Abstract
A novel class of oncogene has been recognised whose loss-of-function results in the expression of the malignant phenotype. Two examples of such genes are the human retinoblastoma predisposition gene (RB1) and the gene encoding the cellular protein p53. These genes are thought to regulate and limit normal proliferation of cells and, as a consequence, can suppress tumongenicity when introduced into transformed cells. They are hence frequently described as 'tumour suppressor genes'. Both RB1 and p53 gene products are bound by various transforming early proteins encoded by the DNA tumour viruses SV40, adenovirus and human papilloma virus. It is thought that they are thus sequestered and rendered inactive. Thus, a coherent model is emerging whereby inactivation, either by mutation of sequestration, of these tumour suppressor genes may contribute to natural and experimental carcinogenic processes.
Original language | English (US) |
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Pages (from-to) | 437-446 |
Number of pages | 10 |
Journal | Seminars in Cancer Biology |
Volume | 1 |
Issue number | 6 |
State | Published - Dec 1990 |
Externally published | Yes |
Keywords
- Anti-oncogene
- RB
- Retinoblastoma gene
- Tumour suppressor genes
- p53
ASJC Scopus subject areas
- Cancer Research