Abstract
Endometrial cancer (EC) is one of the most common cancers with a constantly and steadily growing incidence worldwide. The main reason for EC development, in addition to the female population aging, involves the obesity epidemic and associated hyperinsulinemia. Screening for EC has not been developed. However, endometrial carcinoma (ECa) demonstrates a specific symptomatology and clinical picture, and diagnostic methods are available, sensitive and defined by a certain range of comorbid diseases. These factors allow early ECa diagnosis in 80 %. The methods of treatment are standardized, depending on the stage of RTM and the morphological structure of EC, the age of the patient and allow to achieve 72–76 % of the overall 5-year survival rate. The methods of treatment are standardized, depending on the EC stage, the morphological structure of ECa, and the patient’s age, and allow achieving the 5-year overall survival of 72–76 %. The disease promised a favorable outcome and seemed to be controlled. However, at the end of the last century, researchers started to report the clinical and morphological heterogeneity of ECa, which allowed Ya. V. Bohman to propose a dichotomous division of EC into clinical and pathological variants. Such a division was accepted all over the world and required re-evaluation of the prognostic value of various endometrial adenocarcinoma histotypes depending on the phenotype and hormonogenesis of ECa. Initially, adenosquamous cancer (or endometrioid adenocarcinoma with squamous metaplasia, in the modern classification) was also classified as estrogen-dependent endometrioid adenocarcinoma, and squamous cell endometrial cancer was classified as an unfavorable type with a poor prognosis and without hormonal influence. Interest in the squamous cell component in dimorphic endometrial adenocarcinoma has repeatedly arisen over the past decades due to its unpredictable clinical course. The newest TCGA molecular classification of EC did not clarify the issues, but gave rise to new ones related to the etiology and carcinogenesis of this ECa histotype and its clinical interpretation.
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