, Volume 1, Issue 2, pp 163-175

P53, apoptosis, and breast cancer

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access

Abstract

Wild-type p53 is a tumor suppressor gene that plays a central role in maintaining the genetic integrity of the cell by preventing cells with damaged DNA from further proliferation. Mutation and deletion of p53 are the most common genetic defects seen in clinical cancer. About 40% of breast carcinomas show high levels of stabilized, often mutant, p53 protein in their cells as detected by immunohistochemistry. p53-related defects in tumor cells correlate with a poor prognosis and may also indicate a poor response to chemotherapy. In experimental systems, the p53 status of cells is important in determining their sensitivity to radiation and chemotherapeutic drugs. Cells with functional p53 die by apoptosis, whilst similar cells lacking p53 function continue to proliferate, perpetuating potentially oncogenic mutations. Not only may p53 status be a marker of the biological aggressiveness of individual tumors and of their likely response to therapy, but restoration of normal p53 function is itself already a goal of cancer therapy.