Diethylstilbestrol, genetics, teratogenesis, and tumor spectrum in humans.
Diethylstilbestrol (DES) is the first example of transplacental carcinogenesis in humans, as evidenced by an excess of clear cell adenocarcinoma of the vagina and cervix in exposed women. We hypothesize that: 1) in utero DES exposure will be responsible for a broader spectrum of cancer with variable age of onset as a function of latency effects in exposed humans of both sexes; 2) teratogenicity of DES will be more far-reaching than currently recognized and will harbor cancer implications in the face of known associations between teratogenesis and carcinogenesis; and 3) genetic heterogeneity will be a critical etiologic discriminant in DES associated cancer. This hypothesis embraces a prodigious body of data at the infrahuman level, as well as extant pharmacogenetic and ecogenetic observations in humans which signify heritable variations in response to environmental carcinogenic exposures. This hypothesis has important implications for drug testing with appropriate preventive strategies. Herein, particular restraints with monitoring through governmental legal channels must be employed. Past experience has clearly indicated negligence in shouldering this responsibility by both the pharmaceutical industry and government regulatory bodies.
D000230:Adenocarcinoma / Q000139:chemically induced; D002471:Cell Transformation, Neoplastic / Q000139:chemically induced; D004054:Diethylstilbestrol / Q000009:adverse effects*; D005260:Female; D006801:Humans; D009369:Neoplasms / Q000139:chemically induced* / Q000235:genetics; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D002583:Uterine Cervical Neoplasms / Q000139:chemically induced; D014625:Vaginal Neoplasms / Q000139:chemically induced
D004054:Diethylstilbestrol