Evidence map›Paper›PMID 21062454›Full record

ArticleBreast cancer research : BCR2010

A genome-wide association scan on estrogen receptor-negative breast cancer.

Jingmei Li, Keith Humphreys, Hatef Darabi, Gustaf Rosin, Ulf Hannelius, Tuomas Heikkinen, Kristiina Aittomäki, Carl Blomqvist, Paul Dp Pharoah, Alison M Dunning and 18 more

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact, top 86% 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

22 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
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  7. Previous GWAS hits in relation to young-onset breast cancer.Breast cancer research and treatment · 2017
    Article
  8. Genomic Disparities in Breast Cancer Among Latinas.Cancer control : journal of the Moffitt Cancer Center · 2016
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  14. A genome-wide association study of early-onset breast cancer identifies PFKM as a novel breast cancer gene and supports a common genetic spectrum for breast cancer at any age.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2014
    Article
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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

28 authors at 1 institution in 1 country.

Jingmei LiDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm 17177, Sweden. jingmei.li@ki.se
Keith Humphreys
Hatef Darabi
Gustaf Rosin
Ulf Hannelius
Tuomas Heikkinen
Kristiina Aittomäki
Carl Blomqvist
Paul Dp Pharoah
Alison M Dunning
Shahana Ahmed
Maartje J Hooning
Antoinette Hollestelle
Rogier A Oldenburg
Lars Alfredsson
Aarno Palotie
Leena Peltonen-Palotie
Astrid Irwanto
Hui Qi Low
Garrett Hk Teoh
Anbupalam Thalamuthu
Juha Kere
Mauro D'Amato
Douglas F Easton
Heli Nevanlinna
Jianjun Liu
Kamila Czene
Per Hall
Manchester Academic Health Science Centre · GB

Funding

HORMONE REPLACEMENT THERAPY AND BREAST CANCERR01CA058427 · NCI · UPPSALA UNIVERSITY · PI ADAMI, HANS-OLOV · 1993 to 1995
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Cancer Research UK 10118Cancer Research UK 10119Cancer Research UK 10124Cancer Research UK 11021Cancer Research UK 11022Cancer Research UK A10119Cancer Research UK A10124NCI NIH HHS R01 CA58427
6 · The paper itself

Abstract

introductionBreast cancer is a heterogeneous disease and may be characterized on the basis of whether estrogen receptors (ER) are expressed in the tumour cells. ER status of breast cancer is important clinically, and is used both as a prognostic indicator and treatment predictor. In this study, we focused on identifying genetic markers associated with ER-negative breast cancer risk.

methodsWe conducted a genome-wide association analysis of 285,984 single nucleotide polymorphisms (SNPs) genotyped in 617 ER-negative breast cancer cases and 4,583 controls. We also conducted a genome-wide pathway analysis on the discovery dataset using permutation-based tests on pre-defined pathways. The extent of shared polygenic variation between ER-negative and ER-positive breast cancers was assessed by relating risk scores, derived using ER-positive breast cancer samples, to disease state in independent, ER-negative breast cancer cases.

resultsAssociation with ER-negative breast cancer was not validated for any of the five most strongly associated SNPs followed up in independent studies (1,011 ER-negative breast cancer cases, 7,604 controls). However, an excess of small P-values for SNPs with known regulatory functions in cancer-related pathways was found (global P = 0.052). We found no evidence to suggest that ER-negative breast cancer shares a polygenic basis to disease with ER-positive breast cancer.

conclusionsER-negative breast cancer is a distinct breast cancer subtype that merits independent analyses. Given the clinical importance of this phenotype and the likelihood that genetic effect sizes are small, greater sample sizes and further studies are required to understand the etiology of ER-negative breast cancers.

Indexed as

Biomarkers, TumorPolymorphism, Single NucleotideBreast NeoplasmsCase-Control StudiesFemaleGene ExpressionGenome-Wide Association StudyGenotypeHumansPrognosisReceptors, EstrogenTreatment OutcomeBiomarkers, TumorReceptors, Estrogen

Identifiers

PMID21062454
PMCPMC3046434
OpenAlexW2090004577

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.