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    Targeting DNA damage in SCLC.

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    Authors
    Foy, Victoria
    Schenk, Maximilian W
    Baker, Katie
    Gomes, Fabio
    Lallo, Alice
    Frese, Kristopher K
    Forster, M
    Dive, Caroline
    Blackhall, Fiona H
    Affiliation
    Clinical and Experimental Pharmacology Group, Cancer Research UK Manchester Institute, University of Manchester, UKClinical and Experimental Pharmacology Group, Cancer Research UK Manchester Institute, University of Manchester, UK
    Issue Date
    2017-12
    
    Metadata
    Show full item record
    Abstract
    SCLC accounts for 15% of lung cancer worldwide. Characterised by early dissemination and rapid development of chemo-resistant disease, less than 5% of patients survive 5 years. Despite 3 decades of clinical trials there has been no change to the standard platinum and etoposide regimen for first line treatment developed in the 1970's. The exceptionally high number of genomic aberrations observed in SCLC combined with the characteristic rapid cellular proliferation results in accumulation of DNA damage and genomic instability. To flourish in this precarious genomic context, SCLC cells are reliant on functional DNA damage repair pathways and cell cycle checkpoints. Current cytotoxic drugs and radiotherapy treatments for SCLC have long been known to act by induction of DNA damage and the response of cancer cells to such damage determines treatment efficacy. Recent years have witnessed improved understanding of strategies to exploit DNA damage and repair mechanisms in order to increase treatment efficacy. This review will summarise the rationale to target DNA damage response in SCLC, the progress made in evaluating novel DDR inhibitors and highlight various ongoing challenges for their clinical development in this disease.
    Citation
    Targeting DNA damage in SCLC. 2017, 114:12-22 Lung Cancer
    Journal
    Lung Cancer
    URI
    http://hdl.handle.net/10541/620718
    DOI
    10.1016/j.lungcan.2017.10.006
    PubMed ID
    29173760
    Type
    Article
    Language
    en
    ISSN
    1872-8332
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.lungcan.2017.10.006
    Scopus Count
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