Evidence map›Paper›PMID 25990088›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2015

Bacterial Prostatitis Enhances 2-Amino-1-Methyl-6-Phenylimidazo[4,5-b]Pyridine (PhIP)-Induced Cancer at Multiple Sites.

Karen S Sfanos, Kirstie Canene-Adams, Heidi Hempel, Shu-Han Yu, Brian W Simons, Anthony J Schaeffer, Edward M Schaeffer, William G Nelson, Angelo M De Marzo

Open access · bronzeAbstract read
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2015. 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
1.3field-weighted citation impact, top 18% 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. Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026
    Review
  2. Review
  3. Prostate Cancer: Etiology, Diagnosis, and Treatment.Serican journal of medicine · 2026
    Article
  4. Review
  5. Spot-light on microbiota in obesity and cancer.International journal of obesity (2005) · 2021
    Review
  6. Why Do Epidemiologic Studies Find an Inverse Association Between Intraprostatic Inflammation and Prostate Cancer: A Possible Role for Colliding Bias?Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2021
    Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Prostate carcinogenesis: inflammatory storms.Nature reviews. Cancer · 2020
    Review
  12. The microbiome in prostate inflammation and prostate cancer.Prostate cancer and prostatic diseases · 2018
    Review
  13. Review
  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 2 institutions in 1 country.

Karen S SfanosDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland. Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, Maryland. Department of Urology, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland. ksfanos@jhmi.edu.
Kirstie Canene-AdamsDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Heidi HempelDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Shu-Han YuDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Brian W SimonsDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Anthony J SchaefferDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Edward M SchaefferDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland.
William G NelsonSidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, Maryland. Department of Urology, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Angelo M De MarzoDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland. Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, Maryland. Department of Urology, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Johns Hopkins University · USNorthwestern University · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI WILLIAM George NELSON · 1985 to 2026
$208.6M
Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LEONIDAS C. PLATANIAS · 1993 to 2026
$153.9M
TRAINING PROGRAM IN THE PATHOBIOLOGY OF CANCERT32CA067751 · NCI · JOHNS HOPKINS UNIVERSITY · PI GABRIELSON, EDWARD W. · 1996 to 2011
$4.0M
NCI NIH HHS P30 CA006973NCI NIH HHS P30 CA060553NCI NIH HHS T32 CA067751
6 · The paper itself

Abstract

Dietary carcinogens, such as 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), and chronic inflammation have each been implicated as etiologic agents in prostate cancer. We hypothesized that bacterial prostatitis would accelerate PhIP-induced preinvasive lesions in the rat prostate. Male Fischer 344 rats were assigned into 4 groups: Control (untreated), PhIP (200 ppm in the diet for 20 weeks), Escherichia coli (E. coli, prostatic inoculation in week 10), or PhIP + E. coli. Study animals were monitored for a total of 52 weeks and were euthanized as necessary based on strict criteria for health status and tumor burden. Animals treated with E. coli initially developed acute and chronic inflammation in all lobes of the prostate, whereas inflammation was observed predominantly in the ventral lobe at time of death. PhIP + E. coli-treated animals exhibited a marked decrease in survival compared with PhIP-alone-treated animals as a result of an increase in the number of invasive cancers that developed at multiple sites, including the skin, small intestine, and Zymbal's gland. Despite their earlier mortality, PhIP + E. coli-treated animals developed an increased average number of precancerous lesions within the prostate compared with PhIP-treated animals, with a significantly increased Ki-67 index. Multiplexed serum cytokine analysis indicated an increase in the level of circulating IL6 and IL12 in PhIP + E. coli-treated animals. Elevated serum IL6 levels correlated with the development of precancerous lesions within the prostate. These results suggest that bacterial infections and dietary carcinogens, two conceivably preventable cancer risk factors, may synergistically promote tumorigenesis.

Indexed as

AnimalsCarcinogensCell Transformation, NeoplasticEscherichia coliEscherichia coli InfectionsImidazolesMaleProstatic NeoplasmsProstatitisRatsRats, Inbred F3442-amino-1-methyl-6-phenylimidazo(4,5-b)pyridineCarcinogensImidazoles

Identifiers

PMID25990088
PMCPMC4527940
OpenAlexW2170845300

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.