Evidence map›Paper›PMID 16508751›Full record

ArticleHuman genetics2006

Genome-wide linkage scan for prostate cancer susceptibility genes in men with aggressive disease: significant evidence for linkage at chromosome 15q12.

Ethan M Lange, Lindsey A Ho, Jennifer L Beebe-Dimmer, Yunfei Wang, Elizabeth M Gillanders, Jeffrey M Trent, Leslie A Lange, David P Wood, Kathleen A Cooney

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Human genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. miR-183-5p Inhibits Occurrence and Progression of Acute Myeloid Leukemia via Targeting Erbin.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. The role of the BRCA2 gene in susceptibility to prostate cancer revisited.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2008
    Review
  12. Article
  13. Article
  14. 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

9 authors at 4 institutions in 1 country.

Ethan M LangeDepartment of Genetics, University of North Carolina, 4300D MBRB, CB# 7264, 103 Mason Farm Road, Chapel Hill, NC 27599-7264, USA. ethan_lange@med.unc.edu
Lindsey A Ho
Jennifer L Beebe-Dimmer
Yunfei Wang
Elizabeth M Gillanders
Jeffrey M Trent
Leslie A Lange
David P Wood
Kathleen A Cooney
University of North Carolina at Chapel Hill · USUniversity of Michigan–Ann Arbor · USNational Human Genome Research Institute · USTranslational Genomics Research Institute · US

Funding

Prostate Cancer Susceptibility: The ICPCG StudyU01CA089600 · NCI · MAYO CLINIC ROCHESTER · PI THIBODEAU, STEPHEN NORMAN · 2002 to 2016
$27.3M
GENETIC ANALYSIS OF HEREDITARY PROSTATE CANCER FAMILIESR01CA079596 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COONEY, KATHLEEN A · 1999 to 2009
$3.0M
Genetic Epidemiology of CancerZ01HG200331 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI BAILEY-WILSON, JOAN ELLEN · 2005 to 2008
$1.6M
NCI NIH HHS CA 079596NCI NIH HHS CA 089600
6 · The paper itself

Abstract

Epidemiological and twin studies have consistently demonstrated a strong genetic component to prostate cancer (PCa) susceptibility. To date, numerous linkage studies have been performed to identify chromosomal regions containing PCa susceptibility genes. Unfortunately, results from these studies have failed to form any obvious consensus regarding which regions are most likely to contain genes that may contribute to PCa predisposition. One plausible explanation for the difficulty in mapping susceptibility loci is the existence of considerable heterogeneity in the phenotype of PCa, with significant variation in clinical stage and grade of disease even among family members. To address this issue, we performed a genome-wide linkage scan on 71 informative families with two or more men with aggressive PCa. When only men with aggressive PCa were coded as affected, statistically significant evidence for linkage at chromosome 15q12 was detected (LOD=3.49; genome-wide p=0.005). Furthermore, the evidence for linkage increased when analyses were restricted to Caucasian-American pedigrees (n=65; LOD=4.05) and pedigrees with two confirmed aggressive cases (n=42, LOD=4.76). Interestingly, a 1-LOD support interval about our peak at 15q12 overlaps a region of suggestive linkage, 15q11, identified by a recent linkage study on 1,233 PCa families by the International Consortium for Prostate Cancer Genetics. Using a more rigid definition of PCa in linkage studies will result in a severe reduction in sample sizes available for study, but may ultimately prove to increase statistical power to detect susceptibility genes for this multigenic trait.

Indexed as

Genetic LinkageGenetic Predisposition to DiseaseGenome, HumanAllelesChromosome MappingChromosomes, Human, Pair 15EthnicityGenotypeHumansLod ScoreMaleMicrosatellite RepeatsMiddle AgedPedigreeProstatic Neoplasms

Identifiers

PMID16508751
OpenAlexW2001673896

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.