Tumour predisposition and cancer syndromes as models to study gene-environment interactions.


Journal

Nature reviews. Cancer
ISSN: 1474-1768
Titre abrégé: Nat Rev Cancer
Pays: England
ID NLM: 101124168

Informations de publication

Date de publication:
09 2020
Historique:
accepted: 23 04 2020
pubmed: 31 5 2020
medline: 20 11 2020
entrez: 31 5 2020
Statut: ppublish

Résumé

Cell division and organismal development are exquisitely orchestrated and regulated processes. The dysregulation of the molecular mechanisms underlying these processes may cause cancer, a consequence of cell-intrinsic and/or cell-extrinsic events. Cellular DNA can be damaged by spontaneous hydrolysis, reactive oxygen species, aberrant cellular metabolism or other perturbations that cause DNA damage. Moreover, several environmental factors may damage the DNA, alter cellular metabolism or affect the ability of cells to interact with their microenvironment. While some environmental factors are well established as carcinogens, there remains a large knowledge gap of others owing to the difficulty in identifying them because of the typically long interval between carcinogen exposure and cancer diagnosis. DNA damage increases in cells harbouring mutations that impair their ability to correctly repair the DNA. Tumour predisposition syndromes in which cancers arise at an accelerated rate and in different organs - the equivalent of a sensitized background - provide a unique opportunity to examine how gene-environment interactions influence cancer risk when the initiating genetic defect responsible for malignancy is known. Understanding the molecular processes that are altered by specific germline mutations, environmental exposures and related mechanisms that promote cancer will allow the design of novel and effective preventive and therapeutic strategies.

Identifiants

pubmed: 32472073
doi: 10.1038/s41568-020-0265-y
pii: 10.1038/s41568-020-0265-y
pmc: PMC8104546
mid: NIHMS1595145
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

533-549

Subventions

Organisme : NCI NIH HHS
ID : R01 CA198138
Pays : United States
Organisme : NIGMS NIH HHS
ID : R37 GM026017
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA077852
Pays : United States
Organisme : NCI NIH HHS
ID : R35 CA197706
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA237235
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM026017
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA111295
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA214195
Pays : United States
Organisme : CCR NIH HHS
ID : HHSN261200800001C
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES030948
Pays : United States
Organisme : NCI NIH HHS
ID : HHSN261200800001E
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM050006
Pays : United States

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Auteurs

Michele Carbone (M)

Thoracic Oncology, University of Hawaii Cancer Center, Honolulu, HI, USA. mcarbone@cc.hawaii.edu.

Sarah T Arron (ST)

STA, JEC, Department of Dermatology, University of California, San Francisco, San Francisco, CA, USA.

Bruce Beutler (B)

Center for Genetic Host Defense, University of Texas Southwestern Medical Center, Dallas, TX, USA.

Angela Bononi (A)

Thoracic Oncology, University of Hawaii Cancer Center, Honolulu, HI, USA.

Webster Cavenee (W)

Ludwig Institute, University of California, San Diego, San Diego, CA, USA.

James E Cleaver (JE)

STA, JEC, Department of Dermatology, University of California, San Francisco, San Francisco, CA, USA.

Carlo M Croce (CM)

Department of Cancer Biology and Genetics, Ohio State University, Columbus, OH, USA.

Alan D'Andrea (A)

Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.

William D Foulkes (WD)

Department of Human Genetics, McGill University, Montreal, QC, Canada.

Giovanni Gaudino (G)

Thoracic Oncology, University of Hawaii Cancer Center, Honolulu, HI, USA.

Joanna L Groden (JL)

VC Research, University of Illinois, Chicago, IL, USA.

Elizabeth P Henske (EP)

Center for LAM Research, Brigham & Women's Hospital, Harvard Medical School, Boston, MA, USA.

Ian D Hickson (ID)

Center for Chromosome Stability, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.
Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.

Paul M Hwang (PM)

Cardiovascular Branch, National Institutes of Health, Bethesda, MD, USA.

Richard D Kolodner (RD)

Ludwig Institute, University of California, San Diego, San Diego, CA, USA.

Tak W Mak (TW)

Princess Margaret Cancer Center, University of Toronto, Toronto, ON, Canada.

David Malkin (D)

Division of Haematology/Oncology, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Toronto, ON, Canada.

Raymond J Monnat (RJ)

Department Pathology, Washington University, Seattle, WA, USA.
Department of Genome Science, Washington University, Seattle, WA, USA.

Flavia Novelli (F)

Thoracic Oncology, University of Hawaii Cancer Center, Honolulu, HI, USA.

Harvey I Pass (HI)

Department of Cardiovascular Surgery, New York University, New York, NY, USA.

John H Petrini (JH)

Molecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Laura S Schmidt (LS)

Urologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Basic Science Program, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.

Haining Yang (H)

Thoracic Oncology, University of Hawaii Cancer Center, Honolulu, HI, USA.

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