๐”– Bobbio Scriptorium
โœฆ   LIBER   โœฆ

Loh and mutation analysis of CDKN2 in primary human ovarian cancers

โœ Scribed by Ian G. Campbell; Gareth Beynon; Michael Davis; Pat Englefield


Publisher
John Wiley and Sons
Year
1995
Tongue
French
Weight
735 KB
Volume
63
Category
Article
ISSN
0020-7136

No coin nor oath required. For personal study only.

โœฆ Synopsis


The CDKNZ gene encodes a cell cycle regulatory protein and is located on chromosome 9 ~2 1 , a region deleted in a wide variety of primary tumours. While mutations in the CDKNZ gene itself are frequently observed in tumour cell lines, they are less common in primary turnouts. We have investigated the role of the CDKNZ gene in ovarian cancer by analysis for allelic loss of 9p2 I and single-strand conformational polymorphism analysis of exons I and 2 of CDKNZ in 67 primary ovarian tumoun. Loss of heterozygosity on 9p2I was frequently observed (24/50 informative tumoun) and was common in early-stage tumours, suggesting that it is an early event in ovarian tumorigenesis. Homozygous deletion of the CDKNZ gene was detected in only I tumour. No somatic or germline mutations were observed in CDKNZ, though a codon 140 polymorphism was detected in 2 cases. This suggests that CDKNZ is not involved in ovarian tumorigenesis and that another gene(s) may be the target of the frequent 9p allelic losses observed.

ici 199s Wiley-Liss. Inc.


๐Ÿ“œ SIMILAR VOLUMES


Infrequent CDKN2 mutation in human diffe
โœ William S. Tung; Douglas W. Shevlin; Detlef Bartsch; Jeffrey A. Norton; Samuel A ๐Ÿ“‚ Article ๐Ÿ“… 1996 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 611 KB

We examined t h e frequency of cyclin-dependent kinase (CDK) N2 alterations in differentiated and anaplastic thyroid cancers t o assess the involvement of CDKNZ in the development of these cancers. The CDKNZ gene, which encodes the cell-cycle regulator p16, was recently shown t o be mutated or delet

Deletional, mutational, and methylation
โœ David F. Jarrard; G. Steven Bova; Charles M. Ewing; Sokhom S. Pin; Son H. Nguyen ๐Ÿ“‚ Article ๐Ÿ“… 1997 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 98 KB ๐Ÿ‘ 1 views

The tumor suppressor gene CDKN2 (p16/MTS1) resides on chromosome 9p21 and encodes a 16 kDa inhibitor of the cyclin-dependent kinases. Inactivation of CDKN2 by homozygous deletion, point mutation, and recently described aberrant methylation in the 5' promoter region may increase progression through t

Low frequency of BRAF and CDKN2A mutatio
โœ Helga B. Salvesen; Rajiv Kumar; Ingunn Stefansson; Sabrina Angelini; Nicola MacD ๐Ÿ“‚ Article ๐Ÿ“… 2005 ๐Ÿ› John Wiley and Sons ๐ŸŒ French โš– 196 KB ๐Ÿ‘ 1 views

## Abstract Several pathways have been implicated in the pathogenesis of endometrial carcinoma. Based on recent reports, __BRAF__ mutations provide an alternative route for activation of the RAS signalling pathway. The __CDKN2A (p16)__ tumour suppressor gene is also altered in several tumour types.

Ovarian cancer susceptibility alleles an
โœ Susan J. Ramus; Antonis C. Antoniou; Karoline B. Kuchenbaecker; Penny Soucy; Jon ๐Ÿ“‚ Article ๐Ÿ“… 2012 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 361 KB ๐Ÿ‘ 1 views

Germline mutations in BRCA1 and BRCA2 are associated with increased risks of breast and ovarian cancer. A genome-wide association study (GWAS) identified six alleles associated with risk of ovarian cancer for women in the general population. We evaluated four of these loci as potential modifiers of

Analysis of RAD51C germline mutations in
โœ Ella R. Thompson; Samantha E. Boyle; Julie Johnson; Georgina L. Ryland; Sarah Sa ๐Ÿ“‚ Article ๐Ÿ“… 2011 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 180 KB

There is strong evidence that overtly inactivating mutations in RAD51C predispose to hereditary breast and ovarian cancer but the prevalence of such mutations, and whether they are associated with a particular clinical phenotype, remains unclear. Resolving these questions has important implications