Testicular cancer in prenatally DES-exposed men

Environmental Signaling: What Embryos and Evolution Teach Us About Endocrine Disrupting Chemicals, 2001

Abstracts

DES as a model for developmental estrogenization

Studies in our laboratory and others have helped to define a phenotype typical of male mice exposed in utero to DES and other estrogens. The structural or functional changes associated with the phenotype include undescended testes, cysts of the epididymis, prostatic lesions, distended seminal vesicles, retained Müllerian ducts, reduced fertility, and abnormal spermatogenesis (even in a scrotal testis).

In a smaller number of cases, the occurrence of testicular cancers was noted (see 1979 study, 1985 study, 1986 study). The severity of these changes was dose-dependent as were the appearance of all the lesions in the suite. It was subsequently shown that the epididymal cysts were of Müllerian duct origin; it was apparent that the enlarged prostatic utricle was also the Müllerian contribution to the prostate gland.

Features in the human male

Genital tract defects similar to those seen in DES-treated mice were also observed in men whose mothers had taken DES (study).

A group at the University of Chicago reported that DES-exposed men had a higher incidence of undescended (cryptorchid) testes and epididymal cysts than comparable unexposed men. Gill and colleagues (study) went on to confirm and extend these studies and showed, in addition, a higher incidence of hypoplastic testes and abnormal sperm.

In one study reporting testicular cancer in one DES-exposed man, the possibility of cancer of the testis as a result of prenatal exposure to DES was raised by Gill et al. (study). A few other case reports of testicular cancer (seminoma) and epididymal cysts in prenatally DES-exposed men have been reported (study).

References

  • Environmental Signaling: What Embryos and Evolution Teach Us About Endocrine Disrupting Chemicals, Endocrine Reviews, Volume 22, Issue 3, Pages 319–341 doi.org/10.1210/edrv.22.3.0432, 01 June 2001.
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