Abstract

Ovarian cancer is the fifth most common cause of death due to cancer in women despite being the tenth in incidence. Unfortunately, the five-year survival rate is only 45%, which has not improved much in the past 30 years. Even though the majority of women have successful initial therapy, the low rate of survival is due to the eventual recurrence and succumbing to their disease. With the recent release of the Cancer Genome Atlas for ovarian cancer, it was shown that the PI3K/AKT/mTOR pathway was one of the most frequently mutated or altered pathways in patients’ tumors. Researching how the PI3K/AKT/mTOR pathway affects the progression and tumorigensis of ovarian cancer will hopefully lead to new therapies that will increase survival for women. This review focuses on recent research on the PI3K/AKT/mTOR pathway and its role in the progression and tumorigensis of ovarian cancer.

Highlights

  • Ovarian cancer is the fifth most common cause of death due to cancer in women, despite ranking tenth in incidence [1]

  • The PI3 kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway is a central regulator in both normal cell physiology and in cancer proliferation, tumorigenesis, and metastasis

  • PI3K/AKT/mTOR pathway has demonstrated to play a key role in ovarian cancer tumorigenesis, progression, and chemotherapy resistance

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Summary

Introduction

Ovarian cancer is the fifth most common cause of death due to cancer in women, despite ranking tenth in incidence [1]. The PI3K/Akt/mTOR pathway is a central regulator in both normal cell physiology and in cancer proliferation, tumorigenesis, and metastasis. The PI3K/Akt/mTOR pathway has a key role in promoting cell survival in the normal ovary. PI3K/AKT/mTOR pathway has demonstrated to play a key role in ovarian cancer tumorigenesis, progression, and chemotherapy resistance.

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