Year: 1999
Type: article
Abstract: Deregulation of cell cycle that results in uncontrolled cellular proliferation is the basis of neoplastic process. Bladder tumors are heterogenous in their behavior, and it is very difficult to predict the clinical course in many patients. In order to alleviate this problem, attention has been focused on mutations in various cell cycle regulators and their association with tumor behavior. Mutations of the p16/CDKN2 gene, encoding a cyclin-dependent kinase inhibitor, are common in bladder cancer. In contrast to other tumor suppressor genes, the two most common mechanisms for loss of p16/CDKN2 function are homozygous deletion and loss of transcription associated with hyperméthylation of the 5'CpG island region. Recently, it is found that méthylation of p16/CDKN2 is potentially reversible with exposure to demethylating agents, such as 5- aza-2'-deoxycytidine, which is a well-established inhibitor of DNA méthylation, which may open up new ways to effective tumor management.Key Words: Méthylation, Bladder cancer, Cell cycle
Authors: Cevdet Kaya, Levent Türkeri, A. Akdaş
Institution: Marmara University
Language: Turkish
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2345345138