Molecular Biology for Oncologists by John R. Yarnold (auth.), John R. Yarnold, Michael R.

By John R. Yarnold (auth.), John R. Yarnold, Michael R. Stratton, Trevor J. McMillan (eds.)

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Ponder, B. A. , Easton, D. F. ancl Horwich, A. (eds) (1996) Genetic Predisposition to Cancer, Chapman & Hall, London (in press). Lemoine, N. R. and Hurst, H. C. (1994) Genetics of cancer. Eur. J. Cancer, 30A. Ponder, B. A. , Solomon, E. and Cavenee, W. (eds) (1995) Genetics and Cancer: A Second Look, Cancer Surveys, vol. 25, Cold Spring Harbor Press, New York. Ponder, B. and Waring, M. (eds) (1995) The Genetics of Cancer, Cancer Biology and Medicine, vol. 4, Kluwer Academic Publishers, London.

If the gene is dominant, the risk to siblings will be half that in parents because, on average, the offspring of the parents will inherit the diseasecausing gene 50% of the time. 4 MOLECULAR GENETICS OF CANCER-PREDISPOSITION With the exception of one cancer family syndrome so far, cancer-predisposition genes are tumour suppressor genes. At the gene locus responsible for the predisposition in an individual, one of the alleles is inactivated by mutation in every cell in the body, whereas the other normal allele acts to suppress tumour formation; hence the term tumour suppressor gene.

The alterations in DNA that result in this change in biochemical activity are almost exclusively point mutations. All are missense and hence allow translation of a full length Ras protein. Of particular importance, however, is the restriction of the mutations to certain sites within the gene, namely codons 12, 13 and 61 (that encode amino acids 12,13 and 61 of the Ras protein). Mutations at other sites are not found in human tumours, nor do most of them result in oncogenic activation in experimental models.

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