It was suggested that perhaps diethylstilbestrol increased the incidence of vaginal carcinogenesis by increasing the cell division rate in a system with a fixed mutation rate. Thus, there could be an increase in the number of mutations (leading to cancer) as a result of greater opportunity (i.e., more cell division) for carcinomatous mutations. Pubertal estrogen stimulation of vaginal epithelial growth would then merely be additive to the in utero stimulation of rate of cell division induced by diethylstilbestrol. There may arise a primary cell line as the result of intrauterine estrogen stimulation that serves as the locus of change with later estrogen exposure. Differentiation of vaginal cells into populations with increased or decreased mitotic rates has been observed in experimental situations. The specificity of the neonatal mouse model was questioned because it responds in an abnormal fashion to estrogens, androgens, and progestins. The gestational periods of the mouse and human differ in many important hormonal respects; nevertheless, the mouse models permit examination of events that may ultimately be applicable to the human. The phenomenon of increased growth of vaginal epithelium following neonatal estrogen treatment can be induced in the absence of endogenous gonadal or adrenal hormones and has also been observed after transplantation of the vagina from a treated into an untreated animal. There are some interstrain differences in susceptibility to this effect.
|Original language||English (US)|
|Number of pages||8|
|Issue number||6 II SUPPL.|
|State||Published - Dec 1 1978|
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health