Testicular Dysgenesis Syndrome and Testicular Germ Cell Cancer

Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement, 2009

Abstracts

As discussed below, development of vaginal adenocarcinoma in women exposed fetally to DES and the association of carcinoma in situ in the fetal testis with the development of testicular cancer in adulthood (see Testicular dysgenesis syndrome: possible role of endocrine disrupters, 2006, and Pathways of endocrine disruption during male sexual differentiation and masculinization, 2006) are examples of links between the fetal environment and the occurrence of adult disease.

In the male, cryptorchidism, hypospadias, oligospermia, and testicular cancer have been proposed to be linked as the testicular dysgenesis syndrome (TDS) arising from disturbed prenatal testicular development. Such links are important because they could mean that several disorders occur at different periods throughout life in a single individual as a result of exposure to a given EDC (or mixture) at a particular period.

Testicular Dysgenesis Syndrome TDS

Skakkebaek et al. hypothesized that diminished semen quality, TGCC, and male urogenital tract anomalies may share a common causal pathway. They defined this triad as the TDS. The hypothesis invokes a common pathway by which EDCs, and other environmental chemicals and genetic factors, may lead to abnormal development of the fetal testis, producing testicular dysgenesis that can manifest as an increased risk of urogenital abnormalities in newborn males, as well as altered semen quality and TGCC in young men. As a cautionary note, the manifestations (or symptoms) of TDS have other causes apart from testicular dysgenesis.

It is hypothesized that TDS is due to prenatal Leydig and Sertoli cell dysfunction with secondary androgen insufficiency and impaired germ cell development. This should not be confused with the clinical diagnosis of dysgenetic testes, which is associated with genital ambiguity and a high risk of testicular malignancy. The existence of TDS as a distinct clinical entity and of possible associations with EDCs is an area of active research

Testicular Germ Cell Cancer TGCC

The earliest suggestion of epidemiological evidence related to prenatal estrogen exposure and increased risk of TGCC came from a (DES) study in 1979. However, other studies have not consistently confirmed these earlier results.

References

  • Full study (free access) : Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement, Endocrine Reviews, PMC2726844, 2009 June.
  • Featured image credit tamassetmanagement.
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