Evidence map›Paper›PMID 23066084›Full record

ArticleCarcinogenesis2013

Elevated polycyclic aromatic hydrocarbon-DNA adducts in benign prostate and risk of prostate cancer in African Americans.

Deliang Tang, Oleksandr N Kryvenko, Yun Wang, Michelle Jankowski, Sheri Trudeau, Andrew Rundle, Benjamin A Rybicki

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Race Differences in Telomere Length in Benign Prostate Biopsies and Subsequent Risk of Prostate Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2022
    Article
  4. Article
  5. Review
  6. Occupational exposure to polycyclic aromatic hydrocarbons and risk of prostate cancer.Environmental health : a global access science source · 2021
    Article
  7. Article
  8. Dietary Carcinogens and DNA Adducts in Prostate Cancer.Advances in experimental medicine and biology · 2019
    Review
  9. Review
  10. Article
  11. Article
  12. Polycyclic aromatic hydrocarbon residues in serum samples of autopsied individuals from Tennessee.International journal of environmental research and public health · 2014
    Article
  13. Article
  14. Review
  15. Obesity and future prostate cancer risk among men after an initial benign biopsy of the prostate.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2013
    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

7 authors at 2 institutions in 1 country.

Deliang TangDepartment of Environmental Health Sciences, Columbia University, New York, NY, USA.
Oleksandr N Kryvenko
Yun Wang
Michelle Jankowski
Sheri Trudeau
Andrew Rundle
Benjamin A Rybicki
Henry Ford Health System · USColumbia University · 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 5R01-ES011126NIEHS NIH HHS R01 ES011126
6 · The paper itself

Abstract

Carcinogen-DNA adducts, a marker of DNA damage, are capable of inducing mutations in oncogenes and tumor suppressor genes, resulting in carcinogenesis. We have shown previously that polycyclic aromatic hydrocarbon (PAH)-DNA adduct levels in prostate cancer cases vary by cellular histology and that higher adduct levels are associated with biochemical recurrence. A nested case-control study was conducted in a historical cohort of 6692 men with histopathologically benign prostate specimens. PAH-DNA adduct levels were determined by immunohistochemistry in benign prostate specimens from 536 prostate cancer case-control pairs (59% White and 41% African American). We estimated the overall and race-stratified risk of subsequent prostate cancer associated with higher adduct levels. Prostate cancer risk for men with elevated adduct levels (defined as greater than control group median) was slightly increased [odds ratio (OR) = 1.28, 95% confidence interval (CI) = 0.98-1.67, P = 0.07]. After race stratification, elevated adduct levels were significantly associated with increased risk in African American men (OR = 1.56, CI = 1.00-2.44, *P = 0.05) but not White men (OR = 1.14, CI = 0.82-1.59, P = 0.45). Elevated PAH-DNA adduct levels were significantly associated with 60% increased risk of prostate cancer among cases diagnosed 1-4 years after cohort entry (OR = 1.60, CI = 1.07-2.41) with a greater risk observed in African Americans within the first 4 years of follow-up (OR = 4.71, CI = 1.97-11.26, ***P = 0.0005). Analyses stratified by age or tumor grade revealed no additional significant heterogeneity in risk. Increased prostate cancer risk associated with high PAH-DNA adduct levels in benign prostate was found only in African Americans; risk was greatest within 4 years of follow-up, possibly reflecting a carcinogenic process not yet histologically detectable.

Indexed as

Black PeopleAgedBlack or African AmericanDNA AdductsHumansMaleMiddle AgedPolycyclic CompoundsProstatic HyperplasiaProstatic NeoplasmsDNA AdductsPolycyclic Compounds

Identifiers

PMID23066084
PMCPMC3534199
OpenAlexW2135080120

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.