Apoptosis and carcinogenesis

Lyons, S. K., Clarke, A. R. (1997) Apoptosis and carcinogenesis. Br Med Bull, 53 (3). pp. 554-69. ISSN 0007-1420 (Print)0007-1420 (Linking)

URL: https://www.ncbi.nlm.nih.gov/pubmed/9374037
DOI: 10.1093/oxfordjournals.bmb.a011630

Abstract

Many tumours are characterised by increased levels of apoptosis. This observation establishes significance for this process in tumour development, but it does little to elucidate the nature of this role, nor does it yield information relevant to the early stages of carcinogenesis. To gain a better understanding of the importance of apoptosis, it has been necessary to create a number of transgenic model systems wherein the apoptotic response has been modified. Using this strategy, a number of genetic lesions have been identified which affect both the apoptotic pathway and predisposition to malignancy. These lesions can operate either directly, by blocking the induction of apoptosis; or indirectly, by increasing the selective pressure for further genetic change. The consequent deregulation of growth control and increase in mutation burden represent two key steps in carcinogenesis, underlining the pivotal role played in tumour suppression by the normal induction of apoptosis.

Item Type: Paper
Uncontrolled Keywords: Apoptosis/*genetics Cell Transformation, Neoplastic/*genetics Genes, Retinoblastoma/physiology Genes, bcl-2/physiology Genes, myc/physiology Genes, p53/physiology Genetic Therapy/methods Humans Neoplasms/genetics/pathology/therapy
Subjects: organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > apoptosis
diseases & disorders > cancer > cancer types > retinoblastoma
CSHL Authors:
Communities: CSHL labs > Lyons lab
Depositing User: Matt Covey
Date: 1997
Date Deposited: 12 May 2017 15:08
Last Modified: 12 May 2017 15:08
URI: http://repository.cshl.edu/id/eprint/34718

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