Evidence map›Paper›PMID 24805830›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014

Genome-wide pathway analysis of breast cancer.

Young Ho Lee, Jae-Hoon Kim, Gwan Gyu Song

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Genome-wide association pathway analysis to identify candidate single nucleotide polymorphisms and molecular pathways for gastric adenocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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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 1 institution in 1 country.

Young Ho LeeDivision of Rheumatology, Department of Internal Medicine, Korea University Anam Hospital, Korea University College of Medicine, 126-1 5 ga, Anam-dong, Seongbuk-gu, Seoul, 136-705, Korea, lyhcgh@korea.ac.kr.
Jae-Hoon Kim
Gwan Gyu Song
Korea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to identify candidate single-nucleotide polymorphisms (SNPs) that might affect susceptibility to breast cancer and then elucidate their potential mechanisms and generate SNP-to-gene-to-pathway hypotheses. A genome-wide association study (GWAS) dataset of breast cancer that included 453,852 SNPs from 1,145 breast cancer patients and 1,142 control subjects of European descent was used in this study. The identify candidate causal SNPs and pathways (ICSNPathway) method was applied to the GWAS dataset. ICSNPathway analysis identified 16 candidate SNPs, 13 genes, and 7 pathways, which together revealed 7 hypothetical biological mechanisms. The strongest hypothetical biological mechanism was that rs3168891 and rs2899849 alter the role of MBIP in the inactivation of mitogen-activated protein kinase (MAPK) (p < 0.001; false discovery rate (FDR) = 0.038). The second strongest mechanism was that rs2229714 modulates RPS6KA1 to affect its role in growth hormone signaling (p = 0.001; FDR = 0.039). The third strongest mechanism was that rs2230394 modulates ITGB1 to regulate the PTEN pathway and hsa04360 (axon guidance pathway) (p < 0.001; FDR = 0.039, 0.041). Use of the ICSNPathway to analyze breast cancer GWAS data identified 16 candidate SNPs, 13 genes (including MBIP, RPS6KA1, and ITGB1), and 7 pathways that might contribute to the susceptibility of patients to breast cancer.

Indexed as

Genome-Wide Association StudyPolymorphism, Single NucleotideBreast NeoplasmsFemaleGenetic Predisposition to DiseaseHumansMAP Kinase Signaling SystemPTEN PhosphohydrolaseSignal TransductionPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID24805830
OpenAlexW1992074987

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.