[Molecular epidemiology and cancer prevention].
Environmental factors act in concert with individual susceptibility to cause most human cancers. The modulation of these environmental factors by host susceptibility has rarely been evaluated. Recently, the molecular epidemiology of human cancer has been extended to a study clarifying individual variation and gene-environmental interactions by integrating molecular biology, in vitro and in vivo laboratory models, biochemistry and epidemiology to infer individual cancer risk. This article briefly reviews genetic polymorphisms frequently used in molecular epidemiological studies and shows, as an example, a possible association between the genetic polymorphisms of CYP17 genes and prostate cancer risk.
Kamoto
T
T
Department of Urology, Kyoto University Graduate School of Medicine.
Ogawa
O
O
Habuchi
T
T
Kato
T
T
D000728:Androgens / Q000378:metabolism; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D017720:Molecular Epidemiology; D011110:Polymorphism, Genetic; D011471:Prostatic Neoplasms / Q000453:epidemiology / Q000235:genetics / Q000517:prevention & control*; D011944:Receptors, Androgen / Q000235:genetics; D013254:Steroid 17-alpha-Hydroxylase / Q000235:genetics
D000728:Androgens; D011944:Receptors, Androgen; D013254:Steroid 17-alpha-Hydroxylase