Mutation-selection balance and compensatory mechanisms in tumour evolution.


Journal

Nature reviews. Genetics
ISSN: 1471-0064
Titre abrégé: Nat Rev Genet
Pays: England
ID NLM: 100962779

Informations de publication

Date de publication:
04 2021
Historique:
accepted: 16 10 2020
pubmed: 2 12 2020
medline: 5 5 2021
entrez: 1 12 2020
Statut: ppublish

Résumé

Intratumour heterogeneity and phenotypic plasticity, sustained by a range of somatic aberrations, as well as epigenetic and metabolic adaptations, are the principal mechanisms that enable cancers to resist treatment and survive under environmental stress. A comprehensive picture of the interplay between different somatic aberrations, from point mutations to whole-genome duplications, in tumour initiation and progression is lacking. We posit that different genomic aberrations generally exhibit a temporal order, shaped by a balance between the levels of mutations and selective pressures. Repeat instability emerges first, followed by larger aberrations, with compensatory effects leading to robust tumour fitness maintained throughout the tumour progression. A better understanding of the interplay between genetic aberrations, the microenvironment, and epigenetic and metabolic cellular states is essential for early detection and prevention of cancer as well as development of efficient therapeutic strategies.

Identifiants

pubmed: 33257848
doi: 10.1038/s41576-020-00299-4
pii: 10.1038/s41576-020-00299-4
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, N.I.H., Intramural Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

251-262

Subventions

Organisme : NCI NIH HHS
ID : U54 CA193489
Pays : United States

Commentaires et corrections

Type : ErratumIn

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Auteurs

Erez Persi (E)

National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD, USA. erezpersi@gmail.com.

Yuri I Wolf (YI)

National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD, USA.

David Horn (D)

School of Physics and Astronomy, Raymond & Beverly Sackler Faculty of Exact Sciences, Tel-Aviv University, Tel-Aviv, Israel.

Eytan Ruppin (E)

Cancer Data Science Lab, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

Francesca Demichelis (F)

Department for Cellular, Computational and Integrative Biology, University of Trento, Trento, Italy.
Caryl and Israel Englander Institute for Precision Medicine, New York Presbyterian Hospital, Weill Cornell Medicine, New York, NY, USA.

Robert A Gatenby (RA)

Integrated Mathematical Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.

Robert J Gillies (RJ)

Department of Cancer Physiology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA. Robert.Gillies@moffitt.org.

Eugene V Koonin (EV)

National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD, USA. koonin@ncbi.nlm.nih.gov.

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