We hypothesize that:
- 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;
- 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 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.
- Diethylstilbestrol, genetics, teratogenesis, and tumor spectrum in humans, NCBI, PMID: 3889564, 1985 Mar;16(3):315-32.
More DES DiEthylStilbestrol Resources
- DES studies on cancers and screening.
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- DES studies on in-utero exposure to DES and side-effects.
- DES studies on the genital tract.
- Papers on DES lawsuits.
- DES videos and posts tagged DES, the DES-exposed, DES victims.