Taken together, these observations support a role for mutations of the p53 gene in the development of cisplatin resistance in ovarian cancer as a consequence of loss of the ability of p53 to transactivate bax, an apoptosis-inducing gene.
Loss of heterozygosity on chromosome 5q in ovarian cancer is frequently accompanied by TP53 mutation and identifies a tumour suppressor gene locus at 5q13.1-21.
Although numerous studies have reported p53 expression and mutation in ovarian tumors, none have correlated p53 expression with that of its downstream effector, p21waf1/cip1.
In particular, we examined the association between the lifetime number of ovulatory cycles and mutation of the p53 tumor-suppressor gene (also known as TP53) in ovarian tumors.
These findings provide support for classifying MPSC as a distinct neoplasm of the ovary and suggest that increased expression of wild-type p53 may play a role in its pathogenesis.
Loss of heterozygosity (LOH) in chromosome region 6q27 and p53 mutations were studied to attempt to clarify the genetic etiology of ovarian cancer, with particular reference to clear cell adenocarcinoma (CCC), which has a poor prognosis.
We have further investigated the association between ovulatory history and p53 gene mutation by use of data from a large case-control study of ovarian cancer in Australia.
The purpose of this investigation was to assess p53 alterations in ovarian cancer to determine if p53 overexpression corresponds with mutations in the p53 gene, and to assess whether either predicts clinical outcome in ovarian carcinoma.