Evidence map›Paper›PMID 39663641›Full record

SynthesisInternational journal of cancer2025

Etiology of prostate cancer with the TMPRSS2:ERG fusion: A systematic review of risk factors.

Colleen B McGrath, Alaina H Shreves, Megan R Shanahan, Hannah E Guard, Manelisi V Nhliziyo, Claire H Pernar, Kathryn L Penney, Tamara L Lotan, Michelangelo Fiorentino, Lorelei A Mucci and 1 more

Abstract readSystematic Review
In one paragraph

Synthesis in International journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Precision medicine in prostate cancer: individualized treatment through radiomics, genomics, and biomarkers.Cancer imaging : the official publication of the International Cancer Imaging Society · 2025
    Review
  7. Article
  8. Review
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

11 authors.

Colleen B McGrathDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.ORCID 0000-0003-4542-2955
Alaina H ShrevesDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.ORCID 0000-0002-0127-4391
Megan R ShanahanDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
Hannah E GuardDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
Manelisi V NhliziyoDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
Claire H PernarDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
Kathryn L PenneyDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
Tamara L LotanDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Michelangelo FiorentinoDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
Lorelei A MucciDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
Konrad H StopsackDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.ORCID 0000-0002-0722-1311

Funding

Tumor and Circulating Markers as Links Between Obesity and Lethal Prostate CanceP50CA090381 · NCI · DANA-FARBER CANCER INSTITUTE · PI BALK, STEVEN P., BELTRAN, HIMISHA · 2002 to 2017
$36.2M
Training Program in Cancer EpidemiologyT32CA009001 · NCI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI A. Heather Eliassen, Meir Stampfer · 1985 to 2026
$17.3M
Cancer Epidemiology Cohort in Male Health ProfessionalsU01CA167552 · NCI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI Lorelei Mucci, Walter C. Willett · 2017 to 2026
$17.0M
The Impact of DNA Damage Repair Abnormalities in Prostate CancerP01CA228696 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI OFFIT, KENNETH, POMERANTZ, MARK M. · 2019 to 2024
$8.7M
Comprehensive characterization of prostate stromal gene expression and association with lethal prostate cancerR37CA227190 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI BIRMANN, BRENDA M, TYEKUCHEVA, SVITLANA · 2018 to 2024
$3.6M
Etiologic Heterogeneity Between Molecular Subtypes of Prostate CancerR37CA275914 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI Konrad Hermann Stopsack · 2023 to 2026
$2.7M
Sex-Hormones and the TMPRSS2: ERG Fusion in Prostate Cancer ProgressionR01CA136578 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI MUCCI, LORELEI · 2009 to 2013
$1.7M
NCI NIH HHS P01 CA228696NCI NIH HHS P50 CA090381NCI NIH HHS R01 CA136578NCI NIH HHS R37 CA227190NCI NIH HHS R37 CA275914NCI NIH HHS T32 CA009001NCI NIH HHS U01 CA167552Prostate Cancer Foundation
6 · The paper itself

Abstract

The most common somatic alteration in primary prostate cancer is the TMPRSS2:ERG gene fusion, which may be caused or promoted by distinct etiologic factors. The objective of this systematic review was to assess epidemiologic evidence on etiologic factors for prostate cancer by tumor TMPRSS2:ERG fusion status in human populations. Of 3071 publications identified, 19 cohort or case-control studies from six distinct study populations were included in this systematic review. Etiologic factors included germline genetic variants, circulating hormones, and dietary and lifestyle factors. Taller height, higher total and free testosterone levels, and fewer trinucleotide repeats in AR were possibly associated with higher risk of TMPRSS2:ERG-positive prostate cancer. Excess body weight, greater vigorous physical activity, higher lycopene intake, and the use of calcium channel blockers were associated with lower risk of TMPRSS2:ERG-positive prostate cancer. Diabetes and family history of prostate cancer were associated with both TMPRSS2:ERG-positive and TMPRSS2:ERG-negative prostate cancer. Prostate cancer germline variants had suggestive differential associations with TMPRSS2:ERG-positive or TMPRSS2:ERG-negative prostate cancer. However, results were based on few distinct study populations and generally had low precision, underscoring the need for replication. In conclusion, prostate cancer with TMPRSS2:ERG fusion is an etiologically distinct subtype that may be, in part, preventable by addressing modifiable and hormonally acting etiologic factors that align with the established mechanistic role of TMPRSS2:ERG in androgen, insulin, antioxidant, and growth factor pathways.

Indexed as

Oncogene Proteins, FusionProstatic NeoplasmsGenetic Predisposition to DiseaseHumansMaleRisk FactorsSerine EndopeptidasesTranscriptional Regulator ERGOncogene Proteins, FusionSerine EndopeptidasesTMPRSS2-ERG fusion protein, humanTMPRSS2 protein, humanTranscriptional Regulator ERGetiologygene fusionprostate cancersystematic reviewTMPRSS2:ERG

Identifiers

PMID39663641
PMCPMC11924303

What Socratic 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 Socratic graph.