Early endometrial carcinoma: clinicopathology, hormonal aspects, molecular genetics, diagnosis, and treatment

Abstract

The number of patients with endometrial carcinoma is markedly increasing in Japan. Therefore, understanding of its biological characteristics and establishment of appropriate treatment are important. In this article, we first describe the clinicopathology of the two types of endometrial carcinoma with their hormonal background and genetic alterations, and then discuss the pathways of early endometrial carcinogenesis. In addition, we also review the diagnostic and therapeutic modalities for early endometrial carcinomas with current controversies, especially regarding postoperative treatment strategies.

Biological Roles of Estrogen and Progesterone in Human Endometrial Carcinoma - New developments in potential endocrine therapy for endometrial cancer -

“…This approach is by no means a standard therapy and should not be recommended routinely, even when the patients desire. However, this approach has been supported by several reports in patients desiring to maintain fertility, despite the fact that the subsequent success rate of pregnancy is not necessarily high [55,56]. The initial response rate of MPA ranged from 55% to 100% for endometrial carcinoma and 70 to 100% for atypical hyperplasia [55,56].…”

“…However, this approach has been supported by several reports in patients desiring to maintain fertility, despite the fact that the subsequent success rate of pregnancy is not necessarily high [55,56]. The initial response rate of MPA ranged from 55% to 100% for endometrial carcinoma and 70 to 100% for atypical hyperplasia [55,56]. In a recent multi-center study, Ushijima et al reported the results of 17 cases of atypical endometrial hyperplasia and 28 cases of endometrioid endometrial carcinoma [57].…”

Chemokines and Cancer Progression: A Qualitative Review on the Role of Stromal Cell-derived Factor 1-alpha and CXCR4 in Endometrial Cancer

“…Common epithelial mutations which give rise to endometrial tumors include PTEN inactivation, betacatenin, k-ras, p53, and HER2/neu mutations, as well as microsatellite instability [4]. Importantly, cancer cells continue to communicate with host stromal cells after acquiring these initial mutations.…”

NAC1, a potential stem cell pluripotency factor expression in normal endometrium, endometrial hyperplasia and endometrial carcinoma

“…There are two main clinicopathologic variants of endometrial carcinoma (2). Type I tumors are usually estrogen-related.…”

“…In contrast, type II carcinomas are unrelated to estrogen, are associated with atrophic endometrium, and usually occur at an older age (3,4). Four main molecular genetic alterations have been described in type I endometrial carcinomas, including microsatellite instability (MI), and mutations of the PTEN, K-ras, and B-catenin genes (2)(3)(4)(5). These molecular alterations have also been described in atypical endometrial hyperplasia (2).…”