The Response of Cancer Cell Populations to Therapies

Lindsay, Danika; Garvey, Colleen M.; Mumenthaler, Shannon M.; Foo, Jasmine

doi:10.1016/b978-0-12-804310-3.00010-7

Cited by 1 publication

(1 citation statement)

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“…The vast majority of both current and under development therapies are directed toward killing or suppressing the proliferation of tumor cells. Despite the introduction of highly effective drugs, such as tyrosine kinase inhibitors of EGFR or ALK signaling pathways, our ability to eradicate tumors is limited by ITH in therapy sensitivity, where some tumor cells avoid elimination due to genetic, epigenetic, or microenvironmental differences (Lindsay et al, 2017 ). Development of complex combination therapy schedules that target multiple mechanisms of persistence and resistance operating within the same tumors is limited by availability of drugs and issues of systemic toxicities.…”

Section: Therapeutic Implicationsmentioning

confidence: 99%

The paradox of cooperation among selfish cancer cells

Capp¹,

Thomas

Marusyk

et al. 2023

Evolutionary Applications

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It is traditionally assumed that during cancer development, tumor cells abort their initially cooperative behavior (i.e., cheat) in favor of evolutionary strategies designed solely to enhance their own fitness (i.e., a “selfish” life style) at the expense of that of the multicellular organism. However, the growth and progress of solid tumors can also involve cooperation among these presumed selfish cells (which, by definition, should be noncooperative) and with stromal cells. The ultimate and proximate reasons behind this paradox are not fully understood. Here, in the light of current theories on the evolution of cooperation, we discuss the possible evolutionary mechanisms that could explain the apparent cooperative behaviors among selfish malignant cells. In addition to the most classical explanations for cooperation in cancer and in general (by‐product mutualism, kin selection, direct reciprocity, indirect reciprocity, network reciprocity, group selection), we propose the idea that “greenbeard” effects are relevant to explaining some cooperative behaviors in cancer. Also, we discuss the possibility that malignant cooperative cells express or co‐opt cooperative traits normally expressed by healthy cells. We provide examples where considerations of these processes could help understand tumorigenesis and metastasis and argue that this framework provides novel insights into cancer biology and potential strategies for cancer prevention and treatment.

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Section: Therapeutic Implicationsmentioning

confidence: 99%