Evidence map›Paper›PMID 32472073›Full record

ReviewNature reviews. Cancer2020

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

Michele Carbone, Sarah T Arron, Bruce Beutler, Angela Bononi, Webster Cavenee, James E Cleaver, Carlo M Croce, Alan D'Andrea, William D Foulkes, Giovanni Gaudino and 13 more

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 3 pooled it
11.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

79 citing papers in PubMed, 3 syntheses or guidelines pooled it, 192 citations in OpenAlex.

  1. Pooled it
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  11. Clinical and Pathologic Phenotyping of Mesotheliomas Developing in Carriers of Germline BAP1 Mutations.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2025
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19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors at 15 institutions in 3 countries.

Michele CarboneThoracic Oncology, University of Hawaii Cancer Center, Honolulu, HI, USA. mcarbone@cc.hawaii.edu.ORCID http://orcid.org/0000-0001-8928-8474
Sarah T ArronSTA, JEC, Department of Dermatology, University of California, San Francisco, San Francisco, CA, USA.
Bruce BeutlerCenter for Genetic Host Defense, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID http://orcid.org/0000-0002-3639-246X
Angela BononiThoracic Oncology, University of Hawaii Cancer Center, Honolulu, HI, USA.
Webster CaveneeLudwig Institute, University of California, San Diego, San Diego, CA, USA.
James E CleaverSTA, JEC, Department of Dermatology, University of California, San Francisco, San Francisco, CA, USA.
Carlo M CroceDepartment of Cancer Biology and Genetics, Ohio State University, Columbus, OH, USA.
Alan D'AndreaDana Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0001-6168-6294
William D FoulkesDepartment of Human Genetics, McGill University, Montreal, QC, Canada.ORCID http://orcid.org/0000-0001-7427-4651
Giovanni GaudinoThoracic Oncology, University of Hawaii Cancer Center, Honolulu, HI, USA.ORCID http://orcid.org/0000-0002-1572-6571
Joanna L GrodenVC Research, University of Illinois, Chicago, IL, USA.
Elizabeth P HenskeCenter for LAM Research, Brigham & Women's Hospital, Harvard Medical School, Boston, MA, USA.
Ian D HicksonCenter for Chromosome Stability, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-0583-566X
Paul M HwangCardiovascular Branch, National Institutes of Health, Bethesda, MD, USA.
Richard D KolodnerLudwig Institute, University of California, San Diego, San Diego, CA, USA.
Tak W MakPrincess Margaret Cancer Center, University of Toronto, Toronto, ON, Canada.
David MalkinDivision of Haematology/Oncology, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Toronto, ON, Canada.
Raymond J MonnatDepartment Pathology, Washington University, Seattle, WA, USA.
Flavia NovelliThoracic Oncology, University of Hawaii Cancer Center, Honolulu, HI, USA.
Harvey I PassDepartment of Cardiovascular Surgery, New York University, New York, NY, USA.
John H PetriniMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Laura S SchmidtUrologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Haining YangThoracic Oncology, University of Hawaii Cancer Center, Honolulu, HI, USA.
University of Hawaiʻi at Mānoa · USNational Institutes of Health · USUniversity of California San Diego · USUniversity of California, San Francisco · USUniversity of Toronto · CABrigham and Women's Hospital · USHarvard University · USMcGill University · CAMemorial Sloan Kettering Cancer Center · USNew York University · USThe Ohio State University · USThe University of Texas Southwestern Medical Center · USUniversity of Copenhagen · DKUniversity of Illinois Urbana-Champaign · USUniversity of Washington · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Tumor mutation signaturesP01CA077852 · NCI · UNIVERSITY OF WASHINGTON · PI LOEB, LAWRENCE A · 1999 to 2019
$26.0M
Mitochondrial regulation in cardiovascular and cancer biologyZIAHL005101 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI HWANG, PAUL M. · 2009 to 2025
$19.1M
ENZYMOLOGY OF MISMATCH REPAIR IN YEASTR01GM050006 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Richard D Kolodner · 1994 to 2026
$10.5M
ENZYMATIC MECHANISMS OF GENETIC RECOMBINATIONR01GM026017 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Richard D Kolodner · 1985 to 2026
$10.5M
Cancer Gene Discovery to Identify Targetable TargetsR35CA197706 · NCI · OHIO STATE UNIVERSITY · PI CROCE, CARLO M · 2015 to 2021
$6.4M
The North American Mesothelioma ConsortiumU01CA111295 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUFLEJT, MARGARET ELISABETH, PASS, HARVEY IRA · 2005 to 2016
$4.8M
The EDRN Mesothelioma Biomarker Discovery LaboratoryU01CA214195 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PASS, HARVEY IRA, YANG, HAINING · 2016 to 2021
$3.5M
Mechanisms of BAP1 activity in human cancer developmentR01CA237235 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI CARBONE, MICHELE, YANG, HAINING · 2020 to 2024
$2.1M
Influence of germline mutations on susceptibility to environmental carcinogensR01ES030948 · NIEHS · UNIVERSITY OF HAWAII AT MANOA · PI CARBONE, MICHELE, GRZYMSKI, JOSEPH J · 2019 to 2021
$1.9M
Germline BAP1 Mutations and Malignant Mesothelioma: Mechanisms and Early DetectionR01CA198138 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI CARBONE, MICHELE · 2015 to 2019
$1.7M
ENZYMATIC MECHANISMS OF GENETIC RECOMBINATIONR37GM026017 · NIGMS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI KOLODNER, RICHARD D · 1992 to 2001
$759k
CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001ENCI NIH HHS P01 CA077852NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA198138NCI NIH HHS R01 CA237235NCI NIH HHS R35 CA197706NCI NIH HHS U01 CA111295NCI NIH HHS U01 CA214195NIEHS NIH HHS R01 ES030948NIGMS NIH HHS R01 GM026017NIGMS NIH HHS R01 GM050006NIGMS NIH HHS R37 GM026017
6 · The paper itself

Abstract

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.

Indexed as

Gene-Environment InteractionGenetic Predisposition to DiseaseAnimalsGerm-Line MutationHumansNeoplasms

Identifiers

PMID32472073
PMCPMC8104546
OpenAlexW3032355325

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.