Human |
mts2 |
primary tumors |
The above studies were extended to other chondrosarcoma cell lines and primary tumors, where similar deletions of the CDKN2 and MTS2 genes were found to be present (unpublished data). |
8689636 |
Human |
mts2 |
leukemias |
Recently, two putative tumor suppressor gene(s) CDKN2 and MTS2 have been mapped to the 9p21 region, and shown to be deleted in a large number of tumors including leukemias, melanomas, bladder cancers and brain tumors. |
8689637 |
Human |
mts2 |
brain tumors |
Recently, two putative tumor suppressor gene(s) CDKN2 and MTS2 have been mapped to the 9p21 region, and shown to be deleted in a large number of tumors including leukemias, melanomas, bladder cancers and brain tumors. |
8689637 |
Human |
mts2 |
tumors |
Recently, two putative tumor suppressor gene(s) CDKN2 and MTS2 have been mapped to the 9p21 region, and shown to be deleted in a large number of tumors including leukemias, melanomas, bladder cancers and brain tumors. |
8689637 |
Human |
mts2 |
melanomas |
Recently, two putative tumor suppressor gene(s) CDKN2 and MTS2 have been mapped to the 9p21 region, and shown to be deleted in a large number of tumors including leukemias, melanomas, bladder cancers and brain tumors. |
8689637 |
Human |
mts2 |
bladder cancers |
Recently, two putative tumor suppressor gene(s) CDKN2 and MTS2 have been mapped to the 9p21 region, and shown to be deleted in a large number of tumors including leukemias, melanomas, bladder cancers and brain tumors. |
8689637 |
Human |
mts2 |
myxoid chondrosarcoma |
We have previously reported a similar 9p21 abnormality and deletions of the CDKN2 and MTS2 genes in a myxoid chondrosarcoma cell line and its subclones. |
8689637 |
Human |
mts2 |
chondrosarcoma |
In addition, four of the seven chondrosarcoma cell lines also showed deletions of the CDKN2 and/or MTS2 putative tumor suppressor genes, or the absence of the CDKN2 protein product. |
8689637 |
Human |
mts2 |
tumor |
These data suggest that chromosome 9p21 abnormality, and deletions of the CDKN2 and MTS2 tumor suppressor genes may be a significant event in the development of chondrosarcomas. |
8689637 |
Human |
p15 |
cancers |
These antigens are classified as 1) melanocyte specific melanosomal proteins (MART-1, gp100, tyrosinase and TRP-1), 2) proteins expressed in testis and a variety of cancers (MAGE-1, MAGE-3, BAGE and GAGE), 3) tumor specific mutated proteins (beta-catenin, |
8683899 |
Human |
p15 |
tumor |
These antigens are classified as 1) melanocyte specific melanosomal proteins (MART-1, gp100, tyrosinase and TRP-1), 2) proteins expressed in testis and a variety of cancers (MAGE-1, MAGE-3, BAGE and GAGE), 3) tumor specific mutated proteins (beta-catenin, |
8683899 |
Human |
p15 |
carcinoma |
Immortalized A1N4 and HBL100 cells, as well as ER+, MCF-7 carcinoma cells, expressed high levels of p15 mRNA. |
8712723 |
Human |
mts2 |
tumor |
Candidate tumor suppressor genes, Mts1 (multiple tumor suppressor 1) and Mts2 have been mapped to this region. |
8764131 |
Human |
p15 |
primary malignant lymphoma |
Primary malignant lymphoma of the brain: demonstration of frequent p16 and p15 gene deletions. |
8698617 |
Human |
mts-2 |
tumor |
The p15 (MTS-2) gene, another candidate tumor suppressor gene located in the vicinity of the p16 gene, to which it shows structural and functional similarity, was also found to be deleted in 4 cases. |
8698617 |
Human |
p15 |
tumor |
The p15 (MTS-2) gene, another candidate tumor suppressor gene located in the vicinity of the p16 gene, to which it shows structural and functional similarity, was also found to be deleted in 4 cases. |
8698617 |
Human |
p15 |
primary malignant lymphoma |
Our frequent detection (80%) of p16 and p15 gene deletions might suggest that these deletions are closely related to carcinogenesis in primary malignant lymphoma of the brain. |
8698617 |
Human |
p15 |
malignant astrocytomas |
Abnormalities of p16, p15 and CDK4 genes in recurrent malignant astrocytomas. |
8760309 |
Human |
p15 |
recurrent tumors |
The primary and recurrent tumors in Group A did not show structural alterations in the p16, p15 or CDK4 genes, whereas homozygous codeletion of p16 and p15 was observed in both primary and recurrent tumors in Group B. |
8760309 |
Human |
p15 |
primary tumors |
The primary tumors in Group C had a normal profile of p16, p15 and CDK4 at presentation. |
8760309 |
Human |
p15 |
tumors |
Upon recurrence, however, the tumors sustained either deletion of p16 alone or codeletion of both p16 and p15 or amplification of CDK4. |
8760309 |
Human |
cdkn2b |
human malignant melanoma |
Transfection experiments with CDKN2A and CDKN2B cDNA expression vectors, using mouse A9 cells and three human malignant melanoma cell lines as recipients, provided further evidence in support of this hypothesis. |
8761411 |
Human |
p15 |
cancer |
In this study, we demonstrate the use of MSP to identify promoter region hypermethylation changes associated with transcriptional inactivation in four important tumor suppressor genes (p16, p15, E-cadherin, and von Hippel-Lindau) in human cancer. |
8790415 |
Human |
p15 |
gastric carcinoma |
We examined the genetic status and the expression of CDK inhibitors (p21, p27, p16 and p15), CDK2 and cyclins (A, D1 and E) in eight gastric carcinoma cell lines, in comparison with the status of p53 gene alterations. |
8797888 |
Human |
p15 |
gastric carcinoma |
Homozygous deletion of the p16 and p15 genes was detected in two (MKN-45 and HSC-39) of the eight gastric carcinoma cell lines, p16 protein was not expressed in three cell lines (MKN-28, MKN-74 and KATO-III), as well as MKN-45 and HSC-39. |
8797888 |
Human |
p15 ink4b |
leukemias |
A novel pre-B acute lymphoblastic leukemia cell line with chromosomal translocation between p16(INK4A)/p15(INK4B) tumor suppressor and immunoglobulin heavy chain genes: TGFbeta/IL-7 inhibitory signaling mechanism. p16 INK4A and/or p15 INK4B genes are freq |
8847892 |
Human |
p15 ink4b |
other cancers |
A novel pre-B acute lymphoblastic leukemia cell line with chromosomal translocation between p16(INK4A)/p15(INK4B) tumor suppressor and immunoglobulin heavy chain genes: TGFbeta/IL-7 inhibitory signaling mechanism. p16 INK4A and/or p15 INK4B genes are freq |
8847892 |
Human |
p15 |
melanoma |
The present paper describes mutational analysis by polymerase chain reaction-single-strand conformation polymorphism (PCR/SSCP) and nucleotide sequence analysis of the genes coding for the p15, p53 and N-ras proteins in 26 metastases from 25 melanoma pati |
8826861 |
Human |
p15 |
metastases |
The present paper describes mutational analysis by polymerase chain reaction-single-strand conformation polymorphism (PCR/SSCP) and nucleotide sequence analysis of the genes coding for the p15, p53 and N-ras proteins in 26 metastases from 25 melanoma pati |
8826861 |
Human |
p15 |
parathyroid adenomas |
Loss of chromosome arm 9p DNA and analysis of the p16 and p15 cyclin-dependent kinase inhibitor genes in human parathyroid adenomas. |
8855819 |
Human |
p15 |
parathyroid adenomas |
Because inactivation of the p16 or p15 genes might be expected to result in oncogenic consequences similar to those from cyclin D1 overexpression, we examined 25 parathyroid adenomas for 1) allelic loss of polymorphic DNA loci on chromosome arm 9p, 2) hom |
8855819 |
Human |
p15 |
adenomas |
Heterozygous allelic loss at 9p was observed in 4 of 25 adenomas (16%); their smallest shared region of deletion was 9p21-pter, which includes both the p16 and p15 genes. |
8855819 |
Human |
p15 |
cancers |
However, single strand conformational polymorphism analysis of all 3 exons of the p16 gene and both exons of the p15 gene failed to demonstrate mutation in any of the 25 cases, and homozygous deletions of the p16 and p15 genes, which are present in some h |
8855819 |
Human |
p15 |
parathyroid tumors |
However, single strand conformational polymorphism analysis of all 3 exons of the p16 gene and both exons of the p15 gene failed to demonstrate mutation in any of the 25 cases, and homozygous deletions of the p16 and p15 genes, which are present in some h |
8855819 |
Human |
p15 |
parathyroid adenomas |
These observations indicate that inactivating mutations or homozygous deletions of the p16 and p15 genes occur uncommonly, if ever, in parathyroid adenomas; however, loss of a different tumor suppressor gene (or genes) on 9p appears to contribute to the p |
8855819 |
Human |
p15 |
tumors |
These observations indicate that inactivating mutations or homozygous deletions of the p16 and p15 genes occur uncommonly, if ever, in parathyroid adenomas; however, loss of a different tumor suppressor gene (or genes) on 9p appears to contribute to the p |
8855819 |
Human |
p15 |
malignant melanoma |
Expression of the tumour suppressor genes p15 and p16 in malignant melanoma. |
8873047 |
Human |
p15 |
malignant melanoma |
Recent evidence has suggested the presence of a malignant melanoma (MM)-related gene on human chromosome 9p21, the location of the putative tumour suppressor genes p15 and p16. |
8873047 |
Human |
cdkn2b |
bladder cancer |
The 9p21 region in bladder cancer cell lines: large homozygous deletion inactivate the CDKN2, CDKN2B and MTAP genes. |
8873383 |
Human |
cdkn2b |
tumor |
The identification of two cell cycle regulators, CDKN2 and CDKN2B, that map to the common region of deletion has prompted the hypothesis that they are critical tumor suppressor genes in this malignancy. |
8873383 |
Human |
cdkn2b |
bladder cancer |
To more clearly determine the effect of these 9p21 alterations, we mapped the homozygous deletions and performed a detailed mutational and expression analysis for CDKN2, CDKN2B and a closely linked gene, methylthioadenoside phosphorylase (MTAP), in 16 est |
8873383 |
Human |
p15 |
glioma |
A comparative study of glioma cell lines for p16, p15, p53 and p21 gene alterations. |
8878451 |
Human |
p15 |
glioma |
A total of 10 glioma cell lines were examined for alterations of the p16, p15, p53 and p21 genes, which are tumor suppressor genes or candidates with direct or indirect CDK-inhibitory functions. |
8878451 |
Human |
p15 |
glioma |
When the states of the p16, p15 and p53 genes were compared among cell lines, all the cell lines showed abnormalities in at least 1 gene, often in 2 or 3 genes coincidentally, suggesting that dysfunction of these genes is closely related to glioma cell gr |
8878451 |
Human |
p15 |
primary tumor |
On examination of the primary tumor tissues, the same alterations of the p16/p15 and p53 genes as detected in the cell lines were demonstrated in all 6 cases examined: p16/p15 gene deletion in 1, p16 gene mutation in 1 and p53 gene mutations in 5 cases. |
8878451 |
Human |
p15 |
glioma |
This suggested that the p16/p15 and the p53 gene alterations and their combinations in at least some glioma cell lines reflected those in the primary glioma tissues. |
8878451 |
Human |
p15 |
esophageal tumors |
Alterations in the p16 and p15 cyclin kinase inhibitors, including point mutation and homozygous deletion, have been reported in primary esophageal tumors and/or tumor-derived cell lines. |
8893331 |
Human |
mts2 |
cancer |
Molecular analysis of the cyclin-dependent kinase inhibitor genes p15INK4b/MTS2, p16INK4/MTS1, p18 and p19 in human cancer cell lines. |
8938142 |
Human |
mts2 |
cancer |
Homozygous deletions of the p15INK4b/MTS2 gene were detected in 29 cancer cell lines. |
8938142 |
Human |
mts2 |
cancers |
One group includes p15INK4b/MTS2 and p16INK4/MTS1, in which genetic and epigenetic alterations might contribute to the development of human cancers. |
8938142 |
Human |
p15 |
hematopoietic malignancies |
The p16 and p15 CDKI genes are very frequently altered in a variety of cancers including hematopoietic malignancies. |
8946928 |
Human |
p15 |
cancers |
The p16 and p15 CDKI genes are very frequently altered in a variety of cancers including hematopoietic malignancies. |
8946928 |
Human |
mts2 |
primary carcinomas |
The multiple tumor suppressor 1 (MTS1) and 2 (MTS2) genes, located on chromosome 9p21, have been reported to be deleted or mutated in many malignant cell lines and in a high percentage of some primary carcinomas. |
8957063 |
Human |
ink4b |
medullary thyroid cancer |
A frequent mutation/polymorphism in tumor suppressor gene INK4B (MTS-2) in papillary and medullary thyroid cancer. |
8957499 |
Human |
mts-2 |
medullary thyroid cancer |
A frequent mutation/polymorphism in tumor suppressor gene INK4B (MTS-2) in papillary and medullary thyroid cancer. |
8957499 |
Human |
mts-2 |
tumor |
METHODS: Because MTS-2 encodes the tumor suppressor p15, a protein related to the transforming growth factor-beta inhibition of many epithelial cells such as thyrocytes, we investigated MTS-1 and MTS-2 genes in 87 thyroid cancers (29 papillary, 26 follicu |
8957499 |
Human |
p15 |
tumor |
METHODS: Because MTS-2 encodes the tumor suppressor p15, a protein related to the transforming growth factor-beta inhibition of many epithelial cells such as thyrocytes, we investigated MTS-1 and MTS-2 genes in 87 thyroid cancers (29 papillary, 26 follicu |
8957499 |
Human |
mts-2 |
thyroid cancers |
METHODS: Because MTS-2 encodes the tumor suppressor p15, a protein related to the transforming growth factor-beta inhibition of many epithelial cells such as thyrocytes, we investigated MTS-1 and MTS-2 genes in 87 thyroid cancers (29 papillary, 26 follicu |
8957499 |
Human |
p15 |
thyroid cancers |
METHODS: Because MTS-2 encodes the tumor suppressor p15, a protein related to the transforming growth factor-beta inhibition of many epithelial cells such as thyrocytes, we investigated MTS-1 and MTS-2 genes in 87 thyroid cancers (29 papillary, 26 follicu |
8957499 |
Human |
mts-2 |
thyroid tumors |
RESULTS: We failed to demonstrate homozygous deletions of MTS-1 and MTS-2 in thyroid tumors, but we demonstrated a highly frequent base pair exchange of the MTS-2 gene 27 codons upstream the 5' end of exon 2. |
8957499 |
Human |
p15 |
medullary thyroid cancer |
CONCLUSIONS: We conclude that base pair exchange at this site most likely has biologic importance for the tumor suppressor p15 and may contribute to tumorigenesis and lymphatic spread of differentiated and medullary thyroid cancer. |
8957499 |
Human |
mts2 |
ovarian tumors |
Inactivation of p16/CDKN2 and p15/MTS2 genes in different histological types and clinical stages of primary ovarian tumors. |
8980248 |
Human |
p15 |
ovarian tumors |
Inactivation of p16/CDKN2 and p15/MTS2 genes in different histological types and clinical stages of primary ovarian tumors. |
8980248 |
Human |
mts2 |
ovarian carcinoma |
To define the involvement of p16/CDKN2 and p15/MTS2 inactivation in ovarian tumorigenesis and the association of these inactivation events with histological types and clinical stages of ovarian tumors, we analyzed homozygous deletion and somatic mutation |
8980248 |
Human |
p15 |
ovarian carcinoma |
To define the involvement of p16/CDKN2 and p15/MTS2 inactivation in ovarian tumorigenesis and the association of these inactivation events with histological types and clinical stages of ovarian tumors, we analyzed homozygous deletion and somatic mutation |
8980248 |
Human |
mts2 |
ovarian tumors |
To define the involvement of p16/CDKN2 and p15/MTS2 inactivation in ovarian tumorigenesis and the association of these inactivation events with histological types and clinical stages of ovarian tumors, we analyzed homozygous deletion and somatic mutation |
8980248 |
Human |
p15 |
ovarian tumors |
To define the involvement of p16/CDKN2 and p15/MTS2 inactivation in ovarian tumorigenesis and the association of these inactivation events with histological types and clinical stages of ovarian tumors, we analyzed homozygous deletion and somatic mutation |
8980248 |
Human |
mts2 |
primary tumors |
We found homozygous deletions of p16/CDKN2 and p15/MTS2 in 6 (12%) and 5 (10%) primary tumors, respectively. |
8980248 |
Human |
p15 |
primary tumors |
We found homozygous deletions of p16/CDKN2 and p15/MTS2 in 6 (12%) and 5 (10%) primary tumors, respectively. |
8980248 |
Human |
mts2 |
primary tumor |
Somatic mutation of p16/CDKN2 was found in only 1 primary tumor, but mutation of p15/MTS2 was not detected in any sample. |
8980248 |
Human |
p15 |
primary tumor |
Somatic mutation of p16/CDKN2 was found in only 1 primary tumor, but mutation of p15/MTS2 was not detected in any sample. |
8980248 |
Human |
mts2 |
carcinomas |
Seven of 9 alterations in p16/CDKN2 and p15/MTS2 were observed in serous (3 of 12), endometrioid (3 of 9) and clear-cell (1 of 4) carcinomas. |
8980248 |
Human |
p15 |
carcinomas |
Seven of 9 alterations in p16/CDKN2 and p15/MTS2 were observed in serous (3 of 12), endometrioid (3 of 9) and clear-cell (1 of 4) carcinomas. |
8980248 |
Human |
mts2 |
ovarian tumors |
These results suggest that: (i) homozygous deletion is the main mechanism of inactivation of p16/CDKN2 and p15/MTS2 in ovarian tumorigenesis; (ii) inactivation of p16/CDKN2 and p15/MTS2 may be the histological type-specific events involved in ovarian tumo |
8980248 |
Human |
p15 |
ovarian tumors |
These results suggest that: (i) homozygous deletion is the main mechanism of inactivation of p16/CDKN2 and p15/MTS2 in ovarian tumorigenesis; (ii) inactivation of p16/CDKN2 and p15/MTS2 may be the histological type-specific events involved in ovarian tumo |
8980248 |
Human |
p15 |
lymphoma |
Role of the cyclin-dependent kinase 4 and 6 inhibitor gene family p15, p16, p18 and p19 in leukemia and lymphoma. |
9031081 |
Human |
p15 |
leukemia |
Role of the cyclin-dependent kinase 4 and 6 inhibitor gene family p15, p16, p18 and p19 in leukemia and lymphoma. |
9031081 |
Human |
mts2 |
cancer |
As the genes encoding the CDK4- and CDK6-inhibitors (CDK4/6-inhibitors) p16INK4A/CDKN2/MTS1 and p15INK4B/MTS2 have been found to be altered in many cancer cell lines and primary neoplastic tissues, CDK-inhibitors in general and CDK4/6-inhibitors in partic |
9031081 |
Human |
mts2 |
tumor |
As the genes encoding the CDK4- and CDK6-inhibitors (CDK4/6-inhibitors) p16INK4A/CDKN2/MTS1 and p15INK4B/MTS2 have been found to be altered in many cancer cell lines and primary neoplastic tissues, CDK-inhibitors in general and CDK4/6-inhibitors in partic |
9031081 |
Human |
p15 |
neoplasms |
The p15 and p16 genes map to a region frequently deleted in lymphoid neoplasms. |
9031081 |
Human |
p15 |
human esophageal carcinoma |
Out of eight human esophageal carcinoma cell lines, seven (67.5%) and six (75%) cell lines showed homozygous deletions of the p16 and p15 genes, respectively. |
9414383 |
Human |
mts2 |
non-small cell lung cancers |
In vivo occurrence of p16 (MTS1) and p15 (MTS2) alterations preferentially in non-small cell lung cancers. |
7834619 |
Human |
p15 |
non-small cell lung cancers |
In vivo occurrence of p16 (MTS1) and p15 (MTS2) alterations preferentially in non-small cell lung cancers. |
7834619 |
Human |
p15 |
lung cancer |
In the present study, alterations of p16 and/or p15, a p16-related cyclin-dependent kinase, were observed not only in lung cancer cell lines but also in the corresponding tumor specimens in vivo, excluding the possibility of in vitro artifacts. |
7834619 |
Human |
p15 |
tumor |
In the present study, alterations of p16 and/or p15, a p16-related cyclin-dependent kinase, were observed not only in lung cancer cell lines but also in the corresponding tumor specimens in vivo, excluding the possibility of in vitro artifacts. |
7834619 |
Human |
mts2 |
human leukemias |
Involvement of CDKN2 (p16INK4A/MTS1) and p15INK4B/MTS2 in human leukemias and lymphomas. |
7882348 |
Human |
mts2 |
lymphomas |
Involvement of CDKN2 (p16INK4A/MTS1) and p15INK4B/MTS2 in human leukemias and lymphomas. |
7882348 |
Human |
mts2 |
lymphoma |
In the primary tumors, homozygous deletions of both CDKN2 and MTS2 were found in 35% of the T-ALL/lymphoblastic lymphoma (8 of 23). |
7882348 |
Human |
mts2 |
primary tumors |
In the primary tumors, homozygous deletions of both CDKN2 and MTS2 were found in 35% of the T-ALL/lymphoblastic lymphoma (8 of 23). |
7882348 |
Human |
mts2 |
lymphoma |
These results are consistent with a role for CDKN2 and/or MTS2 in the pathogenesis of some lymphoid leukemia/lymphomas, particularly in T-ALL/lymphoblastic lymphoma. |
7882348 |
Human |
mts2 |
lymphoid leukemia |
These results are consistent with a role for CDKN2 and/or MTS2 in the pathogenesis of some lymphoid leukemia/lymphomas, particularly in T-ALL/lymphoblastic lymphoma. |
7882348 |
Human |
mts2 |
lymphomas |
These results are consistent with a role for CDKN2 and/or MTS2 in the pathogenesis of some lymphoid leukemia/lymphomas, particularly in T-ALL/lymphoblastic lymphoma. |
7882348 |
Human |
mts2 |
metastatic lung cancer |
Mutations in the p16INK4/MTS1/CDKN2, p15INK4B/MTS2, and p18 genes in primary and metastatic lung cancer. |
7882351 |
Human |
mts2 |
malignant gliomas |
Because MTS1/p16/CDKN2 and the homologous MTS2/p15 gene map to a region of chromosome 9p21, which is frequently deleted in malignant gliomas, we searched for lesions of these genes in primary biopsies of glioblastoma multiforme (GBM). |
7887443 |
Human |
p15 |
malignant gliomas |
Because MTS1/p16/CDKN2 and the homologous MTS2/p15 gene map to a region of chromosome 9p21, which is frequently deleted in malignant gliomas, we searched for lesions of these genes in primary biopsies of glioblastoma multiforme (GBM). |
7887443 |
Human |
mts2 |
glioblastoma multiforme |
Because MTS1/p16/CDKN2 and the homologous MTS2/p15 gene map to a region of chromosome 9p21, which is frequently deleted in malignant gliomas, we searched for lesions of these genes in primary biopsies of glioblastoma multiforme (GBM). |
7887443 |
Human |
p15 |
glioblastoma multiforme |
Because MTS1/p16/CDKN2 and the homologous MTS2/p15 gene map to a region of chromosome 9p21, which is frequently deleted in malignant gliomas, we searched for lesions of these genes in primary biopsies of glioblastoma multiforme (GBM). |
7887443 |
Human |
mts2 |
pediatric acute lymphoblastic leukemia |
Frequent deletion of p16INK4a/MTS1 and p15INK4b/MTS2 in pediatric acute lymphoblastic leukemia. |
7727766 |
Human |
mts2 |
adult t-cell leukemia |
Homozygous deletions of the p15 (MTS2) and p16 (CDKN2/MTS1) genes in adult T-cell leukemia. |
7742529 |
Human |
p15 |
adult t-cell leukemia |
Homozygous deletions of the p15 (MTS2) and p16 (CDKN2/MTS1) genes in adult T-cell leukemia. |
7742529 |
Human |
mts2 |
tumors |
The p15 (MTS2) and p16 (CDKN2/MTS1) genes located on chromosome 9p have been implicated as candidate tumor-suppressor genes in several types of tumors. |
7742529 |
Human |
p15 |
tumors |
The p15 (MTS2) and p16 (CDKN2/MTS1) genes located on chromosome 9p have been implicated as candidate tumor-suppressor genes in several types of tumors. |
7742529 |
Human |
p15 |
cancers |
The p15 and p16 CDKI genes are very frequently mutated in a variety of cancers. |
7757974 |
Human |
p15 |
uveal melanoma |
Contribution of germline mutations in BRCA2, P16(INK4A), P14(ARF) and P15 to uveal melanoma. |
12556369 |
Human |
p15 |
uveal melanomas |
Similarly, the association between cutaneous and uveal melanomas in some families, coupled with the high frequency of somatic deletions of the INK4A-ARF locus in uveal melanomas, strongly suggests that mutations in P16(INK4A) and P15 account for a proport |
12556369 |
Human |
p15 |
uveal melanoma |
METHODS: To examine this proposition, a systematically ascertained series of 385 patients with uveal melanoma were screened for germline mutations in BRCA2, P16(INK4A), P14(ARF), and P15. |
12556369 |
Human |
p15 |
uveal melanoma |
CONCLUSIONS: These findings suggest that less than 2% of cases of uveal melanoma can be ascribed to germline mutations in BRCA2, P16(INK4A), P14(ARF), or P15. |
12556369 |
Human |
mts2 |
tumor |
Recently, two genes, p16INK4A and p15INK4B (also called MTS1 and MTS2), have been localized in close proximity at the 9p21 locus, encoding cyclin-dependent kinases 4/6 inhibitors of relative molecular mass 16 kD and 15 kD, respectively and also found to b |
7795238 |
Human |
mts2 |
biliary tract cancers |
Mutations of p16Ink4/CDKN2 and p15Ink4B/MTS2 genes in biliary tract cancers. p16Ink4 and p15Ink4B are cyclin-dependent kinase 4 inhibitors and link to the regulation of cell cycle in mammalian cells. |
7796400 |
Human |
mts2 |
biliary tract cancers |
Twenty-five primary biliary tract cancers were examined for somatic mutations in p16Ink4/CDKN2, p15Ink4B/MTS2, p53, and K-ras genes and allelic loss of 9p21 by microsatellite analysis. |
7796400 |
Human |
mts2 |
biliary tract cancer |
We found frequent homozygous deletions in p16Ink4/CDKN2 and p15Ink4B/MTS2 genes in the biliary tract cancer cell lines. |
7796400 |
Human |
mts2 |
cancer |
Each cancer cell line had alteration of either p16Ink4/CDKN2, p15Ink4B/MTS2, or p53 genes. |
7796400 |
Human |
mts2 |
cancers |
In contrast, no mutation in the p15Ink4B/MTS2 gene, one base change in the K-ras gene, and one loss of heterozygosity at the IFN alpha locus in 25 cancers and one base change in the p53 gene in 19 cancers were observed. |
7796400 |
Human |
p15 |
childhood acute lymphoblastic leukemia |
We evaluated the mutational status of the p15, p16, and p18 genes in 103 childhood acute lymphoblastic leukemia (ALL) samples and correlated these results with both their clinical data and additional results concerning their loss of heterozygosity in the |
7606004 |
Human |
p15 |
non-small cell lung carcinoma |
Codeletion of p15 and p16 genes in primary non-small cell lung carcinoma. |
7606711 |
Human |
p15 |
non-small cell lung carcinoma (nsclc) |
Chromosome band 9p21 is deleted frequently in non-small cell lung carcinoma (NSCLC), and the p15 and p16 cyclin-dependent kinase-4 inhibitor genes map within this deletion region. |
7606711 |
Human |
p15 |
metastases |
Recent studies demonstrated deletion of p15 and p16 in NSCLC metastases and cell lines, suggesting a role for these genes in NSCLC progression. |
7606711 |
Human |
p15 |
tumors |
Codeletion of p15 and p16 was found in 15 of 18 NSCLCs, and 1 of the 3 tumors with normal p15 and p16 copy number had a nonsense mutation in exon 2 of p16. |
7606711 |
Human |
p15 |
malignant mesothelioma |
Codeletion of p15 and p16 in primary malignant mesothelioma. |
7630635 |
Human |
p15 |
other cancers |
The p15 and p16 CDK4 inhibitor genes map within the chromosome band 9p21 region deleted frequently in malignant mesothelioma and other cancers. p16 has been implicated recently as a potential target of 9p21 deletions in mesothelioma, but the role of this |
7630635 |
Human |
p15 |
malignant mesothelioma |
The p15 and p16 CDK4 inhibitor genes map within the chromosome band 9p21 region deleted frequently in malignant mesothelioma and other cancers. p16 has been implicated recently as a potential target of 9p21 deletions in mesothelioma, but the role of this |
7630635 |
Human |
p15 |
malignant mesothelioma |
These findings demonstrate that p15, p16 and/or a closely neighboring gene, are the targets of frequent chromosome 9p deletion in primary malignant mesothelioma. |
7630635 |
Human |
p15 |
glial tumor |
Taken together, these data indicate that inactivation by point mutation of these two cyclin-dependent kinase inhibitors is uncommon in glial tumor carcinogenesis, but that there may be a tumor suppressor gene on 9p in the vicinity of p16 and p15 genes. |
7630644 |
Human |
p15 |
t-cell lymphoma |
Homozygous deletions of either the p16 gene or both the p15 and p16 genes were observed in one diffuse large B-cell lymphoma cell line and two uncultured lymphomas consisting of one large B-cell and one mixed T-cell lymphoma. |
7632961 |
Human |
p15 |
diffuse large b-cell lymphoma |
Homozygous deletions of either the p16 gene or both the p15 and p16 genes were observed in one diffuse large B-cell lymphoma cell line and two uncultured lymphomas consisting of one large B-cell and one mixed T-cell lymphoma. |
7632961 |
Human |
p15 |
lymphomas |
Homozygous deletions of either the p16 gene or both the p15 and p16 genes were observed in one diffuse large B-cell lymphoma cell line and two uncultured lymphomas consisting of one large B-cell and one mixed T-cell lymphoma. |
7632961 |
Human |
p15 |
lymphomas |
These results indicate that the rate of alterations in the p15 and p16 genes is low for lymphomas, but loss of p16 and/or p15 may be involved in the development of some lymphomas. |
7632961 |
Human |
p15 |
hematopoietic malignancies |
A total of 410 tumor specimens from patients with primary hematopoietic malignancies were examined for deletions of the p16 gene as well as the neighboring p15 gene and the nearby interferon alpha gene by Southern blot analysis. |
7632963 |
Human |
p15 |
tumor |
A total of 410 tumor specimens from patients with primary hematopoietic malignancies were examined for deletions of the p16 gene as well as the neighboring p15 gene and the nearby interferon alpha gene by Southern blot analysis. |
7632963 |
Human |
mts2 |
malignant gliomas |
The cyclin-dependent kinase inhibitors p16INK4/MTS1 and p15INK4B/MTS2 have been mapped to a region in chromosome 9 (921) that is deleted frequently in acute lymphoblastic leukemias and malignant gliomas. |
7664273 |
Human |
mts2 |
acute lymphoblastic leukemias |
The cyclin-dependent kinase inhibitors p16INK4/MTS1 and p15INK4B/MTS2 have been mapped to a region in chromosome 9 (921) that is deleted frequently in acute lymphoblastic leukemias and malignant gliomas. |
7664273 |
Human |
p15 |
teratocarcinoma |
The differentiation of the embryonic teratocarcinoma cell line NT2 into postmitotic neurons (hNT) was associated with enhanced expression of p15 and p16 proteins. |
7664273 |
Human |
p15 |
tumor |
These features suggest that p15 may be a tumor suppressor. |
7675459 |
Human |
p15 |
melanoma |
We have also searched for P15 mutations in tumor cell lines and in 9p21-linked melanoma kindreds. |
7675459 |
Human |
p15 |
tumor |
We have also searched for P15 mutations in tumor cell lines and in 9p21-linked melanoma kindreds. |
7675459 |
Human |
p15 |
tumor |
Collectively, these observations suggest a role for p15 in growth regulation, but a limited role for p15 in tumor progression. |
7675459 |
Human |
p15 |
bladder tumors |
Deletion of the p16 and p15 genes in human bladder tumors. |
7563186 |
Human |
p15 |
cancer |
(The encoded polypeptides inactivate specific cyclin-protein kinase complexes that are required for progression through the cell cycle.) Molecular genetic studies have revealed that deletion of the p16 and p15 genes occurs frequently in cancer cell lines |
7563186 |
Human |
p15 |
malignant neoplasms |
(The encoded polypeptides inactivate specific cyclin-protein kinase complexes that are required for progression through the cell cycle.) Molecular genetic studies have revealed that deletion of the p16 and p15 genes occurs frequently in cancer cell lines |
7563186 |
Human |
p15 |
transitional cell bladder cancers |
PURPOSE: We evaluated the frequency of p16 and p15 gene alterations in a well-characterized cohort of human transitional cell bladder cancers, and we explored potential associations between alterations in these genes and tumor stage and/or grade. |
7563186 |
Human |
p15 |
tumor |
PURPOSE: We evaluated the frequency of p16 and p15 gene alterations in a well-characterized cohort of human transitional cell bladder cancers, and we explored potential associations between alterations in these genes and tumor stage and/or grade. |
7563186 |
Human |
p15 |
bladder tumors |
RESULTS: Homozygous deletion (both alleles lost) of the p16 and the p15 genes was observed in 11 and nine bladder tumors, respectively. |
7563186 |
Human |
p15 |
tumors |
Eight of the 11 tumors exhibiting complete loss of the p16 gene also displayed homozygous deletion of the p15 gene. |
7563186 |
Human |
p15 |
tumors |
Hemizygous deletion (one allele lost, also referred to as loss of heterozygosity [LOH] of the p16 and/or p15 genes was observed in eight tumors. Rearrangement of the two genes was indicated in three additional tumors. |
7563186 |
Human |
p15 |
tumors |
The overall frequency of alteration in this cohort of bladder tumors was approximately 18% for each gene (in 20 [18.3%, 95% confidence interval (CI) = 11.1%-25.6%] of 109 informative tumors for the p16 gene and in 18 [18%, 95% CI = 10.5%-25.5%] of 100 inf |
7563186 |
Human |
p15 |
bladder tumors |
The overall frequency of alteration in this cohort of bladder tumors was approximately 18% for each gene (in 20 [18.3%, 95% confidence interval (CI) = 11.1%-25.6%] of 109 informative tumors for the p16 gene and in 18 [18%, 95% CI = 10.5%-25.5%] of 100 inf |
7563186 |
Human |
p15 |
tumors |
A statistically significant association between p16 gene alteration and bladder tumors of low stage (P < .01) and grade (P < .01) was observed; a significant association between p15 gene alteration and tumors of low stage (P < .01) was also detected. |
7563186 |
Human |
p15 |
bladder tumors |
A statistically significant association between p16 gene alteration and bladder tumors of low stage (P < .01) and grade (P < .01) was observed; a significant association between p15 gene alteration and tumors of low stage (P < .01) was also detected. |
7563186 |
Human |
p15 |
bladder cancer |
CONCLUSIONS: Alteration of the p16 and p15 genes, especially coincident homozygous deletion, appears to be a common event in bladder cancer. |
7563186 |
Human |
p15 |
malignant peripheral-nerve-sheath tumors |
We demonstrate potential applications of these novel approaches by evaluating: 1) significance of normal karyotypes in malignant peripheral nerve sheath tumors; 2) p15/p16 copy number in prostate cancer; and 3) clonal chromosome 3p deletion in cytological |
7573365 |
Human |
p15 |
prostate cancer |
We demonstrate potential applications of these novel approaches by evaluating: 1) significance of normal karyotypes in malignant peripheral nerve sheath tumors; 2) p15/p16 copy number in prostate cancer; and 3) clonal chromosome 3p deletion in cytological |
7573365 |
Human |
p15 |
mesothelioma |
We demonstrate potential applications of these novel approaches by evaluating: 1) significance of normal karyotypes in malignant peripheral nerve sheath tumors; 2) p15/p16 copy number in prostate cancer; and 3) clonal chromosome 3p deletion in cytological |
7573365 |
Human |
p15 |
non-hodgkins lymphoma |
Deletion of cyclin-dependent kinase 4 inhibitor genes P15 and P16 in non-Hodgkin's lymphoma. |
7579381 |
Human |
p15 |
tumors |
In this study, we examined the contribution of the cell cycle inhibitor genes P15, P16, and P18 to pathogenesis in a large panel of 209 cytogenetically characterized B-cell NHL tumors representing varied histologic groups. |
7579381 |
Human |
p15 |
small-lymphocytic lymphoma |
We identified the homozygous deletion of P15 and P16 genes in 13 tumors from 12 patients, all belonging to diffuse large-cell histology; 10 had this diagnosis made on presentation, 1 had transformed from small lymphocytic lymphoma, and 1 had transformed f |
7579381 |
Human |
p15 |
tumors |
We identified the homozygous deletion of P15 and P16 genes in 13 tumors from 12 patients, all belonging to diffuse large-cell histology; 10 had this diagnosis made on presentation, 1 had transformed from small lymphocytic lymphoma, and 1 had transformed f |
7579381 |
Human |
mts2 |
lymphoblastic leukaemia |
Homozygous loss of the MTS1/p16 and MTS2/p15 genes in lymphoma and lymphoblastic leukaemia cell lines. |
8547074 |
Human |
p15 |
lymphoblastic leukaemia |
Homozygous loss of the MTS1/p16 and MTS2/p15 genes in lymphoma and lymphoblastic leukaemia cell lines. |
8547074 |
Human |
mts2 |
lymphoma |
Homozygous loss of the MTS1/p16 and MTS2/p15 genes in lymphoma and lymphoblastic leukaemia cell lines. |
8547074 |
Human |
p15 |
lymphoma |
Homozygous loss of the MTS1/p16 and MTS2/p15 genes in lymphoma and lymphoblastic leukaemia cell lines. |
8547074 |
Human |
mts2 |
tumour |
The genes MTS1/p16 and MTS2/p15 located in 9p21 encoding cyclin-dependent kinase-4 inhibitors are homozygously deleted in a number of different tumour cell lines. |
8547074 |
Human |
p15 |
tumour |
The genes MTS1/p16 and MTS2/p15 located in 9p21 encoding cyclin-dependent kinase-4 inhibitors are homozygously deleted in a number of different tumour cell lines. |
8547074 |
Human |
cdkn2b |
esophageal squamous carcinoma |
Genomic DNA and messenger RNA expression alterations of the CDKN2B and CDKN2 genes in esophageal squamous carcinoma cell lines. |
7547637 |
Human |
mts2 |
human tumors |
The genes CDKN2B (MTS2) and CDKN2 (MTS1) encoding the proteins p15 and p16 are both located on chromosomal band 9p21, a locus at which frequent homozygous and heterozygous deletions occur in many primary human tumors, including esophageal carcinoma. |
7547637 |
Human |
p15 |
human tumors |
The genes CDKN2B (MTS2) and CDKN2 (MTS1) encoding the proteins p15 and p16 are both located on chromosomal band 9p21, a locus at which frequent homozygous and heterozygous deletions occur in many primary human tumors, including esophageal carcinoma. |
7547637 |
Human |
cdkn2b |
human tumors |
The genes CDKN2B (MTS2) and CDKN2 (MTS1) encoding the proteins p15 and p16 are both located on chromosomal band 9p21, a locus at which frequent homozygous and heterozygous deletions occur in many primary human tumors, including esophageal carcinoma. |
7547637 |
Human |
mts2 |
esophageal carcinoma |
The genes CDKN2B (MTS2) and CDKN2 (MTS1) encoding the proteins p15 and p16 are both located on chromosomal band 9p21, a locus at which frequent homozygous and heterozygous deletions occur in many primary human tumors, including esophageal carcinoma. |
7547637 |
Human |
p15 |
esophageal carcinoma |
The genes CDKN2B (MTS2) and CDKN2 (MTS1) encoding the proteins p15 and p16 are both located on chromosomal band 9p21, a locus at which frequent homozygous and heterozygous deletions occur in many primary human tumors, including esophageal carcinoma. |
7547637 |
Human |
cdkn2b |
esophageal carcinoma |
The genes CDKN2B (MTS2) and CDKN2 (MTS1) encoding the proteins p15 and p16 are both located on chromosomal band 9p21, a locus at which frequent homozygous and heterozygous deletions occur in many primary human tumors, including esophageal carcinoma. |
7547637 |
Human |
cdkn2b |
esophageal squamous cancer |
To investigate whether CDKN2B and CDKN2 are involved in esophageal tumorigenesis, we studied homozygous deletion, intragenic mutation, and messenger RNA (mRNA) expression of CDKN2 and CDKN2B in nine esophageal squamous cancer cell lines. |
7547637 |
Human |
mts2 |
non-small cell lung cancer |
Mechanism of inactivation of CDKN2 and MTS2 in non-small cell lung cancer and association with advanced stage. |
7478613 |
Human |
mts2 |
cancer |
Conflicting reports of the frequency of CDKN2 alterations in NSCLC tumors prompted us to examine the relationship of these alterations and those of the related gene, MTS2, with patient stage and site of cancer. |
7478613 |
Human |
mts2 |
tumors |
Conflicting reports of the frequency of CDKN2 alterations in NSCLC tumors prompted us to examine the relationship of these alterations and those of the related gene, MTS2, with patient stage and site of cancer. |
7478613 |
Human |
p15 |
human bladder cancer |
In this study, a panel of well-characterised established human bladder cancer cell lines was screened by the polymerase chain reaction for homozygous loss of the cyclin-dependent kinase inhibitor genes p15, p16 and p27. |
7577470 |
Human |
p15 |
bladder cancer |
The p15 and p16 genes are known to be juxtaposed on chromosome 9p21 at the locus of a putative tumour-suppressor gene involved in the initiation of bladder cancer. |
7577470 |
Human |
p15 |
myeloid leukaemias |
Structural integrity of the cyclin-dependent kinase inhibitor genes, p15, p16 and p18 in myeloid leukaemias. |
7577621 |
Human |
p15 |
tumour |
The cyclin-dependent kinase inhibitors known as p15, p16 and p18 have been suggested as candidates for tumour suppressor genes. |
7577621 |
Human |
p15 |
myeloid leukaemias |
The p15 and p16 genes were either deleted or mutated in myeloid leukaemia lines at a high frequency [6/15 (40%) for p15; 8/15 (53%) for p16] but alterations in primary myeloid leukaemias are much less frequent [2/46 (4%) for p15; 3/46 (6%) for p16]. |
7577621 |
Human |
p15 |
myeloid leukaemia |
The p15 and p16 genes were either deleted or mutated in myeloid leukaemia lines at a high frequency [6/15 (40%) for p15; 8/15 (53%) for p16] but alterations in primary myeloid leukaemias are much less frequent [2/46 (4%) for p15; 3/46 (6%) for p16]. |
7577621 |
Human |
p15 |
myeloid leukaemia |
In summary, the deletions of p15 and p16 genes identified in the myeloid leukaemia cell lines probably occurred during their in vitro immortalization. |
7577621 |
Human |
p15 |
acute myeloid leukaemia |
Alterations of the p16 or p15 gene only occurred in primary acute myeloid leukaemia samples that were of mixed myeloid/lymphoid lineage (CD19/CD20-positive acute myeloid leukaemia [AML], CD2/CD19-positive AML, and lymphoid blastic crisis of chronic myeloi |
7577621 |
Human |
p15 |
chronic myeloid leukaemia |
Alterations of the p16 or p15 gene only occurred in primary acute myeloid leukaemia samples that were of mixed myeloid/lymphoid lineage (CD19/CD20-positive acute myeloid leukaemia [AML], CD2/CD19-positive AML, and lymphoid blastic crisis of chronic myeloi |
7577621 |
Human |
mts2 |
glioma |
Homozygous deletion of the MTS1/p16 and MTS2/p15 genes and amplification of the CDK4 gene in glioma. |
7478535 |
Human |
p15 |
glioma |
Homozygous deletion of the MTS1/p16 and MTS2/p15 genes and amplification of the CDK4 gene in glioma. |
7478535 |
Human |
mts2 |
tumors |
We detected losses of one allele and homozygous deletions at loci, including those of the MTS1/p16 and MTS2/p15 genes, in 10 and 3 tumors, respectively. |
7478535 |
Human |
p15 |
tumors |
We detected losses of one allele and homozygous deletions at loci, including those of the MTS1/p16 and MTS2/p15 genes, in 10 and 3 tumors, respectively. |
7478535 |
Human |
mts2 |
malignant gliomas |
The CDK4 gene was amplified in two malignant gliomas without homozygous deletion of the MTS1/p16 and MTS2/p15 genes and one malignant glioma with an allelic loss of the genes. |
7478535 |
Human |
p15 |
malignant gliomas |
The CDK4 gene was amplified in two malignant gliomas without homozygous deletion of the MTS1/p16 and MTS2/p15 genes and one malignant glioma with an allelic loss of the genes. |
7478535 |
Human |
mts2 |
malignant glioma |
The CDK4 gene was amplified in two malignant gliomas without homozygous deletion of the MTS1/p16 and MTS2/p15 genes and one malignant glioma with an allelic loss of the genes. |
7478535 |
Human |
p15 |
malignant glioma |
The CDK4 gene was amplified in two malignant gliomas without homozygous deletion of the MTS1/p16 and MTS2/p15 genes and one malignant glioma with an allelic loss of the genes. |
7478535 |
Human |
p15 |
bladder tumors |
Homozygous deletions but no sequence mutations in coding regions of p15 or p16 in human primary bladder tumors. |
7576106 |
Human |
p15 |
tumor |
To map the deletion at 9p21 in bladder tumors, we analyzed DNA from 28 tumor and normal pairs at five microsatellite markers that flank the region occupied by the putative tumor suppressor genes p16 and p15. |
7576106 |
Human |
p15 |
bladder tumors |
To map the deletion at 9p21 in bladder tumors, we analyzed DNA from 28 tumor and normal pairs at five microsatellite markers that flank the region occupied by the putative tumor suppressor genes p16 and p15. |
7576106 |
Human |
p15 |
bladder tumors |
Loss of heterozygosity (LOH) at the markers human interferon (HIFN) alpha and D9S171, which are adjacent to the p15 and p16 loci, was detected in 41% and 33%, respectively, of informative cases of bladder tumors. |
7576106 |
Human |
p15 |
bladder tumors |
No sequence mutations were detected in exons 1 or 2 of either p15 or p16 in any of the bladder tumors. |
7576106 |
Human |
p15 |
tumors |
Six of 11 tumors with LOH at surrounding markers had homozygous deletions of the marker c5.1, which is located within the p16 gene; and two tumors appeared to have homozygous deletions within p15 (RN1.1) but not p16 (c5.1). |
7576106 |
Human |
p15 |
tumor |
Although these data could not be used to identify p16 or p15 as the definitive tumor suppressor gene in this region that is involved in bladder carcinogenesis, they suggest that homozygous deletion is a common mechanism of loss of tumor suppressor gene fu |
7576106 |
Human |
p15 |
tumour |
Six deletions involved p16 but not the related and adjacent gene p15 and one tumour had an intragenic deletion of p16. |
8541841 |
Human |
mts2 |
human lung cancers |
Loss of heterozygosity at 9p21 loci and mutations of the MTS1 and MTS2 genes in human lung cancers. |
7591275 |
Human |
mts2 |
tumors |
To elucidate the involvement of abnormalities of the MTS1/p16 and MTS2/p15 genes located at chromosomal region 9p21 in human lung cancers, we analyzed DNA from 30 primary lung cancers and detected loss of heterozygosity at the 9p21-p23 region in 15 tumors |
7591275 |
Human |
p15 |
tumors |
To elucidate the involvement of abnormalities of the MTS1/p16 and MTS2/p15 genes located at chromosomal region 9p21 in human lung cancers, we analyzed DNA from 30 primary lung cancers and detected loss of heterozygosity at the 9p21-p23 region in 15 tumors |
7591275 |
Human |
mts2 |
human lung cancers |
To elucidate the involvement of abnormalities of the MTS1/p16 and MTS2/p15 genes located at chromosomal region 9p21 in human lung cancers, we analyzed DNA from 30 primary lung cancers and detected loss of heterozygosity at the 9p21-p23 region in 15 tumors |
7591275 |
Human |
p15 |
human lung cancers |
To elucidate the involvement of abnormalities of the MTS1/p16 and MTS2/p15 genes located at chromosomal region 9p21 in human lung cancers, we analyzed DNA from 30 primary lung cancers and detected loss of heterozygosity at the 9p21-p23 region in 15 tumors |
7591275 |
Human |
mts2 |
primary lung cancers |
To elucidate the involvement of abnormalities of the MTS1/p16 and MTS2/p15 genes located at chromosomal region 9p21 in human lung cancers, we analyzed DNA from 30 primary lung cancers and detected loss of heterozygosity at the 9p21-p23 region in 15 tumors |
7591275 |
Human |
p15 |
primary lung cancers |
To elucidate the involvement of abnormalities of the MTS1/p16 and MTS2/p15 genes located at chromosomal region 9p21 in human lung cancers, we analyzed DNA from 30 primary lung cancers and detected loss of heterozygosity at the 9p21-p23 region in 15 tumors |
7591275 |
Human |
mts2 |
tumors |
Single-strand-conformation-polymorphism analysis of polymerase-chain-reaction products from the MTS1 and MTS2 genes and determination of the nucleotide sequences revealed the presence of a mutated MTS1 gene in 2 of 15 tumors with a loss of corresponding l |
7591275 |
Human |
mts2 |
malignant gliomas |
Deletion and transfection analysis of the p15/MTS2 gene in malignant gliomas. |
8526910 |
Human |
p15 |
malignant gliomas |
Deletion and transfection analysis of the p15/MTS2 gene in malignant gliomas. |
8526910 |
Human |
mts2 |
glioblastoma |
We also expressed MTS2 and MTS1, encoding the contiguous and highly homologous CDK inhibitor p16, in U-87 human glioblastoma cells. |
8526910 |
Human |
mts2 |
tumor |
As a whole, the data assign a tumor suppressor role to p15 and confirm homozygous deletions as the favorite mechanism for the inactivation of MTS1 and MTS2 in glioblastomas. |
8526910 |
Human |
p15 |
tumor |
As a whole, the data assign a tumor suppressor role to p15 and confirm homozygous deletions as the favorite mechanism for the inactivation of MTS1 and MTS2 in glioblastomas. |
8526910 |
Human |
mts2 |
glioma |
Homozygous deletions of p16INK4A/MTS1 and p15INK4B/MTS2 genes in glioma cells and primary glioma tissues. |
7497469 |
Human |
mts2 |
human tumors |
The p16INK4A/MTS1 (p16) and p15INK4B/MTS2 (p15) genes map to 9p21 where genetic alterations have been frequently reported in various human tumors. |
7497469 |
Human |
p15 |
human tumors |
The p16INK4A/MTS1 (p16) and p15INK4B/MTS2 (p15) genes map to 9p21 where genetic alterations have been frequently reported in various human tumors. |
7497469 |
Human |
p15 |
glioma |
In 12 short-term cultures of cells derived from primary glioma samples, 5 (41.7%) and 2 (16.7%) glioblastoma-derived cells had homozygous deletion of all or any of the three exons of the p16 gene and exon 2 of the p15 gene, respectively. |
7497469 |
Human |
p15 |
glioblastoma |
Our results indicate that loss of the p16 and p15 genes may be involved in tumor progression in human gliomas, especially in the development of glioblastoma, that this loss may give growth advantage to the cells in culture, and that it is not the result o |
7497469 |
Human |
p15 |
tumor |
Our results indicate that loss of the p16 and p15 genes may be involved in tumor progression in human gliomas, especially in the development of glioblastoma, that this loss may give growth advantage to the cells in culture, and that it is not the result o |
7497469 |
Human |
p15 |
head and neck squamous cell carcinoma |
The study of p16 and p15 gene methylation in head and neck squamous cell carcinoma and their quantitative evaluation in plasma by real-time PCR. |
12932666 |
Human |
p15 |
head and neck squamous cell carcinomas |
Epigenetic silencing of the p16 and p15 genes by promoter methylation are commonly observed in human epithelial malignancies, including head and neck squamous cell carcinomas (HNSCC). |
12932666 |
Human |
p15 |
primary tumour |
The frequencies of p16 and p15 methylation in the primary tumour were 49% and 60%, respectively. |
12932666 |
Human |
p15 |
tumour |
Concordant methylation of p16 and p15 in tumour samples and metastatic lymph nodes was found in 59 and 38% of cases, respectively. |
12932666 |
Human |
p15 ink4b |
myelodysplastic syndromes |
Gene silencing of the p15/INK4B cell-cycle inhibitor by hypermethylation: an early or later epigenetic alteration in myelodysplastic syndromes? |
12970776 |
Human |
p15 |
acute myeloid leukemia |
Hypermethylation of the three genes was studied in 81 patients with therapy-related myelodysplasia (t-MDS) or acute myeloid leukemia (t-AML) by methylation-specific PCR, and p15 methylation additionally by bisulfite genomic sequencing. |
12970781 |
Human |
p15 |
tumor |
Gene inactivation ('silencing') of tumor suppressor and growth inhibitory genes (e.g. the cyclin-dependent kinase inhibitors p16, p15, p21) is frequently mediated by DNA methylation of gene promoters. |
14528273 |
Human |
ink4b |
pediatric acute lymphoblastic leukemia |
No rearrangements or deletions of the INK4d gene were observed in Southern blot analysis of selected cases of pediatric acute lymphoblastic leukemia (ALL) containing a variant (1;19)(q23;p13) translocation that lacks rearrangement of either E2A or PBX1, o |
8575754 |
Human |
cdkn2b |
human esophageal cancers |
Intragenic mutations of CDKN2B and CDKN2A in primary human esophageal cancers. |
8595411 |
Human |
p15 |
human tumors |
The CDKN2A and CDKN2B genes, encoding p16 and p15 respectively, are located on chromosome 9p21, a locus at which frequent homozygous and heterozygous deletions occur in many primary human tumors, including esophageal carcinoma. |
8595411 |
Human |
cdkn2b |
human tumors |
The CDKN2A and CDKN2B genes, encoding p16 and p15 respectively, are located on chromosome 9p21, a locus at which frequent homozygous and heterozygous deletions occur in many primary human tumors, including esophageal carcinoma. |
8595411 |
Human |
p15 |
esophageal carcinoma |
The CDKN2A and CDKN2B genes, encoding p16 and p15 respectively, are located on chromosome 9p21, a locus at which frequent homozygous and heterozygous deletions occur in many primary human tumors, including esophageal carcinoma. |
8595411 |
Human |
cdkn2b |
esophageal carcinoma |
The CDKN2A and CDKN2B genes, encoding p16 and p15 respectively, are located on chromosome 9p21, a locus at which frequent homozygous and heterozygous deletions occur in many primary human tumors, including esophageal carcinoma. |
8595411 |
Human |
cdkn2b |
esophageal cancers |
In order to determine whether CDKN2A and CDKN2B are frequent targets of 9p21 deletion in esophageal carcinogenesis, we have now analyzed 60 primary esophageal cancers for mutations in both exons 1 and 2 of CDKN2A and CDKN2B by direct sequencing of PCR amp |
8595411 |
Human |
cdkn2b |
esophageal carcinomas |
In conjunction with our previously published data, we have identified a total of eight nucleic acid substitutions among 60 esophageal carcinomas; here, we describe one new CDKN2B nonsense mutation and one new silent CDKN2B mutation that occurred somatical |
8595411 |
Human |
cdkn2b |
esophageal cancer |
Taken together, these results suggest that intragenic mutations in CDKN2A and CDKN2B occur in esophageal cancer, but that they are infrequent events. |
8595411 |
Human |
cdkn2b |
esophageal cancers |
In view of the known high frequency of loss of heterozygosity at the chromosome 9p21 locus in esophageal cancers, the current data suggest that intragenic mutation is not the predominant mode of inactivation of CDKN2A and CDKN2B or that other genes are ta |
8595411 |
Human |
cdkn2b |
cancers |
In view of the known high frequency of loss of heterozygosity at the chromosome 9p21 locus in esophageal cancers, the current data suggest that intragenic mutation is not the predominant mode of inactivation of CDKN2A and CDKN2B or that other genes are ta |
8595411 |
Human |
p15 |
superficial bladder cancers |
Infrequent somatic mutations of the p16 and p15 genes in human bladder cancer: p16 mutations occur only in low-grade and superficial bladder cancers. |
8747595 |
Human |
p15 |
human bladder cancer |
Infrequent somatic mutations of the p16 and p15 genes in human bladder cancer: p16 mutations occur only in low-grade and superficial bladder cancers. |
8747595 |
Human |
p15 |
human bladder cancers |
To investigate structural alterations of p16 and a neighboring gene, p15, we examined human bladder cancers for mutations in the entire coding region of these genes using polymerase chain reaction and single-strand conformational polymorphism analysis. |
8747595 |
Human |
p15 |
bladder cancers |
We found no p15 gene mutations in these 50 bladder cancers. |
8747595 |
Human |
p15 |
non-small cell lung cancers |
Homozygous deletions at chromosome 9p21 and mutation analysis of p16 and p15 in microdissected primary non-small cell lung cancers. |
9816033 |
Human |
p15 |
tumor |
The recently cloned p16 and p15 genes, mapped to 9p21, are likely candidates for such tumor suppressors. |
9816033 |
Human |
p15 |
tumors |
To map the deletion at chromosome 9p21 in non-small cell lung tumors, we analyzed DNA from 25 tumors and matching normal DNAs at six microsatellite markers that flank the region occupied by the p16 and p15 genes. |
9816033 |
Human |
p15 |
tumor |
Screening for mutations in p16 and p15 revealed one tumor with a non-sense mutation in exon 2 of p16, but no mutations were detected in p15 in any of the tumors. |
9816033 |
Human |
p15 |
tumors |
Screening for mutations in p16 and p15 revealed one tumor with a non-sense mutation in exon 2 of p16, but no mutations were detected in p15 in any of the tumors. |
9816033 |
Human |
p15 |
tumor |
The apparent lack of other mutations in p16 and p15 in the tumors with loss of heterozygosity leaves open the possibility of an unidentified gene in this region that may function as a tumor suppressor. |
9816033 |
Human |
p15 |
tumors |
The apparent lack of other mutations in p16 and p15 in the tumors with loss of heterozygosity leaves open the possibility of an unidentified gene in this region that may function as a tumor suppressor. |
9816033 |
Human |
p15 |
tumours |
The gene encoding p15 is located on chromosome 9 adjacent to the p16 gene at a frequent site of chromosomal abnormality in human tumours (9p21). |
8078588 |
Human |
p15 |
therapy-related myelodysplastic syndrome |
Aberrant p15 gene promoter methylation in therapy-related myelodysplastic syndrome and acute myeloid leukaemia: clinicopathological and karyotypic associations. |
12648079 |
Human |
p15 |
acute myeloid leukaemia |
Aberrant p15 gene promoter methylation in therapy-related myelodysplastic syndrome and acute myeloid leukaemia: clinicopathological and karyotypic associations. |
12648079 |
Human |
p15 |
therapy-related myelodysplastic syndrome |
Seventeen patients with therapy-related myelodysplastic syndrome/acute myeloid leukaemia (t-MDS/AML) were examined for aberrant p15 gene methylation by methylation-specific polymerase chain reaction. |
12648079 |
Human |
p15 |
acute myeloid leukaemia |
Seventeen patients with therapy-related myelodysplastic syndrome/acute myeloid leukaemia (t-MDS/AML) were examined for aberrant p15 gene methylation by methylation-specific polymerase chain reaction. |
12648079 |
Human |
cdkn2b |
childhood acute lymphoblastic leukemia |
CDKN2A, CDKN2B, and MTAP gene dosage permits precise characterization of mono- and bi-allelic 9p21 deletions in childhood acute lymphoblastic leukemia. |
12661005 |
Human |
p15 |
brain tumors |
Deletion of p16 and p15 genes in brain tumors. |
7987828 |
Human |
p15 |
glioblastoma |
We found that p16 and a neighboring gene, p15, were often homozygously deleted in glioblastoma multiformes but not in medulloblastomas or ependymomas. |
7987828 |
Human |
p15 |
glioblastoma multiforme |
These data suggest that the target of deletion in glioblastoma multiforme includes both p15 and p16 genes. |
7987828 |
Human |
mts2 |
b-cell lineage acute lymphoblastic leukemias |
Candidate tumor-suppressor genes MTS1 (p16INK4A) and MTS2 (p15INK4B) display frequent homozygous deletions in primary cells from T- but not from B-cell lineage acute lymphoblastic leukemias. |
7994022 |
Human |
mts2 |
acute lymphoblastic leukemia (all) |
Using a Southern blot approach, deletions of MTS1 (multiple tumor-suppressor gene 1) and MTS2 (multiple tumor-suppressor gene 2) candidate tumor-suppressor genes have been studied in primary neoplastic cells from 55 acute lymphoblastic leukemia (ALL) pati |
7994022 |
Human |
mts2 |
human leukemia |
The high frequency of MTS1 and MTS2 homozygous deletions in T-ALLs supports the view that inactivation of these genes plays an important role in the pathogenesis of this type of human leukemia. |
7994022 |
Human |
p15 |
oral squamous-cell carcinoma |
Promoter hypermethylation profile of tumor-associated genes p16, p15, hMLH1, MGMT and E-cadherin in oral squamous cell carcinoma. |
12672028 |
Human |
p15 |
oral squamous-cell carcinoma (oscc) |
Using a sensitive restriction-multiplex PCR method, we studied the promoter hypermethylation profile of the p16, p15, hMLH1, MGMT and E-cad genes in oral squamous cell carcinoma (OSCC) of Indians. |
12672028 |
Human |
p15 |
esophageal cancer |
Also p15 and p16 have been identified to be involved in the pathogenesis of esophageal cancer by influencing the cyclin kinase inhibitor cascade and DNA mismatch repair processes. |
15138356 |
Human |
p15 |
acute myeloblastic leukemia |
Transcriptional repression of the p15 gene predicts the clinical outcome of acute myeloblastic leukemia with intermediate and adverse cytogenetics. |
15085158 |
Human |
p15 |
multiple myeloma |
METHODS: The methylation patterns of the genes p16(INK4a) (p16), tissue inhibitor of metalloproteinase 3 (TIMP3), p15(INK4b) (p15), E-cadherin (ECAD), death-associated protein kinase (DAPK), p73, RAS-association domain family 1A (RASSF1A), p14, O(6)-methy |
15197802 |
Human |
p15 |
plasma-cell leukemia |
METHODS: The methylation patterns of the genes p16(INK4a) (p16), tissue inhibitor of metalloproteinase 3 (TIMP3), p15(INK4b) (p15), E-cadherin (ECAD), death-associated protein kinase (DAPK), p73, RAS-association domain family 1A (RASSF1A), p14, O(6)-methy |
15197802 |
Human |
p15 |
monoclonal gammopathy of undetermined significance |
METHODS: The methylation patterns of the genes p16(INK4a) (p16), tissue inhibitor of metalloproteinase 3 (TIMP3), p15(INK4b) (p15), E-cadherin (ECAD), death-associated protein kinase (DAPK), p73, RAS-association domain family 1A (RASSF1A), p14, O(6)-methy |
15197802 |
Human |
p15 |
smoldering multiple myeloma |
METHODS: The methylation patterns of the genes p16(INK4a) (p16), tissue inhibitor of metalloproteinase 3 (TIMP3), p15(INK4b) (p15), E-cadherin (ECAD), death-associated protein kinase (DAPK), p73, RAS-association domain family 1A (RASSF1A), p14, O(6)-methy |
15197802 |
Human |
p15 |
myeloma |
Of the eight diagnostic myeloma marrow samples, hypermethylation of p15, p16, E-CAD, DAPK and ER occurred in six (75%), four (50%), seven (87.5%), eight (100%), and six (75%) patients. |
15109538 |
Human |
p15 |
malt lymphomas |
METHODS: To better understand the pathogenesis of H. pylori dependent and independent MALT lymphomas, we analysed the methylation profiles of eight independent CpG islands, including p15, p16, p73, hMLH1, death associated protein kinase, MINT1, MINT2, and |
12692046 |
Human |
p15 |
acute promyelocytic leukemia (apl) |
We evaluated the methylation status of p15 gene in a series of 65 patients with newly diagnosed acute promyelocytic leukemia (APL) receiving homogeneous treatment. |
12750706 |
Human |
p15 |
tumors |
Six normal NP tissues, 43 M&T rinsing fluid, 37 NP swabs and 43 peripheral blood from healthy non-smokers and non-drinkers without a family history of NPC, and 30 NPC tumors and their matched body fluid were analyzed for the presence of hypermethylated p1 |
12767073 |
Human |
p15 |
cell lymphomas |
Twenty-five primary tumours and 105 serial biopsies taken at various time points after treatment were examined using a methylation-specific polymerase chain reaction (MSP) for a panel of genes, comprising p73, p16, hMLH1, RARbeta and p15, previously shown |
12823347 |
Human |
p15 |
primary tumours |
Twenty-five primary tumours and 105 serial biopsies taken at various time points after treatment were examined using a methylation-specific polymerase chain reaction (MSP) for a panel of genes, comprising p73, p16, hMLH1, RARbeta and p15, previously shown |
12823347 |
Human |
p15 |
primary tumours |
Primary tumours showed the frequent methylation of the genes p73 (92%), p16 (71%), hMLH1 (61%), RARbeta (56%) and p15 (48%). |
12823347 |
Human |
cdkn2b |
primary testicular lymphoma |
We studied the methylation status of E-cadherin, CDKN2B, CDKN2A, BRCA1, RB1, VHL, RASSF1A, RARB, and GSTP1 by use of TGCT tissues and testicular malignant lymphoma tissues (25 primary TGCT tissues and three primary testicular lymphoma tissues). |
12874790 |
Human |
cdkn2b |
malignant lymphoma |
We studied the methylation status of E-cadherin, CDKN2B, CDKN2A, BRCA1, RB1, VHL, RASSF1A, RARB, and GSTP1 by use of TGCT tissues and testicular malignant lymphoma tissues (25 primary TGCT tissues and three primary testicular lymphoma tissues). |
12874790 |
Human |
cdkn2b |
testicular lymphoma |
In contrast, all three (100%) of the testicular lymphoma tissues demonstrated hypermethylation of E-cadherin, RASSF1A, and RARB, but not CDKN2B, CDKN2A, BRCA1, RB1, VHL, and GSTP1. |
12874790 |
Human |
p15 |
neoplasia |
The pRB cell cycle regulatory cascade is frequently perturbed in neoplasia by overexpression of a component of the pRB-phosphorylating cyclin D1/CDK4 complex or by inactivation of pRB or the CDK4 inhibitors p16 and p15. |
9393981 |
Human |
p15 |
neoplasia |
Hypermethylation within the promoters of some genes appear to be an early event in the pathogenesis of neoplasia (ER, P15), while other genes seem to become methylated during the progression of leukemias (HIC1, c-abl). |
9130685 |
Human |
p15 |
neoplasias |
Demethylation of a hypermethylated P15/INK4B gene in patients with myelodysplastic syndrome by 5-Aza-2'-deoxycytidine (decitabine) treatment. p16 and p15, 2 inhibitors of cyclin-dependent kinases, are frequently hypermethylated in hematologic neoplas |
12351408 |
Human |
p15 |
mds |
We examined p15 and p16 methylation status in bone marrow mononuclear cells from patients with high-risk MDS during treatment with decitabine, using a methylation-sensitive primer extension assay (Ms-SNuPE) to quantitate methylation, and denaturing gradie |
12351408 |
Human |
p15 |
mds |
The emergence of partially demethylated epigenotypes and re-establishment of normal p15 protein expression following the initial decitabine courses implicate pharmacologic demethylation as a possible mechanism resulting in hematologic response in MDS. |
12351408 |
Human |
p15 |
mds |
Relationship between methylation of the p15 gene and ectopic expression of the EVI-1 gene in myelodysplastic syndromes (MDS). |
11417490 |
Human |
p15 |
mds |
In myelodysplastic syndrome (MDS), the expression of the cyclin-dependent kinase inhibitor p15(ink4B) (p15) is frequently decreased because of the aberrant methylation of the gene promoter; p15 is normally up-regulated during megakaryocytic differentiatio |
11435325 |
Human |
p15 |
mds |
It was hypothesized that p15 methylation and deregulation of gene expression contribute to defective megakaryocytopoiesis in patients with MDS. |
11435325 |
Human |
p15 |
mds |
This TGF-beta1-dependent pathway is altered in MDS CD34(+) progenitors because of p15 methylation. |
11435325 |
Human |
p15 |
mds |
Ras mutations are the molecular abnormalities most frequently found in MDS, followed by p15 gene hypermethylation, FLT3 duplications, and p53 mutations, but none of these abnormalities are specific for MDS. |
11503956 |
Human |
p15 |
mds |
Many of the MDS-derived cell lines carry cytogenetic and molecular genetic abnormalities typically associated with MDS: gain or loss of all or parts of chromosomes 5, 7, 8 and 20 (-5/5q-, -7/7q-, + 8, 20q-); alterations of oncogenes and tumor suppressor g |
10654445 |
Human |
p15 |
mds |
Here, p15 is most often inactivated, at particularly high frequencies in the disorders lacking any p15/p16 deletions: 40-80% p15met in AML, MDS and multiple myeloma. |
9639410 |
Human |
p15 |
mds |
In summary, genetic abnormalities of the p15, p16, p18 and p19 genes are rare events in the development and/or progression of MDS. |
9111168 |
Human |
p15 |
myelodysplastic syndromes |
Relationship between methylation of the p15 gene and ectopic expression of the EVI-1 gene in myelodysplastic syndromes (MDS). |
11417490 |
Human |
p15 |
myelodysplastic syndromes |
Molecular analysis of the cyclin-dependent kinase inhibitor genes, p15, p16, p18 and p19 in the myelodysplastic syndromes. |
9111168 |
Human |
p15 |
myelodysplasia |
Hypermethylation of the three genes was studied in 81 patients with therapy-related myelodysplasia (t-MDS) or acute myeloid leukemia (t-AML) by methylation-specific PCR, and p15 methylation additionally by bisulfite genomic sequencing. |
12970781 |
Human |
cdkn2b |
cll |
We examined CDKN2A methylation status at diagnosis in 42 B-cell chronic lymphocytic leukaemia (CLL) patients, in 19 cases the CDKN2B methylation status was also analysed. |
9375748 |
NA |
mts2 |
gliomas |
We analysed the DNAs from 37 gliomas of several grades of malignancy for allelic loss of chromosome 9p and aberrations of the MTS1/p16 and MTS2/p15 genes. |
7478535 |
NA |
mts2 |
malignancy |
We analysed the DNAs from 37 gliomas of several grades of malignancy for allelic loss of chromosome 9p and aberrations of the MTS1/p16 and MTS2/p15 genes. |
7478535 |
NA |
p15 |
gliomas |
We analysed the DNAs from 37 gliomas of several grades of malignancy for allelic loss of chromosome 9p and aberrations of the MTS1/p16 and MTS2/p15 genes. |
7478535 |
NA |
p15 |
malignancy |
We analysed the DNAs from 37 gliomas of several grades of malignancy for allelic loss of chromosome 9p and aberrations of the MTS1/p16 and MTS2/p15 genes. |
7478535 |
NA |
p15 |
medulloblastomas |
In this study, p15, p16, CDK4 and cyclin D1 genes were analyzed in 69 nonastrocytic human brain tumors, including 17 oligodendrogliomas, 16 medulloblastomas/primitive neuroectodermal tumors (PNETs), 14 ependymomas and 22 meningiomas. |
8621248 |
NA |
p15 |
ependymomas |
In this study, p15, p16, CDK4 and cyclin D1 genes were analyzed in 69 nonastrocytic human brain tumors, including 17 oligodendrogliomas, 16 medulloblastomas/primitive neuroectodermal tumors (PNETs), 14 ependymomas and 22 meningiomas. |
8621248 |
NA |
p15 |
oligodendrogliomas |
In this study, p15, p16, CDK4 and cyclin D1 genes were analyzed in 69 nonastrocytic human brain tumors, including 17 oligodendrogliomas, 16 medulloblastomas/primitive neuroectodermal tumors (PNETs), 14 ependymomas and 22 meningiomas. |
8621248 |
NA |
p15 |
gastric tumors |
METHODS: Thirty-six primary gastric tumors and 9 gastric carcinoma cell lines were examined for alterations of the p16 and p15 genes. |
9366289 |
NA |
p15 |
rb |
We examined the expression levels of the p16, p15, p14, and retinoblastoma-susceptibility (RB) genes in primary prostate cancers and human prostate cancer cell lines, and correlated this with the DNA methylation levels of two loci in p16. |
10797499 |
NA |
p15 |
osteosarcomas |
We examined alterations of the p16INK4, p14ARF, p15, TP53, and MDM2 genes in 30 osteosarcomas and 24 Ewing sarcomas. |
10942797 |
NA |
p15 |
minimal residual disease |
PURPOSE: To investigate the frequency of p15 and p16 gene promoter methylation in acute promyelocytic leukemia (APL), and to define its value in the detection of minimal residual disease (MRD) and treatment prognostication. |
11283136 |
NA |
p15 |
mrd |
PURPOSE: To investigate the frequency of p15 and p16 gene promoter methylation in acute promyelocytic leukemia (APL), and to define its value in the detection of minimal residual disease (MRD) and treatment prognostication. |
11283136 |
NA |
p15 |
aml |
In this study, we used sodium bisulfite sequencing to obtain a complete map of the 5-methylcytosine status of 80 CpGs covering approximately 900 bp in the 5' p15 CpG island, and 53 CpGs covering approximately 700 bp in the 5' p16 CpG island in t |
11532526 |
NA |
p15 |
rb |
METHODS: We simultaneously analyzed methylation and expression profiles of five putative tumor suppressor genes (p15, p16, Rb, BRCA1, and E-cadherin) in 14 different cell lines using bisulfite genomic sequencing and reverse transcriptase-polymerase chain |
12559313 |
NA |
p15 |
apl |
In this study, methylation-specific polymerase chain reaction (MSP) was used to define the methylation status of a panel of nine genes, comprising p15, p16, RARbeta, oestrogen receptor (ER), E-cadherin (E-CAD), p73, caspase 8 (CASP8), VHL and MGMT, in 29 |
12899712 |
NA |