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PI3K/AKT/mTOR signaling pathway as a therapeutic target for ovarian cancer
HaiXia Li1, JianFang Zeng, Keng Shen
1Department of Obstetrics and Gynecology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, 100005, China.
Background:
Ovarian cancer is one of the major causes of death in women worldwide. Despite improvements in conventional treatment approaches, such as surgery and chemotherapy, a majority of patients with advanced ovarian cancer experience relapse and eventually succumb to the disease; the outcome of patients remains poor. Hence, new therapeutic strategies are urgently required. The phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) is activated in approximately 70 % of ovarian cancers, resulting in hyperactive signaling cascades that relate to cellular growth, proliferation, survival, metabolism, and angiogenesis. Consistent with this, a number of clinical studies are focusing on PI3K pathway as an attractive target in the treatment of ovarian cancer. In this review, we present an overview of PI3K pathway as well as its pathological aberrations reported in ovarian cancer. We also discuss inhibitors of PI3K pathway that are currently under clinical investigations and the challenges these inhibitors face in future clinical utility.
Methods:
PubMed was searched for articles of relevance to ovarian cancer and the PI3K pathway. In addition, the ClinicalTrials.gov was also scanned for data on novel therapeutic inhibitors targeting the PI3K pathway.
Results:
Genetic aberrations at different levels of PI3K pathway are frequently observed in ovarian cancer, resulting in hyperactivation of this pathway. The alterations of this pathway make the PI3K pathway an attractive therapeutic target in ovarian cancer. Currently, several inhibitors of PI3K pathway, such as PI3K/AKT inhibitors, rapamycin analogs for mTOR inhibition, and dual PI3K/mTOR inhibitors are in clinical testing in patients with ovarian cancer.
Conclusions:
PI3K pathway inhibitors have shown great promise in the treatment of ovarian cancer. However, further researches on selection patients that respond to PI3K inhibitors and exploration of effective combinatorial therapies are required to improve the management of ovarian cancer.
Insights
Targeting the phosphatidylinositol 3-kinase (PI3K) pathway offers new hope for ovarian cancer treatment. Inhibitors are in clinical trials, but patient selection and combination therapies need further research for improved outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Ovarian cancer remains a leading cause of cancer death in women, with poor outcomes for advanced stages despite current treatments.
- The phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway is hyperactivated in ~70% of ovarian cancers, driving tumor growth and survival.
- This pathway's dysregulation makes it a critical therapeutic target for novel ovarian cancer treatments.
Purpose of the Study:
- To review the role of the PI3K pathway in ovarian cancer.
- To discuss pathological aberrations of the PI3K pathway in ovarian cancer.
- To examine current clinical investigations of PI3K pathway inhibitors and their challenges.
Main Methods:
- Literature search of PubMed for ovarian cancer and PI3K pathway relevance.
- Scanned ClinicalTrials.gov for data on novel therapeutic inhibitors targeting the PI3K pathway.
Main Results:
- Frequent genetic aberrations in the PI3K pathway lead to its hyperactivation in ovarian cancer.
- Several PI3K pathway inhibitors, including PI3K/AKT inhibitors and dual PI3K/mTOR inhibitors, are under clinical investigation.
- These inhibitors represent a promising therapeutic strategy for ovarian cancer.
Conclusions:
- PI3K pathway inhibitors demonstrate significant promise for ovarian cancer treatment.
- Further research is needed to identify patient populations responsive to PI3K inhibitors.
- Exploring effective combinatorial therapies is crucial for enhancing ovarian cancer management.
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