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Updated: May 22, 2026
Strategy for Biobanking of Ovarian Cancer Organoids: Addressing the Interpatient Heterogeneity across Histological Subtypes and Disease Stages
Published on: February 23, 2024
Dissecting "PI3Kness": the complexity of personalized therapy for ovarian cancer
Robert C Bast1, Gordon B Mills
1Department of Experimental Therapeutics and Systems Biology, University of Texas MD Anderson Cancer Center, Houston, Texas, USA. rbast@mdanderson.org
Abstract:
Epithelial ovarian cancers exhibit marked heterogeneity and can be divided into low-grade type I and more prevalent high-grade type II lesions that differ in stage at diagnosis, rate of growth, and susceptibility to platinum-based chemotherapy. Activation of the phosphatidylinositol 3' kinase (PI3K) pathway occurs in a significant fraction of both types of ovarian cancer, driven predominantly by mutations in type I and amplification in type II. Available cell lines do not often reflect the genotype of type II ovarian cancers, but studies with cell lines driven by mutation suggest that blocking activated AKT is necessary, but not sufficient to inhibit cancer cell growth. Inhibition of multiple signaling pathways will likely be required to achieve effective personalized therapy for patients whose cancers exhibit "PI3Kness."
Insights
Targeting the phosphatidylinositol 3' kinase (PI3K) pathway is crucial for ovarian cancer treatment. Blocking AKT alone is insufficient; inhibiting multiple signaling pathways is necessary for effective personalized therapy in "PI3Kness" cancers.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Epithelial ovarian cancers show heterogeneity, classified as type I (low-grade) and type II (high-grade).
- The phosphatidylinositol 3' kinase (PI3K) pathway is activated in a substantial portion of both ovarian cancer types.
- Type I activation is mutation-driven, while type II is driven by amplification.
Purpose of the Study:
- To investigate the role of the PI3K pathway in epithelial ovarian cancer.
- To evaluate the efficacy of targeting the PI3K pathway for personalized therapy.
Main Methods:
- Analysis of ovarian cancer cell lines and their genotypes.
- Studies involving the inhibition of activated AKT and other signaling pathways.
Main Results:
- Cell lines often do not accurately represent type II ovarian cancer genotypes.
- Blocking activated AKT is a necessary but insufficient step for inhibiting cancer cell growth.
- Effective inhibition requires targeting multiple signaling pathways.
Conclusions:
- Personalized therapy for ovarian cancers with "PI3Kness" necessitates a multi-targeted approach.
- Inhibiting multiple signaling pathways is essential for successful treatment outcomes.
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