Evidence map›Paper›PMID 19520778›Full record

ReviewEndocrinology2009

Epigenetic alterations in human prostate cancers.

William G Nelson, Angelo M De Marzo, Srinivasan Yegnasubramanian

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
12.7field-weighted citation impact, top 1% 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

82 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Differential DNA Methylation in the Benign and Cancerous Prostate Tissue of African American and European American Men.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2025
    Article
  5. Article
  6. Article
  7. Race and prostate cancer: genomic landscape.Nature reviews. Urology · 2022
    Review
  8. Review
  9. Review
  10. Article
  11. Promoter Demethylation UpregulatesLife (Basel, Switzerland) · 2021
    Article
  12. Article
  13. Review
  14. Epigenetic field alterations in non-tumor prostate tissues detect prostate cancer in urine.American journal of clinical and experimental urology · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Prostate Cancer Epigenetics: From Basic Mechanisms to Clinical Implications.Cold Spring Harbor perspectives in medicine · 2019
    Review
  20. Prostate Cancer Energetics and Biosynthesis.Advances in experimental medicine and biology · 2019
    Review

22 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

William G NelsonSidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231-1000, USA. bnelson@jhmi.edu
Angelo M De Marzo
Srinivasan Yegnasubramanian
Sidney Kimmel Comprehensive Cancer Center · US

Funding

TRANSGENIC MODELS FOR PROSTATE CANCER AND AUTOIMMUNITYP50CA058236 · NCI · JOHNS HOPKINS UNIVERSITY · PI DENMEADE, SAMUEL R · 1992 to 2020
$43.9M
GSTPI PROMOTOR HYPERMETHYLATION IN HUMAN PROSTATE CANCERR01CA070196 · NCI · JOHNS HOPKINS UNIVERSITY · PI NELSON, WILLIAM GEORGE · 1996 to 2012
$3.9M
NCI NIH HHS P50 CA058236NCI NIH HHS P50CA58236NCI NIH HHS R01 CA070196NCI NIH HHS R01 CA70196
6 · The paper itself

Abstract

Human prostate cancer cells carry a myriad of genome defects, including both genetic and epigenetic alterations. These changes, which can be maintained through mitosis, generate malignant phenotypes capable of selective growth, survival, invasion, and metastasis. During prostatic carcinogenesis, epigenetic changes arise earlier than genetic defects, linking the appearance of epigenetic alterations in some way to disease etiology. The most common genetic defect thus far described, leading to fusion transcripts between the androgen-regulated gene TMPRSS2 and genes from the ETS family of transcription factors, likely endows prostate cancer cells with the ability to co-opt androgen signaling, the major prostate differentiation pathway, to support the malignant phenotype. Whether epigenetic changes promote the appearance of TMPRSS2-ETS family fusion transcripts or collaborate with fusion transcript expression in the pathogenesis of prostate cancer has not been established. However, a growing list of epigenetic alterations has provided new opportunities for clinical tests that might aid in prostate cancer screening, detection, diagnosis, staging, and risk stratification. The epigenetic changes appear to be more attractive than genetic changes as prostate cancer biomarkers because epigenetic alterations are present in a greater fraction of prostate cancer cases than any of the known genetic defects. In addition, an emerging generation of assay strategies for detection of specific DNA sequences carrying (5-me)C, the major epigenetic genome mark, has pushed somatic epigenetic alterations to the forefront of molecular biomarker assay development for cancer. Finally, a growing portfolio of epigenetic drugs, capable of reversing the phenotypic consequences of somatic epigenetic defects, has entered clinical trials for prostate cancer in the search for a new rational therapy for the disease.

Indexed as

Epigenesis, GeneticCpG IslandsDNA MethylationEarly Detection of CancerGlutathione S-Transferase piHumansMaleProstateProstatic NeoplasmsGlutathione S-Transferase piGSTP1 protein, human

Identifiers

PMID19520778
PMCPMC2736081
OpenAlexW2036485388

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.