Evidence map›Paper›PMID 35247880›Full record

ArticleCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology2022

Race Differences in Telomere Length in Benign Prostate Biopsies and Subsequent Risk of Prostate Cancer.

Benjamin A Rybicki, Sudha M Sadasivan, Yalei Chen, Ian Loveless, Nilesh S Gupta, Dhananjay A Chitale, Sean R Williamson, Andrew G Rundle, Deliang L Tang

Open access · bronzeAbstract read
In one paragraph

Article in Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

7 citing papers in PubMed, 12 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

9 authors at 3 institutions in 1 country.

Benjamin A RybickiDepartment of Public Health Sciences, Henry Ford Hospital, Detroit, Michigan.ORCID 0000-0003-3190-3467
Sudha M SadasivanDepartment of Public Health Sciences, Henry Ford Hospital, Detroit, Michigan.
Yalei ChenDepartment of Public Health Sciences, Henry Ford Hospital, Detroit, Michigan.
Ian LovelessDepartment of Public Health Sciences, Henry Ford Hospital, Detroit, Michigan.
Nilesh S GuptaDepartment of Pathology, Henry Ford Hospital, Detroit, Michigan.
Dhananjay A ChitaleDepartment of Pathology, Henry Ford Hospital, Detroit, Michigan.ORCID 0000-0002-4421-6431
Sean R WilliamsonDepartment of Pathology, Cleveland Clinic, Cleveland, Ohio.ORCID 0000-0002-3898-1460
Andrew G RundleDepartment of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York.ORCID 0000-0003-0211-7707
Deliang L TangDepartment of Environmental Heath Sciences, Mailman School of Public Health, Columbia University, New York, New York.
Henry Ford Hospital · USColumbia University · USCleveland Clinic · US

Funding

GENE-ENVIRONMENT INTERACTION IN PROSTATE CANCERR01ES011126 · NIEHS · HENRY FORD HEALTH SYSTEM · PI RYBICKI, BENJAMIN A. · 2000 to 2017
$8.0M
NIEHS NIH HHS R01 ES011126
6 · The paper itself

Abstract

backgroundTelomere shortening is linked to aging and may be associated with increased risk for cancer. Most cancer studies have used telomere length in leukocytes rather than in the target tissue of cancer origin.

methodsA case-control study of 524 case-control pairs with a benign prostate biopsy nested within a historical cohort of 10,478 men was conducted to determine whether premalignant prostate telomere length (assessed using a modified qRT-PCR) is associated with prostate cancer risk.

resultsTelomere lengths in benign prostate biopsies of cases versus controls were similar (1.46 ± 0.38 vs. 1.45 ± 0.42; P = 0.49). African American (AA) men had significantly shorter telomeres compared with White men (1.51 ± 0.38 vs. 1.63 ± 0.39; P < 0.0001). In race-stratified analyses, increasing telomere length was more strongly associated with prostate cancer risk in White men, wherein those with telomere length in the highest quartile had 1.9-fold greater adjusted risk of prostate cancer compared with men with prostate telomere lengths in the lowest quartile [OR = 1.90; 95% confidence interval (CI) = 1.08-3.36]. Men in the highest telomere length quartile also had a greater risk of aggressive prostate cancer compared with men with telomere lengths in the lowest quartile (OR = 2.78; 95% CI = 1.25-6.19).

conclusionsWhite men have longer telomeres in benign prostate tissue compared with AA men, and those with the longest telomeres may be at increased risk for prostate cancer, particularly the more aggressive form of the disease. IMPACT: Race-specific telomere length measures may be an early biomarker of aggressive prostate cancer.

Indexed as

ProstateProstatic NeoplasmsBiopsyCase-Control StudiesHumansLeukocytesMaleRace FactorsRisk FactorsTelomere

Identifiers

PMID35247880
PMCPMC9081233
OpenAlexW4220709174

What OpenQuestion holds

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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.