Dissecting "PI3Kness": The complexity of personalized therapy for ovarian cancer

Robert C. Bast, Gordon B. Mills

    Research output: Contribution to journalArticle

    23 Scopus citations

    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."

    Original languageEnglish (US)
    Pages (from-to)16-18
    Number of pages3
    JournalCancer discovery
    Volume2
    Issue number1
    DOIs
    StatePublished - Jan 1 2012

    ASJC Scopus subject areas

    • Oncology

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