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    How the evolution of multicellularity set the stage for cancer

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    Author
    Trigos, AS; Pearson, RB; Papenfuss, AT; Goode, DL
    Date
    2018-01-23
    Source Title
    British Journal of Cancer
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Goode, David; Pearson, Richard; Papenfuss, Anthony
    Affiliation
    Sir Peter MacCallum Department of Oncology
    Medical Biology (W.E.H.I.)
    Metadata
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    Document Type
    Journal Article
    Citations
    Trigos, A. S., Pearson, R. B., Papenfuss, A. T. & Goode, D. L. (2018). How the evolution of multicellularity set the stage for cancer. BRITISH JOURNAL OF CANCER, 118 (2), pp.145-152. https://doi.org/10.1038/bjc.2017.398.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/255869
    DOI
    10.1038/bjc.2017.398
    NHMRC Grant code
    NHMRC/1052904
    NHMRC/1053792
    Abstract
    Neoplastic growth and many of the hallmark properties of cancer are driven by the disruption of molecular networks established during the emergence of multicellularity. Regulatory pathways and molecules that evolved to impose regulatory constraints upon networks established in earlier unicellular organisms enabled greater communication and coordination between the diverse cell types required for multicellularity, but also created liabilities in the form of points of vulnerability in the network that when mutated or dysregulated facilitate the development of cancer. These factors are usually overlooked in genomic analyses of cancer, but understanding where vulnerabilities to cancer lie in the networks of multicellular species would provide important new insights into how core molecular processes and gene regulation change during tumourigenesis. We describe how the evolutionary origins of genes influence their roles in cancer, and how connections formed between unicellular and multicellular genes that act as key regulatory hubs for normal tissue homeostasis can also contribute to malignant transformation when disrupted. Tumours in general are characterised by increased dependence on unicellular processes for survival, and major dysregulation of the control structures imposed on these processes during the evolution of multicellularity. Mounting molecular evidence suggests altered interactions at the interface between unicellular and multicellular genes play key roles in the initiation and progression of cancer. Furthermore, unicellular network regions activated in cancer show high degrees of robustness and plasticity, conferring increased adaptability to tumour cells by supporting effective responses to environmental pressures such as drug exposure. Examining how the links between multicellular and unicellular regions get disrupted in tumours has great potential to identify novel drivers of cancer, and to guide improvements to cancer treatment by identifying more effective therapeutic strategies. Recent successes in targeting unicellular processes by novel compounds underscore the logic of such approaches. Further gains could come from identifying genes at the interface between unicellular and multicellular processes and manipulating the communication between network regions of different evolutionary ages.

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