Transplacental Carcinogenesis by Stilbestrol

TLDR

Transplacental exposure to diethylstilbestrol (DES) is believed to initiate malignant changes in fetal vaginal tissue that manifest as adenocarcinoma after puberty, raising concerns about residual DES in livestock products. The editorial argues that DES exposure causes vaginal adenocarcinoma, proposes local progestational therapy to prevent future cases, and calls for banning DES in foodstuffs.

Abstract

This editorial argues the cause-and-effect relationship between in utero exposure to diethylstilbestrol (DES) and incidence of vaginal adenocarcinoma among young women. It is conjectured that the mechanism by which DES induces tumors is a result of transplacental carcinogenesis; i.e., DES causes a malignant change in any fetal cell of future vaginal tissue, resulting in a genetic defect which may not be realized until puberty, when endogenous hormone production acts as a promoter of the malignancy initiated by DES exposure during gestation. If this theory is correct, local progestational therapy may arrest future adenocarcinoma cases. Though it is obvious that DES therapy must be avoided in the future in the population of pregnant women, of more concern is the presence of residual DES in foodstuffs, particularly livestock meat. A ban of such diet supplementation of human foodstuffs is called for.