The pathogenesis of endometrial carcinomas at menopause: facts and figures

Abstract

Almost a third of the life of a woman is now postmenopausal, and during this period over 80% of endometrial carcinomas develop. This is by far the most common gynaecological malignancy in the industrialised world and, probably, the less completely understood with regard to its pathogenesis after the menopause. For while it is generally thought that these neoplasms are non-oestrogen-induced, we are, at the same time, informed that oestrogenic stimulation is continuous during menopause through increases to oestrone formation in the adipose tissue from androgens of adrenal and ovarian origin. Furthermore, the postmenopausal endometrium has been typified as atrophic, which is indeed true, but is also implied as being inactive, which in fact it is not; in most cases, the postmenopausal endometrium appears to be weakly proliferative with potential to give rise to an endometrial carcinoma. It is also assumed that postmenopausal endometrial tumours are predominantly of serous papillary and clear cell type, and, in general, they are not well-differentiated endometrioid carcinomas; in reality, no more than 15% are serous papillary and clear cell carcinomas, and no less than 55% are well-differentiated endometrioid neoplasms. The overall prognosis is presumed to be poor, yet postmenopausal patients harbouring well-differentiated endometrioid carcinomas have the same excellent prognosis as those premenopausal women having endometrioid tumours of similar grade and stage. This brief account of endometrial carcinogenesis at menopause re-evaluates these issues and, in the light of new and old evidence, proposes the separation of G1 endometrioid adenocarcinomas (low-grade tumours) from all others (high-grade tumours).

Morphological and Functional Changes in the Thyroid Follicles of the Aged Murine and Humans

“…Cystic atrophy is not infrequently found in the postmenopausal endometrium. In the absence of ovarian function, the endometrium experiences cystic atrophy, having a thin uterine mucosa, cystically dilated endometrial glands, and a flattened inactive epithelium [12]. The pathogenesis of cystic atrophy of the endometrium has not yet been established.…”

Pathophysiology of Heavy Menstrual Bleeding

“…However, EC is a hormonally driven disease and the continuous, unopposed effect of the mitotic action of estrogen is thought to be the primary oncogenic promoter in at least 80% of endometrial cancers [5]. Therefore, conditions that dysregulate the sequential exposure to pro-future science group Pathophysiology of heavy menstrual bleeding Review gesterone of the estrogen primed endometrium, such as obesity, PCOS, diabetes, estrogen secreting ovarian tumors and tamoxifen use, among others, will increase the risk of EC [69,70]. The usual pattern of the bleeding associated with EC is irregular and continuous rather than regular HMB and is thought to be secondary to disruption of endometrial vessels due to invasion by malignant cells and abnormal neovasculogenesis [37].…”

Role of estrogen receptor β in gynecological cancer

“…In western countries, endometrial cancer is the most common cancer type of the female genital tract [49]. It occurs predominantly in postmenopausal women [49,50]. Especially excessive exposure to estrogens, particularly in the absence of progesterone, increases endometrial cancer risk [49][50][51][52].…”