Evidence map›Paper›PMID 21085629›Full record

ArticlePLoS genetics2010

Analysis of the 10q11 cancer risk locus implicates MSMB and NCOA4 in human prostate tumorigenesis.

Mark M Pomerantz, Yashaswi Shrestha, Richard J Flavin, Meredith M Regan, Kathryn L Penney, Lorelei A Mucci, Meir J Stampfer, David J Hunter, Stephen J Chanock, Eric J Schafer and 9 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 5 pooled it
7.2field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 5 syntheses or guidelines pooled it, 87 citations in OpenAlex.

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  20. Contribution ofOncotarget · 2019
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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

19 authors at 8 institutions in 3 countries.

Mark M PomerantzDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, United States of America.
Yashaswi Shrestha
Richard J Flavin
Meredith M Regan
Kathryn L Penney
Lorelei A Mucci
Meir J Stampfer
David J Hunter
Stephen J Chanock
Eric J Schafer
Jennifer A Chan
Josep Tabernero
José Baselga
Andrea L Richardson
Massimo Loda
William K Oh
Philip W Kantoff
William C Hahn
Matthew L Freedman
Harvard University · USBrigham and Women's Hospital · USBroad Institute · USDana-Farber Cancer Institute · USVall d'Hebron Institute of OncologyIcahn School of Medicine at Mount Sinai · USNational Cancer Institute · USUniversity of Calgary · CA

Funding

Laboratory of Translational GenomicsZIACP010201 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI PROKUNINA-OLSSON, LIUDMILA · 2010 to 2025
$91.2M
Tumor and Circulating Markers as Links Between Obesity and Lethal Prostate CanceP50CA090381 · NCI · DANA-FARBER CANCER INSTITUTE · PI GARRAWAY, LEVI A. · 2002 to 2017
$36.2M
Fine mapping and characterization of the 8q24 prostate cancer risk locusR01CA129435 · NCI · DANA-FARBER CANCER INST · PI FREEDMAN, MATTHEW L · 2007 to 2009
$1.5M
Howard Hughes Medical InstituteNCI NIH HHS 5P50CA90381NCI NIH HHS P50 CA090381NCI NIH HHS R01 CA129435
6 · The paper itself

Abstract

Genome-wide association studies (GWAS) have established a variant, rs10993994, on chromosome 10q11 as being associated with prostate cancer risk. Since the variant is located outside of a protein-coding region, the target genes driving tumorigenesis are not readily apparent. Two genes nearest to this variant, MSMB and NCOA4, are strong candidates for mediating the effects of rs109939934. In a cohort of 180 individuals, we demonstrate that the rs10993994 risk allele is associated with decreased expression of two MSMB isoforms in histologically normal and malignant prostate tissue. In addition, the risk allele is associated with increased expression of five NCOA4 isoforms in histologically normal prostate tissue only. No consistent association with either gene is observed in breast or colon tissue. In conjunction with these findings, suppression of MSMB expression or NCOA4 overexpression promotes anchorage-independent growth of prostate epithelial cells, but not growth of breast epithelial cells. These data suggest that germline variation at chromosome 10q11 contributes to prostate cancer risk by influencing expression of at least two genes. More broadly, the findings demonstrate that disease risk alleles may influence multiple genes, and associations between genotype and expression may only be observed in the context of specific tissue and disease states.

Indexed as

Genetic Predisposition to DiseaseCell AdhesionCell ProliferationChromosomes, Human, Pair 10Epithelial CellsGenetic LociHumansMaleNuclear Receptor CoactivatorsPrecancerous ConditionsProstateProstatic NeoplasmsProstatic Secretory ProteinsRisk Factorsbeta-microseminoproteinNCOA4 protein, humanNuclear Receptor CoactivatorsProstatic Secretory Proteins

Identifiers

PMID21085629
PMCPMC2978684
OpenAlexW2112856704

What OpenQuestion holds

Textmetadata
LicenceCC0
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.