We examined the genomic status of the p161NK4A (inhibitor of cyclin-dependent kinase 4 A) and cyclin-dependent kinase 4 (CDK4) genes in 62 human hepatocellular carcinomas (HCCs), 5 cholangiocellular carcinomas and 6 cell lines derived from human liver canceo. Although no samples showed the homozygou
Alterations of the p16INK4A gene in human ovarian cancers
โ Scribed by Tatsuya Kanuma; Jun-ichi Nishida; Tomonao Gima; J. Carl Barrett; Norio Wake
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 394 KB
- Volume
- 18
- Category
- Article
- ISSN
- 0899-1987
No coin nor oath required. For personal study only.
โฆ Synopsis
The p16 INK4A gene, which encodes the cell-cycle regulatory protein cyclin-dependent kinase 4 inhibitor, is a putative tumor-suppressor gene. We examined p16 gene alterations in 30 primary ovarian cancers and 11 ovarian cancer cell lines. Five of the primary cancers (16.7%) had lost both p16 INK4A genes. In addition, four cancers (13.3%) contained five kinds of missense mutations and a one-base deletion. Three cell lines had homozygous deletions of p16 genes, and one cell line had multiple intragenic mutations. There was also suppressed transcription of the p16 gene in one cell line. Some point mutations occurred in the conserved ankylin consensus region. These observations suggest that p16 is a functional target for ovarian carcinogenesis and that p16 alterations occurred in the primary cancers.
๐ SIMILAR VOLUMES
## Background: It has been suggested that cyclin-dependent kinase inhibitors (cdkis), including p16 and p15, are tumor suppressor genes. alterations of cdkis have been found in most types of cancer. however, little is known about the status of p16 and p15 genes, including methylation of the promote
We have examined the roles of 2 putative tumor-suppressor genes, the p16 and p15 inhibitor-of-cyclin-dependentkinase genes, in the most commonly occurring epithelial tumors of the human ovary. Expression of p16 mRNA, examined by RT-PCR, was significantly reduced in 15 of the 48 tumors. Aberrant expr
Cell-cycle regulation depends on a fine balance between cyclin-cyclin-dependent kinase complexes and a family of kinase inhibitors that bind cyclin-cdk complexes and block their activity. To investigate the role of mechanisms regulating cell-cycle progression in human osteosarcomas (OS), pRb/p16/cdk
In primary breast cancer, mutations of the p53 tumor suppressor gene lead to loss of growth-suppressive properties and poor outcome. Recently, a p53-related gene, termed p73, has been cloned and its gene product possesses a function similar to p53. p73 has been mapped at chromosome 1p36.3, a region