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  1. Cancer progression as a sequence of atavistic reversions.Charles H. Lineweaver, Kimberly J. Bussey, Anneke C. Blackburn & Paul C. W. Davies - 2021 - Bioessays 43 (7):2000305.
    It has long been recognized that cancer onset and progression represent a type of reversion to an ancestral quasi‐unicellular phenotype. This general concept has been refined into the atavistic model of cancer that attempts to provide a quantitative analysis and testable predictions based on genomic data. Over the past decade, support for the multicellular‐to‐unicellular reversion predicted by the atavism model has come from phylostratigraphy. Here, we propose that cancer onset and progression involve more than a one‐off multicellular‐to‐unicellular reversion, and are (...)
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  • From developmental to atavistic bet‐hedging: How cancer cells pervert the exploitation of random single‐cell phenotypic fluctuations.Jean-Pascal Capp & Frédéric Thomas - 2022 - Bioessays 44 (9):2200048.
    Stochastic gene expression plays a leading developmental role through its contribution to cell differentiation. It is also proposed to promote phenotypic diversification in malignant cells. However, it remains unclear if these two forms of cellular bet‐hedging are identical or rather display distinct features. Here we argue that bet‐hedging phenomena in cancer cells are more similar to those occurring in unicellular organisms than to those of normal metazoan cells. We further propose that the atavistic bet‐hedging strategies in cancer originate from a (...)
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  • Erosion of cooperation in ageing tissue enables the emergence of the cancer phenotype.Beata Ujvari - 2021 - Bioessays 43 (2):2000301.
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  • Cancer progression: A journey through the past (with the same stops)?Simon P. Castillo - 2021 - Bioessays 43 (7):2100088.
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