Endometrial cancer (EC), which arises in the lining of the uterus, is the most common gynecologic malignancy. Approximately 90% of cases of EC are sporadic, whereas the remaining 10% of cases are hereditary. Although most ECs are diagnosed early, mainly due to symptomatic postmenopausal metrorrhagia, up to 20% of the lesions progress to a high-stage tumor. Unfortunately, the five-year survival in these women drops to 15%, compared to 90% in women diagnosed with confined disease. In the past twenty years, there has been a shift in the EC paradigm to consider it as a multiplicity of disease types rather than a single disease. For EC, four molecular subgroups have undergone extensive studies in recent years: POLE ultramutated, mismatch repair-deficient, p53 mutant and EC lacking any of these alterations, referred to as NSMP. Nonetheless, patients with histologically similar ECs may have very different outcomes, notably in patients with high-grade EC. Improved understanding of the molecular basis for EC could reveal potential biomarkers of disease diagnosis and progression, as well as lead to the identification of molecular targets for novel therapeutic strategies of treatment. Numerous agents targeting different components have been developed and studied as single agents or in combination with traditional cytotoxic agents; additionally, molecular targeted therapies can be combined to deliver increased benefits to patients. Continued investigation into the molecular pathways of EC development and progression are needed to increase our knowledge of this disease process and will lead to the discovery of novel, superior treatment options for patients.

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• Endometrial cancer
• Liquid biopsy
• Molecular biology
• Predictive and prognostic biomarker