Evidence map›Paper›PMID 28627265›Full record

ReviewInternational journal of radiation biology2017

ATM, radiation, and the risk of second primary breast cancer.

Jonine L Bernstein, WECARE Study Collaborative Group, Patrick Concannon

Open access · greenAbstract readReview
In one paragraph

Review in International journal of radiation biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

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  9. Therapeutics Targeting p53-MDM2 Interaction to Induce Cancer Cell Death.International journal of molecular sciences · 2022
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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

3 authors at 2 institutions in 1 country.

Jonine L Bernsteina Department of Epidemiology and Biostatistics , Memorial Sloan Kettering Cancer Center , New York , NY , U.S.A.
WECARE Study Collaborative Group
Patrick Concannonb Genetics Institute and Department of Pathology, Immunology and Laboratory Medicine , University of Florida , Gainesville , FL , U.S.A.
University of Florida · USMemorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Elisa de Stanchina · 1985 to 2026
$347.4M
Genome-Wide Association Study of Radiation Exposure and Bilateral Breast CancerR01CA129639 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI BERNSTEIN, JONINE L. · 2009 to 2013
$15.6M
BREAST CANCER, RADIATION EXPOSURE, AND THE ATM GENEU01CA083178 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI BERNSTEIN, JONINE LISA · 1999 to 2003
$9.3M
Interaction of Radiation, BRCA1/2, and Breast CancerR01CA097397 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI BERNSTEIN, JONINE LISA · 2002 to 2006
$4.1M
Breast Cancer, Radiation and the ATM-CHEK2 PathwayR01CA114236 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI BERNSTEIN, JONINE L. · 2005 to 2008
$1.8M
Novel DNA damage response gene from genomic screeningR01ES027121 · NIEHS · UNIVERSITY OF FLORIDA · PI CONCANNON, PATRICK · 2016 to 2020
$1.6M
NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA097397NCI NIH HHS R01 CA114236NCI NIH HHS R01 CA129639NCI NIH HHS U01 CA083178NIEHS NIH HHS R01 ES027121
6 · The paper itself

Abstract

purposeIt was first suggested more than 40 years ago that heterozygous carriers for the human autosomal recessive disorder Ataxia-Telangiectasia (A-T) might also be at increased risk for cancer. Subsequent studies have identified the responsible gene, Ataxia-Telangiectasia Mutated (ATM), characterized genetic variation at this locus in A-T and a variety of different cancers, and described the functions of the ATM protein with regard to cellular DNA damage responses. However, an overall model of how ATM contributes to cancer risk, and in particular, the role of DNA damage in this process, remains lacking. This review considers these questions in the context of contralateral breast cancer (CBC).

conclusionsHeterozygous carriers of loss of function mutations in ATM that are A-T causing, are at increased risk of breast cancer. However, examination of a range of genetic variants, both rare and common, across multiple cancers, suggests that ATM may have additional effects on cancer risk that are allele-dependent. In the case of CBC, selected common alleles at ATM are associated with a reduced incidence of CBC, while other rare and predicted deleterious variants may act jointly with radiation exposure to increase risk. Further studies that characterize germline and somatic ATM mutations in breast cancer and relate the detected genetic changes to functional outcomes, particularly with regard to radiation responses, are needed to gain a complete picture of the complex relationship between ATM, radiation and breast cancer.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsBreast NeoplasmsGenetic Predisposition to DiseaseHumansMutationNeoplasms, Radiation-InducedNeoplasms, Second PrimaryAtaxia Telangiectasia Mutated Proteinsallelic heterogeneityAtaxia-TelangiectasiaATMbreast cancerradiation therapy

Identifiers

PMID28627265
PMCPMC6113688
OpenAlexW2673887781

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.