Putative homeostatic role of cancer driver mutations

Avanthika Venkatachalam; Eli Pikarsky; Yinon Ben-Neriah

doi:10.1016/j.tcb.2021.07.002

Putative homeostatic role of cancer driver mutations

Avanthika Venkatachalam, Eli Pikarsky^*, Yinon Ben-Neriah

^*Corresponding author for this work

Department of Immunology and Cancer Research

Research output: Contribution to journal › Review article › peer-review

7 Scopus citations

Abstract

Somatic mutations have traditionally been associated with cancer, yet more recently, it was realized that they also appear in nontransformed cells beginning in early life. Remarkably, some of these mutations, commonly viewed as cancer driver mutations, are widely spread among cells of noncancerous tissues, sometimes affecting the majority of the tissue cells. This spreading process intensifies upon aging or exposure to extrinsic insults, such as UV irradiation, inhaling smoke, and inflammatory cues. Whereas classic driver mutations in normal cells are mostly viewed as a first step in the carcinogenesis process, here, we speculate that in certain states, they can play beneficial homeostatic roles while confronting stress and aging tissue repair.

Original language	English
Pages (from-to)	8-17
Number of pages	10
Journal	Trends in Cell Biology
Volume	32
Issue number	1
DOIs	https://doi.org/10.1016/j.tcb.2021.07.002
State	Published - Jan 2022

Bibliographical note

Funding Information:
Research work in the labs of E.P. and Y.B-N. was supported by the Israel Science Foundation (ISF) Centers of Excellence (2084/15 and 3165/20), ISF 3165/19 within the Israel Precision Medicine Program, the European Research Council within the FP-7 (294390 PICHO and 88352 ONCODESTROYER to Y.B-N. and 281738 LIVERMICROENV to E.P.), the Adelson Medical Research Foundation (to E.P. and Y.B-N.), and the Israel Cancer Research Fund Professorship (to Y.B-N.). The authors declare no competing interests. No interests are declared.

Funding Information:
Research work in the labs of E.P. and Y.B-N. was supported by the Israel Science Foundation (ISF) Centers of Excellence (2084/15 and 3165/20), ISF 3165/19 within the Israel Precision Medicine Program, the European Research Council within the FP-7 (294390 PICHO and 88352 ONCODESTROYER to Y.B-N. and 281738 LIVERMICROENV to E.P.), the Adelson Medical Research Foundation (to E.P. and Y.B-N.), and the Israel Cancer Research Fund Professorship (to Y.B-N.). The authors declare no competing interests.

Publisher Copyright:
© 2021 Elsevier Ltd

Keywords

Tp53 hotspot mutations
beneficial mutations
clonal expansion
clonal fitness
clonal hematopoiesis
Aging/genetics
Hematopoiesis
Mutation/genetics
Humans
Neoplasms/genetics
Carcinogenesis/genetics

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.tcb.2021.07.002

Cite this

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abstract = "Somatic mutations have traditionally been associated with cancer, yet more recently, it was realized that they also appear in nontransformed cells beginning in early life. Remarkably, some of these mutations, commonly viewed as cancer driver mutations, are widely spread among cells of noncancerous tissues, sometimes affecting the majority of the tissue cells. This spreading process intensifies upon aging or exposure to extrinsic insults, such as UV irradiation, inhaling smoke, and inflammatory cues. Whereas classic driver mutations in normal cells are mostly viewed as a first step in the carcinogenesis process, here, we speculate that in certain states, they can play beneficial homeostatic roles while confronting stress and aging tissue repair.",

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Putative homeostatic role of cancer driver mutations

Abstract

Bibliographical note

Keywords

UN SDGs

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