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Tumor suppressor genes: new pathways in gynecological cancer
  1. J. A. TIDY and
  2. D. WREDE
  1. Department of Gynaecological Oncology, Samaritan Hospital for Women, Marylebone Road, London NW1 5YE and Ludwig Institute for Cancer Research, St Mary's Hospital Medical School, Norfolk Place, London W2 1PG
  1. Address for correspondence: David Wrede, Ludwig Institute for Cancer Research, St Mary's Hospital Medical School, Norfolk Place, London W2 1PG, UK.


The Retinoblastoma (Rb-1) and p53 genes appear to play an important role in controlling cell division, and mutations in Rb-1 and p53 have been reported widely in non-gynecological cancers. Unlike other cancer-related genes, which become activated during carcinogenesis, it is the loss of wild type p53 and Retinoblastoma protein (RB) function that is thought to contribute to cancer development. These genes therefore, have been called tumor suppressor genes since normal function appears to be necessary for negative control of cell growth. Several viral oncoproteins have been shown to interact with RB and p53. It seems likely that the formation of these complexes inactivates the cellular protein resulting in an overall effect similar to somatic mutation of the Rb-1 or p53 genes. The HPV16 transforming proteins E7 and E6 complex with protein products of Rb-1 and p53, respectively. In HPV positive anal and cervical tumors the normal function of RB and p53 may be inhibited by these viral proteins and so mutation within the RB-1 and p53 gene coding sequences would not appear to be a necessary step in the genesis of these tumors. However, in HPV negative tumors from the same tissues, loss of wild type Rb-1 and p53 activity may only be achieved by somatic mutation of these genes.

  • HPV
  • p53
  • Rb
  • tumor suppressor genes

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