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    Toward Targeting Antiapoptotic MCL-1 for Cancer Therapy

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    Author
    Kelly, GL; Strasser, A
    Editor
    Jacks, T; Sawyers, CL
    Date
    2020-01-01
    Source Title
    ANNUAL REVIEW OF CANCER BIOLOGY, VOL 4
    Publisher
    ANNUAL REVIEWS
    University of Melbourne Author/s
    Kelly, Gemma; Strasser, Andreas
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
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    Document Type
    Chapter
    Citations
    Kelly, G. L. & Strasser, A. (2020). Toward Targeting Antiapoptotic MCL-1 for Cancer Therapy. Jacks, T (Ed.). Sawyers, CL (Ed.). ANNUAL REVIEW OF CANCER BIOLOGY, VOL 4, 4, pp.299-313. ANNUAL REVIEWS.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/252362
    DOI
    10.1146/annurev-cancerbio-030419-033510
    Abstract
    <jats:p> Apoptosis is critical for embryonic development, tissue homeostasis, and the removal of infected or otherwise dangerous cells. It is controlled by three subgroups of the BCL-2 protein family—the BH3-only proteins that initiate cell death; the effectors of cell killing, BAX and BAK; and the antiapoptotic guardians, including MCL-1 and BCL-2. Defects in apoptosis can promote tumorigenesis and render malignant cells refractory to anticancer therapeutics. Activation of cell death by inhibiting antiapoptotic BCL-2 family members has emerged as an attractive strategy for cancer therapy, with the BCL-2 inhibitor venetoclax leading the way. Large-scale cancer genome analyses have revealed frequent amplification of the locus encoding antiapoptotic MCL-1 in human cancers, and functional studies have shown that MCL-1 is essential for the sustained survival and expansion of many types of tumor cells. Structural analysis and medicinal chemistry have led to the development of three distinct small-molecule inhibitors of MCL-1 that are currently undergoing clinical testing. </jats:p>

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