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- W2116714440 abstract "In common with all other malignancies, gynaecological cancers are caused by the accumulation of mutations in growth regulating genes. These mutations may be inherited in a minority of individuals with ovarian or endometrial cancer and are caused predominantly by viral agents in cervical cancer. Hereditary predisposition to ovarian cancer is often found in conjunction with breast cancer and the major predisposing gene BRCA1 has now been identified. Susceptibility to endometrial cancer may be inherited as part of a familial predisposition to colorectal cancer and four genes causing this pattern of cancers in families have recently been identified as DNA repair genes. Hormonal factors contribute to genetic changes in both the endometrium and ovary and drugs which have oestrogenic activity may alter the risks of developing malignancies at these sites. Recent years have seen an enormous improvement in our understanding of the mechanisms of carcinogenesis. Most cancers require a number of genetic changes in a single cell before an invasive turnout results. These changes occur predominantly in two types of growth regulatory gene. An oncogene if activated by a mutation will accelerate cell growth and division. In contrast, most mutations in turnout suppressor genes inactivate the growth suppressor function and again this leads to proliferation. However, the classical model for a growth suppressor gene inactivation requires loss of both functional copies of the gene. In practice this will not always be the case as some mutations will produce a protein product which interferes with the normal 'wild type' protein from the normally functioning copy (allele) of the gene. Few gynaecological turnouts are likely to be caused purely by the loss of two tumour suppressor genes as in the classical model of retinoblastoma, and the number of changes probably varies between four and 10. A" @default.
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- W2116714440 date "1995-12-01" @default.
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- W2116714440 title "The genetics of gynaecological cancer" @default.
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- W2116714440 doi "https://doi.org/10.1016/s0957-5847(95)80004-2" @default.
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