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- W3158275180 endingPage "1895" @default.
- W3158275180 startingPage "1886" @default.
- W3158275180 abstract "Cancer is characterized by loss of the regulatory mechanisms that preserve homeostasis in multicellular organisms, such as controlled proliferation, cell-cell adhesion, and tissue differentiation. The breakdown of multicellularity rules is accompanied by activation of selfish, unicellular-like life features, which are linked to the increased adaptability to environmental changes displayed by cancer cells. Mechanisms of stress response, resembling those observed in unicellular organisms, are actively exploited by mammalian cancer cells to boost genetic diversity and increase chances of survival under unfavorable conditions, such as lack of oxygen/nutrients or exposure to drugs. Unicellular organisms under stressful conditions (e.g., antibiotic treatment) stop replicating or slowly divide and transiently increase their mutation rates to foster diversity, a process known as adaptive mutability. Analogously, tumor cells exposed to drugs enter a persister phenotype and can reduce DNA replication fidelity, which in turn fosters genetic diversity. The implications of adaptive evolution are of relevance to understand resistance to anticancer therapies." @default.
- W3158275180 created "2021-05-10" @default.
- W3158275180 creator A5044490291 @default.
- W3158275180 creator A5064011158 @default.
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- W3158275180 date "2021-05-05" @default.
- W3158275180 modified "2023-10-14" @default.
- W3158275180 title "Adaptive Evolution: How Bacteria and Cancer Cells Survive Stressful Conditions and Drug Treatment" @default.
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