Targeting the PI3K pathway and DNA damage response as a therapeutic strategy in ovarian cancer

Area of Science:

• Oncology
• Molecular Biology
• Genetics

Background:

• Ovarian cancer remains a leading cause of cancer death globally.
• Despite advances, treatment resistance remains a significant challenge.
• The phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway is often dysregulated in ovarian cancer, promoting cell survival and resistance.

Purpose of the Study:

• To review the expanded role of the PI3K/AKT/mTOR pathway in DNA damage response and cell cycle regulation.
• To explore novel combination treatment strategies for ovarian cancer.
• To enhance the efficacy of PI3K pathway inhibitors through combination therapy.

Main Methods:

• Literature review of current research on PI3K pathway inhibitors and DNA damage response (DDR) in ovarian cancer.
• Analysis of emerging data on the involvement of the PI3K pathway in DNA replication and genome stability.
• Synthesis of information regarding combination treatment strategies.

Main Results:

• The PI3K/AKT/mTOR pathway plays a complex role in ovarian cancer, contributing to cell survival and chemoresistance.
• Emerging evidence indicates the PI3K pathway's involvement in DNA replication and maintaining genome stability.
• Combining PI3K pathway inhibitors with DNA damage response (DDR) inhibitors presents a promising therapeutic strategy.

Conclusions:

• The PI3K/AKT/mTOR pathway is a critical target in ovarian cancer, but inhibitors have shown limited success alone.
• The PI3K pathway's role in DNA damage response suggests synergistic potential with DDR inhibitors.
• Combination therapy of PI3K pathway inhibitors and DDR blockades offers a novel approach to improve ovarian cancer treatment outcomes.