Evidence map›Paper›PMID 17562079›Full record

ArticleJournal of cancer research and clinical oncology2007

A multigenic study on breast cancer risk associated with genetic polymorphisms of ER Alpha, COMT and CYP19 gene in BRCA1/BRCA2 negative Shanghai women with early onset breast cancer or affected relatives.

Zhen Hu, Chuan-Gui Song, Jing-Song Lu, Jian-Min Luo, Zhen-Zhou Shen, Wei Huang, Zhi-Ming Shao

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 9 pooled it
1.4field-weighted citation impact, top 17% 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, 9 syntheses or guidelines pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  5. Association Between ESR1 PvuII, XbaI, and P325P Polymorphisms and Breast Cancer Susceptibility: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Pooled it
  6. The Val158Met polymorphism in the COMT gene is associated with increased cancer risks in Chinese population.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  7. Catechol-O-methyltransferase Val158Met polymorphism and breast cancer risk in Asian population.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
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  10. Trial
  11. Journal of Cancer · 2018
    Review
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  18. Prevalence of ERα-397 PvuII C/T, ERα-351 XbaI A/G and PGR PROGINS polymorphisms in Brazilian breast cancer-unaffected women.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2012
    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

7 authors at 3 institutions in 2 countries.

Zhen HuBreast Cancer Institute, Cancer Hospital, Department of Oncology, Shanghai Medical College, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Chuan-Gui Song
Jing-Song Lu
Jian-Min Luo
Zhen-Zhou Shen
Wei Huang
Zhi-Ming Shao
Fudan University Shanghai Cancer Center · CNChinese National Human Genome Center at Shanghai · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High penetrance genes such as BRCA1 or BRCA2 account for only a small proportion of familial breast cancer in Chinese population. Estrogen has been proposed to participate in the proliferation and carcinogenesis of breast cancer. To investigate the association between genetic polymorphisms in genes encoding estrogen metabolizing, estrogen biosynthesizing enzyme and estrogen receptor and the breast cancer risk in BRCA1/BRCA2 negative Shanghai women, we conducted a case-control study including 114 cases with early-onset breast cancer or affected relatives and 121 healthy controls. The genotypes of estrogen receptor alpha (ERalpha), aromatase (CYP19), and catechol-O-methyltransferase (COMT) genes were analyzed by direct DNA-sequencing. Compared with H/H genotype of COMT Val158Met, COMT Val158Met L/L genotype was associated with a nonsignificantly elevated risk of breast cancer (OR: 3.72; 95% CI: 0.99-13.96, P=0.051). There was no statistically significant difference in genotype frequency of the ERalpha PvuII, ERalpha XbaI and CYP19 Arg264Cys polymorphism between controls and cases. When stratified by menopausal status, COMT Val158Met L/L (OR: 11.94; 95% CI: 1.48-96.03, P=0.02) and ERalpha PvuII P/p genotypes (OR: 2.67; 95% CI: 1.01-7.05, P=0.048) were associated with a significantly elevated risk of breast cancer in premenopausal women, and there was a association between ERalpha XbaI x/x genotype and the nonsignificantly increased risk of breast cancer in premenopausal women (OR: 6.88; 95% CI: 0.80-59.15, P=0.079). The multigenic analysis showed maybe these high risk genotypes had combined effect on breast cancer risk. Our findings suggest that polymorphism of genes involving estrogen-metabolizing pathway, estrogen- biosynthesizing pathway and estrogen receptor pathway may play an important role in the etiology of BRCA1/2 negative breast cancer with hereditary predisposing factors.

Indexed as

Genes, BRCA1Genes, BRCA2Polymorphism, GeneticAdultAromataseBase SequenceBreast NeoplasmsCase-Control StudiesCatechol O-MethyltransferaseChinaEstrogen Receptor alphaFamily HealthFemaleGenetic Predisposition to DiseaseHumansMiddle AgedAromataseCatechol O-MethyltransferaseEstrogen Receptor alpha

Identifiers

PMID17562079
PMCPMC12160827
OpenAlexW2025461420

What OpenQuestion holds

Textmetadata
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.