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    Glucuronidation of SN-38 and NU/ICRF 505 in human colon cancer and adjacent normal colon.

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    Authors
    Cummings, Jeffrey
    Ethell, Brian T
    Jardine, Lesley
    Burchell, Brian
    Affiliation
    Cancer Research UK, Edinburgh Oncology Unit, Western General Hospital, Edinburgh, UK. jcummings@picr.man.ac.uk
    Issue Date
    2006
    
    Metadata
    Show full item record
    Abstract
    BACKGROUND: Glucuronidation represents a novel mechanism of intrinsic drug resistance in colon cancer cells. To safely reverse this mechanism in vivo, it is essential to identify which isoforms of UDP-glucuronosyltransferases are responsible for catalysing this drug metabolism in tumour tissue. MATERIALS AND METHODS: LC-MS was applied to measure rates of glucuronidation of two anticancer compounds (SN-38 and NU/ICRF 505) by patient colon cancer biopsies and paired normal colon. RESULTS: Three independent lines of enquiry indicated that, in the tumour specimens, SN-38 was glucuronidated primarily by UGT1A1, the isozyme generally recognised as being responsible for hepatic detoxification of this compound, while with NU/ICRF 505 two candidate isoforms emerged - UGT1A8 and/or UGT1A10 - both of which are not normally expressed in the liver. CONCLUSION: These data suggest that tumour selective modulation of this drug resistance mechanism in patients may be feasible with NU/ICRF 505 but more difficult to realise with SN-38. De novo drug resistance is recognised as contributing significantly to the poor response rates of colorectal cancer (CRC) to chemotherapy (1). Nonetheless, the underlying mechanisms responsible for drug insensitivity remain
    Citation
    Glucuronidation of SN-38 and NU/ICRF 505 in human colon cancer and adjacent normal colon., 26 (3B):2189-96 Anticancer Res.
    Journal
    Anticancer Research
    URI
    http://hdl.handle.net/10541/73078
    PubMed ID
    16821585
    Type
    Article
    Language
    en
    ISSN
    0250-7005
    Collections
    All Paterson Institute for Cancer Research

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