The role of genetic factors in bladder cancer was reviewed in four specific sections: the familial aggregation; the association of genetic polymorphisms with bladder cancer cases; the role of the genetically determined acetylation system in workers exposed to aromatic amines; and the identification of specific activated cellular oncogenes and chromosomal changes in bladder cancer. Unless some compromising experience occurs, the genetic influence does not appear to be expressed as a familial propensity toward bladder cancer development. These experiences include occupational exposures or cigarette smoking. Some genetic factors have been identified in bladder cancer but the precise role of genetic factors was not known. One suggested pathway involves spontaneous or externally caused mutation of a germ cell with subsequent transmission of the defective gene to bladder cells of the offspring. These cells may be thus rendered vulnerable to carcinogenesis or to a second mutational event that provokes the emergence of a malignant clone of cells. Genetically conditioned factors such as slow acetylator phenotype and certain HLA haplotypes can render individuals more specific at certain times to bladder cancer development. According to the author, the suggested relationship between HLA-B5 or HLA-CW4, or blood type-A in nonexposed bladder cancer cases needs further investigation. Whether all persons have oncogenes that can be activated if conditions are right or whether certain individuals are more susceptible remains to be examined.
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