Evidence map›Paper›PMID 17117180›Full record

ArticleBritish journal of cancer2006

HapMap-based study of the 17q21 ERBB2 amplicon in susceptibility to breast cancer.

P R Benusiglio, P D Pharoah, P L Smith, F Lesueur, D Conroy, R N Luben, G Dew, C Jordan, A Dunning, D F Easton and 1 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2006. 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
2.5field-weighted citation impact, top 11% 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, 41 citations in OpenAlex.

  1. Trial
  2. Article
  3. The potential markers of endocrine resistance among HR+ /HER2+ breast cancer patients.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Article
  4. [Study on the effect and mechanism of hepatitis B virus X protein transactivates gene 4 in HepG2 cell apoptosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2019
    Article
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  18. Heritable variation of ERBB2 and breast cancer risk.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2009
    Article
  19. Mitotic deregulation by survivin in ErbB2-overexpressing breast cancer cells contributes to Taxol resistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Article
  20. Article
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

11 authors at 2 institutions in 3 countries.

P R BenusiglioStrangeways Research Laboratory, Cancer Research UK Department of Oncology, University of Cambridge, UK, and Department of Internal Medecine, Hôpital Cantonal Universitaire de Genève, Switzerland. pbenusiglio@yahoo.com
P D Pharoah
P L Smith
F Lesueur
D Conroy
R N Luben
G Dew
C Jordan
A Dunning
D F Easton
B A J Ponder
University of Cambridge · GBCancer Research UK · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ERBB2 is frequently amplified in breast tumours as part of a wide region of amplification on chromosome 17q21. This amplicon contains many candidate genes for breast cancer susceptibility. We used a genetic association study design to determine if common genetic variation (frequency>or=5%) in a 400-kb region surrounding ERBB2 and containing the PPARBP, CRK7, NEUROD2, PPP1R1B, STARD3, TCAP, PNMT, CAB2, ERBB2, C17ORF37, GRB7 and ZNFN1A3 genes, was associated with breast cancer risk. Sixteen tagging single-nucleotide polymorphisms (tSNPs) selected within blocks of linkage disequilibrium from the HapMap database, one HapMap singleton SNP, and six additional SNPs randomly selected from dbSNP were genotyped using Taqman in a large study set of British women (2275 cases, 2280 controls). We observed no association between any of the genotypes or associated haplotypes and disease risk. In order to simulate unidentified SNPs, we performed the leave-one-out cross-validation procedure on the HapMap data; over 90% of the common genetic variation was well represented by tagging polymorphisms. We are therefore likely to have tagged any common variants present in our population. In summary, we found no association between common genetic variation in the 17q21 ERBB2 amplicon and breast cancer risk in British women.

Indexed as

Gene AmplificationGenetic Predisposition to DiseaseAdultAgedAged, 80 and overBreast NeoplasmsCase-Control StudiesChromosomes, Human, Pair 17Erb-b2 Receptor Tyrosine KinasesFemaleGenomicsHaplotypesHumansMiddle AgedPolymorphism, Single NucleotideErb-b2 Receptor Tyrosine Kinases

Identifiers

PMID17117180
PMCPMC2360759
OpenAlexW1984658341

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.