Dissecting "PI3Kness"

The complexity of personalized therapy for ovarian cancer

Robert C. Bast, Gordon Mills

Research output: Contribution to journalArticle

23 Citations (Scopus)

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
Externally publishedYes

Fingerprint

Ovarian Neoplasms
Phosphatidylinositol 3-Kinase
Cell Line
Mutation
Growth
Platinum
Neoplasms
Genotype
Drug Therapy
Therapeutics
Ovarian epithelial cancer

ASJC Scopus subject areas

  • Oncology

Cite this

Dissecting "PI3Kness" : The complexity of personalized therapy for ovarian cancer. / Bast, Robert C.; Mills, Gordon.

In: Cancer Discovery, Vol. 2, No. 1, 01.01.2012, p. 16-18.

Research output: Contribution to journalArticle

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