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    Tandem Duplication of KIT Exon 11 Influences the Proteome of Canine Mast Cell Tumours (2012)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Schlieben, P
    Meyer, A
    Weise, C
    Bondzio, A
    Gruber, A D
    Klopfleisch, R
    Quelle
    Journal of Comparative Pathology; 148(4) — S. 318–322
    ISSN: 0021-9975
    Sprache
    Englisch
    Verweise
    DOI: 10.1016/j.jcpa.2012.07.006
    Pubmed: 22935087
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    Abstract / Zusammenfassung

    Mutations with permanent activation of the stem cell factor receptor KIT have been identified as one potential cause for canine cutaneous mast cell tumours (MCTs). The exact changes in global gene expression patterns associated with permanent activation of KIT in these tumours are unknown. The present study compares, by the use of two dimensional difference gel electrophoresis and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry, the proteomes of canine MCTs, with and without KIT exon 11 tandem duplication. Fifteen differentially expressed proteins were identified in mutated MCTs. These are mainly involved in cytoskeleton structure and cell motility (ACTR2, ACTB and CAPPA1), cell signalling (ARHGDIA) and lipid metabolism (ALOX15 and ACSBG4), or are serum proteins. The results therefore support the notion that KIT mutation is associated with changes in the proteome of affected cells with a major effect on the composition of the cytoskeletal proteome and cell motility proteins. No overlaps were identified when the results were compared with a recent study on the proteomic differences between low- and high-grade tumours, suggesting that KIT-mutated tumours may be regarded as a separate entity of high-grade tumours with potential relevance to therapeutic strategies.