Abstract
Simple SummaryEndometrial cancer (EC) represents 90% of uterine cancer and to date its standard clinical approach is still surgery and/or chemo- and radiotherapy. This mini-review illustrates the state of the art in the disease management. In particular, we aim to point out the following features: the hormonal nature of the pathology and the role of steroid receptors in EC promotion and progression; the importance of molecular and histopathological assessment for driving the clinic decision and the promising immunotherapeutic approaches with immune checkpoint blockade.EC is the most common cancer in the female genital tract in developed countries, and with its increasing incidence due to risk factors, such as aging and obesity, tends to become a public health issue. Although EC is a hormone-dependent neoplasm, there are no recommendations for the determination of steroid hormone receptors in the tumor tissue and no hormone therapy has ever been assessed in the adjuvant setting. Furthermore, its immune environment has been slightly characterized, but recent evidences point out how EC microenvironment may increase self-tolerance by reducing the recruitment of cytotoxic immune cells to the tumor site and/or modifying their phenotype, making these cells no longer able to suppress tumor growth. Here we highlight insights for EC management from diagnosis to a desirable trend of personalized treatment.
Highlights
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Over 90% of uterine cancers are adenocarcinomas of which ~80% are related to a surplus of estrogens associated to insulin resistance and obesity [3], while the remaining 20% are of unknown etiology [1]
EC is classified based on light microscopic features using the World Health Organization (WHO) classification system, which remains the gold standard in the diagnostic arena [15]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. About 80% of all ECs are type I lesions, related to long-lasting unopposed estrogen exposure, especially in pre- and peri-menopausal status. They usually have endometrioid histology, low tumor grade, indolent activities, and arise against a background of endometrial atypical complex hyperplasia (ACH). About 20% of all ECs, by contrast, are Type II lesions, not related to long-lasting unopposed estrogen exposure. They usually have a more aggressive behavior when compared with type I, and they often have a non-endometrioid histology, usually serous papillary and clear cell. Several molecular studies have confirmed this dualistic classification, emphasizing relevant differences between the two types; several molecular markers have been investigated [18]
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