In this short review, we explore the relationship between endometrial cancer and the mTOR pathway and its downstream regulation of protein synthesis. Advances in the molecular genotyping of endometrial cancers have led to an intense focus on molecularly targeted agents that act on the mTOR pathway, and this approach has shown some of the best responses in the treatment of advanced and recurrent disease.

Current combination therapies are highly toxic and of limited efficacy for the treatment of patients who require systemic therapy. Although it is highly curable by surgery when diagnosed at an early stage and grade, the burden of advanced stage and recurrent disease is substantial. ©2011 AACR.Įndometrial cancer remains the most common gynecologic malignancy.

We also highlight laboratory and clinical research findings that will provide new avenues for future research and clinical development. Here, we discuss the potential benefit of targeting mTOR combined with existing chemotherapies by monitoring its impact on translational regulatory pathways and key translation targets in endometrial cancer. Given the poor rate of success for treatment of late-stage endometrial cancer, increasing attention is being directed to the development of new therapeutic approaches, including targeting the mTOR pathway. Less well developed in the study of endometrial cancer is an understanding of mTOR signaling to its major downstream effector, translational control. Endometrial cancers show a significant reliance on the mTOR pathway for survival, and studies to date have revealed a clinical advantage in targeting this pathway. A molecular and genetic understanding of endometrial cancer involves the mTOR signaling pathway, an emerging target for treatment of type I disease (the most common presentation). Although it is highly treatable in the early stages of disease, therapies for advanced and recurrent disease are rarely curative. Endometrial cancer is the most common gynecologic malignancy.

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