Abstract:
To investigate proliferation in disease free postmenopausal endometrium
and that harbouring endometrial adenocarcinoma—is there a dynamic,
yet lurking, potential for atrophic endometrium to give rise to
endometrial adenocarcinoma? The study comprised 84 disease free
endometria from asymptomatic postmenopausal women who had
undergone hysterectomy for prolapse, and 50 endometrioid cell type
endometrial adenocarcinomas with adjacent uninvolved postmenopausal
endometrium. The non-neoplastic tissues were separated histologically
into active, inactive, and mixed forms, although only the first two
categories were studied immunohistochemically for oestrogen and
progesterone receptors (ERs, PRs), epidermal growth factor receptor
(EGFR), Ki-67, and angiogenic activity. All postmenopausal endometria
were atrophic, but only 42 were inactive; of the remaining samples, 22
were weakly proliferative and 20 were mixed active and inactive. In
contrast, the nonneoplastic component of 43 of the 50 endometrial
adenocarcinomas examined was of the active form; four specimens were
of the pure and 39 of the mixed form. Interestingly, high ER and PR
expression was seen in active and inactive endometria, but only the
former were EGFR positive and had high proliferative (Ki-67) and
angiogenic activity. A similar trend was also shown by the nonneoplastic atrophic endometrium adjacent to endometrial
adenocarcinoma. At least half of the disease free postmenopausal
atrophic endometria show a weak proliferative pattern, either diffuse or
focal, probably as a response to continuous low level oestrogenic
stimulation. These tissues have a latent, although very small,
carcinogenic potential, as demonstrated by the immunohistochemical
profile and their frequent association with adjacent endometrial
adenocarcinoma.
