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    Quantitative cell signalling analysis reveals down-regulation of MAPK pathway activation in colorectal cancer.

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    Authors
    Gulmann, Christian
    Sheehan, Katherine M
    Conroy, Ronán M
    Wulfkuhle, Julia D
    Espina, Virginia
    Mullarkey, Michelle J
    Kay, Elaine W
    Liotta, Lance A
    Petricoin, Emanuel F
    Affiliation
    Department of Pathology, Beaumont Hospital, Dublin, Ireland. christiangulmann@beaumont.ie
    Issue Date
    2009-08
    MeSH
    Aged
    Aged, 80 and over
    Blotting, Western
    Colorectal Neoplasms
    DNA Mismatch Repair
    Down-Regulation
    Enzyme Activation
    Female
    Gene Expression Profiling
    Humans
    Immunohistochemistry
    Isoenzymes
    MAP Kinase Kinase 4
    MAP Kinase Signaling System
    Male
    Middle Aged
    Mitogen-Activated Protein Kinases
    Neoplasm Staging
    Oligonucleotide Array Sequence Analysis
    Phosphorylation
    p38 Mitogen-Activated Protein Kinases
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    Citation
    Quantitative cell signalling analysis reveals down-regulation of MAPK pathway activation in colorectal cancer. 2009, 218 (4):514-9 J. Pathol.
    Journal
    The Journal of pathology
    URI
    http://hdl.handle.net/10147/127609
    DOI
    10.1002/path.2561
    PubMed ID
    19396842
    Abstract
    Mitogen-activated protein kinases (MAPK) are considered to play significant roles in colonic carcinogenesis and kinase inhibitor therapy has been proposed as a potential tool in the treatment of this disease. Reverse-phase microarray assays using phospho-specific antibodies can directly measure levels of phosphorylated protein isoforms. In the current study, samples from 35 cases of untreated colorectal cancer colectomies were laser capture-microdissected to isolate epithelium and stroma from cancer as well as normal (i.e. uninvolved) mucosa. Lysates generated from these four tissue types were spotted onto reverse-phase protein microarrays and probed with a panel of antibodies to ERK, p-ERK, p38, p-p38, p-JNK, MEK and p-MEK. Whereas total protein levels were unchanged, or slightly elevated (p38, p = 0.0025) in cancers, activated isoforms, including p-ERK, p-p38 and p-JNK, were decreased two- to four-fold in cancers compared with uninvolved mucosa (p < 0.0023 in all cases except for p-JNK in epithelium, where decrement was non-significant). This was backed up by western blotting. Dukes' stage B and C cancers displayed lower p-ERK and p-p38 expression than Dukes' stage A cancers, although this was not statistically significant. It is concluded that MAPK activity may be down-regulated in colorectal cancer and that further exploration of inhibitory therapy in this system should be carefully evaluated if this finding is confirmed in larger series.
    Item Type
    Article
    Language
    en
    ISSN
    1096-9896
    ae974a485f413a2113503eed53cd6c53
    10.1002/path.2561
    Scopus Count
    Collections
    Beaumont Hospital

    entitlement

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