P53, cell cycle control and apoptosis: implications for cancer.

Published

Journal Article (Review)

Cellular proliferation depends on the rates of both cell division and cell death. Tumors frequently have decreased cell death as a primary mode of increased cell proliferation. Genetic changes resulting in loss of programmed cell death (apoptosis) are likely to be critical components of tumorigenesis. Many of the gene products which appear to control apoptotic tendencies are regulators of cell cycle progression; thus, cell cycle control and cell death appear to be tightly linked processes. P53 protein is an example of a gene product which affects both cell cycle progression and apoptosis. The ability of p53 overexpression to induce apoptosis may be a major reason why tumor cells frequently disable p53 during the transformation process. Unfortunately, the same genetic changes which cause loss of apoptosis during tumor development, may also result in tumor cell resistance to anti-neoplastic therapies which kill tumor cells by apoptosis. Elucidation of the genetic and biochemical controls of these cellular responses may provide insights into ways to induce cell death and thus hopefully suggest new targets for improving therapeutic index in the treatment of malignancies.

Full Text

Duke Authors

Cited Authors

  • Kastan, MB; Canman, CE; Leonard, CJ

Published Date

  • March 1995

Published In

Volume / Issue

  • 14 / 1

Start / End Page

  • 3 - 15

PubMed ID

  • 7606818

Pubmed Central ID

  • 7606818

International Standard Serial Number (ISSN)

  • 0167-7659

Digital Object Identifier (DOI)

  • 10.1007/bf00690207

Language

  • eng

Conference Location

  • Netherlands