Quantitative mass spectrometry for colorectal cancer proteomics

Authors

  • Juan Martínez-Aguilar,

    1. Australian Proteome Analysis Facility (APAF), Department of Chemistry & Biomolecular Sciences, Macquarie University, Sydney, Australia
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  • Jenny Chik,

    1. Australian Proteome Analysis Facility (APAF), Department of Chemistry & Biomolecular Sciences, Macquarie University, Sydney, Australia
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  • Judith Nicholson,

    1. Australian Proteome Analysis Facility (APAF), Department of Chemistry & Biomolecular Sciences, Macquarie University, Sydney, Australia
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  • Crystal Semaan,

    1. Australian Proteome Analysis Facility (APAF), Department of Chemistry & Biomolecular Sciences, Macquarie University, Sydney, Australia
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  • Matthew J. McKay,

    1. Australian Proteome Analysis Facility (APAF), Department of Chemistry & Biomolecular Sciences, Macquarie University, Sydney, Australia
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  • Mark P. Molloy

    Corresponding author
    • Australian Proteome Analysis Facility (APAF), Department of Chemistry & Biomolecular Sciences, Macquarie University, Sydney, Australia
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  • Colour Online: See the article online to view Fig. 1 in colour.

Correspondence: Dr. Mark P. Molloy, APAF, Macquarie University, Sydney 2109, Australia.

E-mail: mmolloy@proteome.org.au

Fax: +612 9850 6200

Abstract

This review documents the uses of quantitative MS applied to colorectal cancer (CRC) proteomics for biomarker discovery and molecular pathway profiling. Investigators are adopting various labeling and label-free MS approaches to quantitate differential protein levels in cells, tumors, and plasma/serum. We comprehensively review recent uses of this technology to examine mouse models of CRC, CRC cell lines, their secretomes and subcellular fractions, CRC tumors, CRC patient plasma/serum, and stool samples. For biomarker discovery these approaches are uncovering proteins with potential diagnostic and prognostic utility, while in vitro cell culture experiments are characterizing proteomic and phosphoproteomic responses to disrupted signaling pathways due to mutations or to inhibition of drugable enzymes.

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