Evidence map›Paper›PMID 22460812›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2012

Inflammation and preneoplastic lesions in benign prostate as risk factors for prostate cancer.

Oleksandr N Kryvenko, Michelle Jankowski, Dhananjay A Chitale, Deliang Tang, Andrew Rundle, Sheri Trudeau, Benjamin A Rybicki

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
6.8field-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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Geographic Differences in Baseline Prostate Inflammation and Relationship with Subsequent Prostate Cancer Risk: Results from the Multinational REDUCE Trial.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018
    Article
  16. Article
  17. Evolution of Premalignant Disease.Cold Spring Harbor perspectives in medicine · 2017
    Review
  18. Revisiting the hallmarks of cancer.American journal of cancer research · 2017
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Oleksandr N KryvenkoDepartment of Pathology, Henry Ford Hospital, Detroit, MI, USA.
Michelle Jankowski
Dhananjay A Chitale
Deliang Tang
Andrew Rundle
Sheri Trudeau
Benjamin A Rybicki
Henry Ford Hospital · USColumbia University · USHenry Ford Health System · 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

Benign changes ranging from atrophy and inflammation to high-grade prostatic intraepithelial neoplasia (HGPIN) are common findings on prostate core needle biopsies. Although atrophy and inflammation may be precursors of prostate cancer, only HGPIN is currently recommended to be included in surgical pathology reports. To determine whether these benign findings increase prostate cancer risk, we conducted a case-control study nested within a historical cohort of 6692 men with a benign prostate specimen collected between 1990 and 2002. The analytic sample included 574 case-control pairs comprised of cases diagnosed with prostate cancer a minimum of 1 year after cohort entry and controls matched to cases on date and age at cohort entry, race, and type of specimen. The initial benign specimen was reviewed for presence of HGPIN, atrophy (simple, lobular, and partial) and inflammation (glandular and/or stromal). HGPIN significantly increased risk for prostate cancer (odds ratio (OR)=2.00; 95% confidence interval (CI)=1.25-3.20). Inflammation within the stromal compartment was associated with decreased risk (OR=0.66; CI=0.52-0.84), and diffuse stromal inflammation of severe grade had the strongest inverse association with risk (OR=0.21; CI=0.07-0.62). In a model adjusted for prostate-specific antigen (PSA) level at cohort entry and inflammation, simple atrophy was associated with a 33% increased prostate cancer risk that was marginally significant (P=0.03). Clinicians should consider patterns and extent of inflammation when managing high-risk patients with negative biopsy results. Identifying benign inflammatory processes that underlie high PSA levels would help to reduce the number of unnecessary repeated prostate biopsies.

Indexed as

AgedAtrophyCase-Control StudiesHumansInflammationMalePrecancerous ConditionsPrevalenceProstate-Specific AntigenProstatic Intraepithelial NeoplasiaProstatic NeoplasmsRisk FactorsProstate-Specific Antigen

Identifiers

PMID22460812
PMCPMC3589982
OpenAlexW2001655892

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.