Putative homeostatic role of cancer driver mutations

Avanthika Venkatachalam, Eli Pikarsky*, Yinon Ben-Neriah

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

4 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 languageAmerican English
Pages (from-to)8-17
Number of pages10
JournalTrends in Cell Biology
Volume32
Issue number1
DOIs
StatePublished - 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

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