Evidence map›Paper›PMID 22801071›Full record

ArticleProstate cancer and prostatic diseases2012

Identification of genetic risk associated with prostate cancer using ancestry informative markers.

L J Ricks-Santi, V Apprey, T Mason, B Wilson, M Abbas, W Hernandez, S Hooker, M Doura, G Bonney, G Dunston and 2 more

Open access · greenAbstract read
In one paragraph

Article in Prostate cancer and prostatic diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 14% 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, 20 citations in OpenAlex.

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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

12 authors at 3 institutions in 1 country.

L J Ricks-SantiDivision of Genetics, Department of Pediatrics and Child Health, Howard University College of Medicine, Washington, DC 20060, USA. LRicks-Santi@howard.edu
V Apprey
T Mason
B Wilson
M Abbas
W Hernandez
S Hooker
M Doura
G Bonney
G Dunston
R Kittles
C Ahaghotu
Howard University · USUniversity of Chicago · USGeorge Washington University · US

Funding

STRUCTURAL/FUNCTIONAL CHARACTERIZATION OF AMINOGLYCOSIDEG12RR003048 · NCRR · HOWARD UNIVERSITY · PI SOUTHERLAND, WILLIAM M. · 1985 to 2011
$19.0M
Resources and Infrastructure: Faculty RecruitmentU54CA091431 · NCI · HOWARD UNIVERSITY · PI ADAMS-CAMPBELL, LUCILE LAUREN · 2001 to 2010
$15.9M
Georgetown-Howard Universities Center for Clinical and Translational Science (GHUUL1RR031975 · NCRR · GEORGETOWN UNIVERSITY · PI MELLMAN, THOMAS A, VERBALIS, JOSEPH G · 2010 to 2011
$14.6M
Georgetown-Howard Universities Center for Clinical and Translational Science (GHUKL2TR000102 · NCATS · GEORGETOWN UNIVERSITY · PI MELLMAN, THOMAS A, VERBALIS, JOSEPH G · 2012 to 2014
$1.7M
NCATS NIH HHS KL2 TR000102NCI NIH HHS U54 CA091431NCRR NIH HHS G12 RR003048NCRR NIH HHS UL1 RR031975NCRR NIH HHS UL1RR031975
6 · The paper itself

Abstract

backgroundProstate cancer (PCa) is a common malignancy and a leading cause of cancer death among men in the United States with African-American (AA) men having the highest incidence and mortality rates. Given recent results from admixture mapping and genome-wide association studies for PCa in AA men, it is clear that many risk alleles are enriched in men with West African genetic ancestry.

methodsA total of 77 ancestry informative markers (AIMs) within surrounding candidate gene regions were genotyped and haplotyped using Pyrosequencing in 358 unrelated men enrolled in a PCa genetic association study at the Howard University Hospital between 2000 and 2004. Sequence analysis of promoter region single-nucleotide polymorphisms (SNPs) to evaluate disruption of transcription factor-binding sites was conducted using in silico methods.

resultsEight AIMs were significantly associated with PCa risk after adjusting for age and West African ancestry. SNP rs1993973 (intervening sequences) had the strongest association with PCa using the log-additive genetic model (P=0.002). SNPs rs1561131 (genotypic, P=0.007), rs1963562 (dominant, P=0.01) and rs615382 (recessive, P=0.009) remained highly significant after adjusting for both age and ancestry. We also tested the independent effect of each significantly associated SNP and rs1561131 (P=0.04) and rs1963562 (P=0.04) remained significantly associated with PCa development. After multiple comparisons testing using the false discovery rate, rs1993973 remained significant. Analysis of the rs156113-, rs1963562-rs615382l and rs1993973-rs585224 haplotypes revealed that the least frequently found haplotypes in this population were significantly associated with a decreased risk of PCa (P=0.032 and 0.0017, respectively).

conclusionsThe approach for SNP selection utilized herein showed that AIMs may not only leverage increased linkage disequilibrium in populations to identify risk and protective alleles, but may also be informative in dissecting the biology of PCa and other health disparities.

Indexed as

Genetic MarkersAfrica, WesternAgedBlack or African AmericanBlack PeopleGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeHaplotypesHumansLinkage DisequilibriumMaleMiddle AgedProstatic NeoplasmsRisk FactorsUnited StatesGenetic Markers

Identifiers

PMID22801071
PMCPMC4291058
OpenAlexW2052484012

What OpenQuestion holds

Textmetadata
LicenceTDM
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.