A New Mutational aktivation in the PI3K Pathway

Joan Brugge, Mien Chie Hung, Gordon B. Mills

    Research output: Contribution to journalShort survey

    188 Scopus citations

    Abstract

    Although multiple members of the phosphatidylinositol-3-kinase pathway (PI3K) are targeted by germline or somatic mutations, functional mutations in the three akt isoforms have proven elusive. This is somewhat surprising, as AKT represents a key node in the PI3K pathway, exhibiting transforming activity when incorporated into the AKT8 retrovirus. A recent report in Nature identifies a transforming E17K PH domain mutation in akt1 in breast (8%), colorectal (6%), and ovarian (2%) cancers. E17K-akt1 transforming activity appears due to PtdIns(3,4)P2- and PtdIns(3,4,5)P3-independent recruitment of AKT1 to the membrane. This novel observation raises important theoretical and clinical questions.

    Original languageEnglish (US)
    Pages (from-to)104-107
    Number of pages4
    JournalCancer Cell
    Volume12
    Issue number2
    DOIs
    StatePublished - Aug 14 2007

    ASJC Scopus subject areas

    • Oncology
    • Cell Biology
    • Cancer Research

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