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ISSN: 2638-5945

Open Access Journal of Oncology and Medicine

Mini Review(ISSN: 2638-5945)

Microenvironmental Stress as the Driver of Cell Plasticity and Tumour Autonomy

Volume 3 - Issue 5

Dan V Nicolau1,2 and Sunil R Lakhani3

  • Author Information Open or Close
    • 1School of Mathematical Sciences, Queensland University of Technology, Australia.
    • 2Nuffield Department of Experimental Medicine, University of Oxford, Australia
    • 3University of Queensland Centre for Clinical Research and Pathology Queensland, Royal Brisbane Women’s Hospital, Australia.

    *Corresponding author: Dan V Nicolau, School of Mathematical Sciences, Queensland University of Technology, Australia

Received: June 18, 2020;   Published: July 17, 2020

DOI: 10.32474/OAJOM.2020.03.000173

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It is well established that the tumour microenvironment (TME) plays a key role in cancer progression, from local invasion all the way to metastasis. In particular, the tumour cell is subjected to various challenges within the TME, from hypoxia to attack by immune cells, collectively rendering its local habitat hostile. The resulting selection pressure essentially encourages invasive behavior by favouring plastic phenotypes. Epigenetic changes then appear to confer on the tumour cell enhanced motility, reduced cell-cell adhesion, the epithelial-mesenchymal transition and other features that have been linked with unicellularity, particularly in the context of the atavistic model of cancer. While some of these changes do indeed appear to be ‘regressive’ and connected to ancient genes, the atavistic model fails to explain why many others are ‘innovative’, recapitulating - in pathological form - programmes requiring exquisite, multicellular cooperation, including angiogenesis and immune evasion. Taking these aspects of cancer progression together suggests a model whereby the hostile TME selects for autonomy, rather than unicellularity, and hints at a deep duality between cellular autonomy and a failure of support for the selective advantages usually conferred by existence within a coordinated, multicellular community.

Keywords: Cancer Progression; Tumour Microenvironment; Plasticity; Atavistic Model

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