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Updated: May 21, 2026

Murine Model for Non-invasive Imaging to Detect and Monitor Ovarian Cancer Recurrence
Published on: November 2, 2014
Investigational agents in development for the treatment of ovarian cancer
Shannon N Westin1, Thomas J Herzog, Robert L Coleman
1Department of Gynecologic Oncology and Reproductive Medicine, University of Texas MD Anderson Cancer Center, Houston, TX, USA. swestin@mdanderson.org
Abstract:
Although significant success has been achieved in the treatment of advanced and recurrent ovarian cancer, there is clearly room for improvement. The use of targeted agents in this patient population has the promise to provide improved survival and quality of life. There are a myriad of relevant pathways under exploration in all settings of ovarian cancer. Clinical trial data are accumulating for antiangiogenic therapy, including vascular endothelial growth factor (VEGF)-specific inhibitors and multiple angiogenic signaling target inhibitors, as well as poly-ADP-ribose polymerase (PARP) inhibitors. Other types of tumorigenic pathway inhibitors, including those that target phosphatidylinositol-3-kinase (PI3K), mammalian target of rapamycin (mTOR), protein kinase B (AKT), Src, folate receptor alpha, and insulin-like growth factor-1 receptor (IGF-1R) pathways are in earlier phases of development for ovarian cancer. Attempts to target the epidermal growth factor receptor (EGFR) of ovarian tumors have been met with limited success; however, newer agents that inhibit this pathway show promise. Finally, with recognition of the role of Wee-1 in p53-deficient tumors, an inhibitor of this tyrosine kinase is being evaluated in recurrent ovarian cancer. The logistical challenge is to determine the optimal timing and proper combinations of novel agents independently as well as concomitantly with conventional chemotherapeutics. Reported results have been modest; however, our growing understanding of these pathways will be potentially reflected in greater impact on response and survival.
Insights
Targeted therapies, including antiangiogenic and poly-ADP-ribose polymerase (PARP) inhibitors, show promise for advanced ovarian cancer. Further research into novel agents and combinations aims to improve patient survival and quality of life.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Advanced and recurrent ovarian cancer treatment has seen success, but significant room for improvement remains.
- Targeted agents offer potential for enhanced survival and quality of life in ovarian cancer patients.
- Numerous molecular pathways are under investigation for therapeutic intervention in ovarian cancer.
Purpose of the Study:
- To review current and emerging targeted therapies for advanced and recurrent ovarian cancer.
- To discuss the role of various signaling pathways and their inhibitors in ovarian cancer treatment.
- To highlight the challenges and future directions in optimizing targeted agent combinations.
Main Methods:
- Review of accumulating clinical trial data for targeted agents.
- Exploration of antiangiogenic therapies, including vascular endothelial growth factor (VEGF) inhibitors.
- Evaluation of poly-ADP-ribose polymerase (PARP) inhibitors and other pathway-specific inhibitors (PI3K, mTOR, AKT, Src, folate receptor alpha, IGF-1R, EGFR, Wee-1).
Main Results:
- Antiangiogenic therapies and poly-ADP-ribose polymerase (PARP) inhibitors are accumulating clinical data.
- Inhibitors targeting PI3K, mTOR, AKT, Src, folate receptor alpha, and IGF-1R pathways are in early development.
- Epidermal growth factor receptor (EGFR) pathway inhibition shows promise with newer agents, and Wee-1 inhibitors are being evaluated for recurrent ovarian cancer.
Conclusions:
- Modest results have been reported for current targeted agents in ovarian cancer.
- Optimal timing and combination strategies for novel agents with conventional chemotherapy are critical logistical challenges.
- A deeper understanding of these pathways will likely lead to greater impact on treatment response and survival in ovarian cancer.
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