Evidence map›Paper›PMID 19088016›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2008

Genetic susceptibility loci for breast cancer by estrogen receptor status.

Montserrat Garcia-Closas, Stephen Chanock

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 2% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Identification and functional analysis of Rattus norvegicus Mammary carcinoma susceptibility 1b (Mcs1b) nominated variants.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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  14. FAM84B promotes prostate tumorigenesis through a network alteration.Therapeutic advances in medical oncology · 2019
    Article
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  19. Transposon insertional mutagenesis in mice identifies human breast cancer susceptibility genes and signatures for stratification.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  20. Article

7 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

2 authors at 2 institutions in 1 country.

Montserrat Garcia-ClosasDivision of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland 20852, USA. montse@nih.gov
Stephen Chanock
Division of Cancer Epidemiology and GeneticsNational Cancer Institute · US

Funding

HORMONE-RELATED CANCERSZ01CP010126 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI BRINTON, LOUISE · 1996 to 2008
$11.2M
Intramural NIH HHS Z01 CP010126Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

Breast cancer is a heterogeneous disease, and risk factors could be differentially associated with the development of distinct tumor subtypes that manifest different biological behavior and progression. In support of this view, there is growing evidence that known breast cancer risk factors vary by hormone receptor status and perhaps other pathologic characteristics of disease. Recent work from large consortial studies has led to the discovery of novel breast cancer susceptibility loci in genic (CASP8, FGFR2, TNRC9, MAP3K1, LSP1) and nongenic regions (8q24, 2q35, 5p12) of the genome, and to the finding of substantial heterogeneity by tumor characteristics. In particular, susceptibility loci in FGFR2, TNRC9, 8q24, 2q35, and 5p12 have stronger associations for estrogen receptor-positive (ER+) disease than estrogen receptor-negative (ER -) disease. These findings suggest that common genetic variants can influence the pathologic subtype of breast cancer, and provide further support for the hypothesis that ER+ and ER(-) disease result from different etiologic pathways. Current studies had limited power to detect susceptibility loci for less common tumor subtypes, such as ER(-) disease including triple-negative and basal-like tumors. Ongoing work targeting uncommon subtypes is likely to identify additional tumor-specific susceptibility loci in the near future. Characterization of etiologic heterogeneity of breast cancer may lead to improvements in the understanding of the biological mechanisms for breast cancer, and ultimately result in improvements in prevention, early detection, and treatment.

Indexed as

Genetic Predisposition to DiseaseApoptosis Regulatory ProteinsBreast NeoplasmsChromosome MappingFemaleGenome-Wide Association StudyHigh Mobility Group ProteinsHumansReceptors, EstrogenReceptors, ProgesteroneTrans-ActivatorsApoptosis Regulatory ProteinsHigh Mobility Group ProteinsReceptors, EstrogenReceptors, ProgesteroneTOX3 protein, humanTrans-Activators

Identifiers

PMID19088016
PMCPMC2668137
OpenAlexW2161129973

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.