Malignant Neoplasms
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
Molecular genetic studies have revealed that deletion of the p16 and p15 genes occurs frequently in cancer cell lines and in certain malignant neoplasms.
|
7563186 |
1995 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
This is the first report of screening for alteration of the p16 gene in testicular, ovarian and endometrial malignancies.
|
7563391 |
1995 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
These results are consistent with the idea that p16 allelic variants that decrease Cdk interaction predispose individuals who carry them to an increased risk of cancer.
|
7566978 |
1995 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Molecular genetic techniques have been used to explore the role of p16 in normal development and cancer.
|
7606716 |
1995 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Loss of the p16 gene is frequent in and highly specific to lymphoid malignancies (54 of 183 [30%] in lymphoid tumor v2 of 219 [1%] in myeloid tumors; P < .0001).
|
7632963 |
1995 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Our findings suggest that homozygous deletion of the p16 gene is seen in about 15% of ALL cases, is not restricted to cases with cytogenetically detectable 9p deletion, and could have a pathogenetic role in this malignancy.
|
7833469 |
1995 |
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Our data confirm the predicted reciprocity between Rb inactivation and p16 expression in a common human malignancy and define differential p16 expression as a fundamental distinction between NSCLC and SCLC.
|
7834618 |
1995 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
For example, the CDKI genes p16 and p15 are frequently deleted in various malignancies and are thought to contribute to cellular transformations.
|
8630967 |
1996 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These results indicate that MTAP deficiency in cancer is primarily due to codeletion of the MTAP and p16 genes.
|
8650244 |
1996 |
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We previously reported that p16 levels are low to undetectable in normal human uroepithelial cells (HUCs) and in immortalized uroepithelial cells with functional pRb, whereas p16 levels are markedly elevated in immortal HUCs with altered pRb (T. Yeager et al., Cancer Res., 55: 493-497, 1995).
|
8674033 |
1996 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The p16 and p15 CDKI genes are very frequently altered in a variety of cancers including hematopoietic malignancies.
|
8946928 |
1996 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Astrocytomas representing all World Health Organization (WHO) grades of malignancy were analyzed in a correlative study using multiplex polymerase chain reaction (PCR) analysis to detect deletions of the p16 gene together with immunohistochemistry to detect loss of the protein in archival specimens of the same tumors.
|
9098651 |
1997 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
(Cancer Res 55:2053-2055, 1995), which showed no p16 mutations or homozygous deletions in 18 primary neuroblastomas and nine tumor-derived cell lines.
|
9115582 |
1997 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
These observations suggest that p16 is a functional target for ovarian carcinogenesis and that p16 alterations occurred in the primary cancers.
|
9115583 |
1997 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In a subset of gastric MALT lymphomas, homozygous p16 deletions are acquired and may contribute to the transformation from a low-grade to a high-grade malignancy.
|
9178679 |
1997 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
It is suggested that alterations of the p16 gene affect a subset of PILs that contain mutations of the K-ras gene and that these mutations might identify high-risk precursors of the invasive malignancy.
|
9187111 |
1997 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The cyclin-dependent kinase inhibitor p16 gene (P16, MTS1, CDKN2) has been shown to be altered by deletion or point mutation in some human tumours and cancer cell lines, suggesting that it works as a tumour suppressor.
|
9231912 |
1997 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, these data support a new model in which overcoming senescence plays a critical role in human cancer pathogenesis and requires at least two genetic changes that occur in several combinations that can include either p16 or pRb loss and at least one additional alteration, such as +20q11-q12, -3p13-p14, or -8p21-pter.
|
9436977 |
1998 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
A variety of cancer syndromes involving the P16 and BRCA2 genes, for example, also lead to pancreatic cancer, but the gene responsible for familial pancreatic cancer has not been identified so far.
|
9438603 |
1997 |
Malignant Neoplasms
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
Recently, an alternative mechanism of p16 inactivation involving methylation of the CpG island in the 5' region of the gene has been demonstrated in a number of malignancies and cell lines.
|
9454653 |
1998 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Based on these studies, we conclude that p16-mediated cytotoxicity is tightly associated with the presence of functional pRb in human cancer cells, and that tumor cells which are mutant or null for p16 are candidates for Adp16 mediated cancer gene therapy.
|
9464545 |
1998 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Inactivation of the tumor-suppressor gene p16 (MTS1/ CDKN2/INK4a) has been described in various human malignancies.
|
9495360 |
1998 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
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 |
1998 |
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Indeed, known phenotypes associated with germ-line p16 mutations and an apparent correlation between the deletion span and tumor spectrum in the two families suggest a new model of cancer pathogenesis based on the inactivation of contiguous tumor suppressor genes, an alternative to the established pleiotropic effects of single-gene disruption.
|
9622062 |
1998 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The product of the p16/INK4a/CDKN2/MTS1 tumor-suppressor gene acts as a negative cell cycle regulator by inhibiting G1 cyclin-dependent kinases that phosphorylate the retinoblastoma protein. p16 is inactivated in a wide range of human malignancies, including familial melanoma.
|
9694617 |
1998 |