Evidence map›Paper›PMID 26581226›Full record

ReviewEndocrine connections2015

Linking obesogenic dysregulation to prostate cancer progression.

Renea A Taylor, Jennifer Lo, Natasha Ascui, Matthew J Watt

Open access · goldAbstract readReview
In one paragraph

Review in Endocrine connections, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Role of CD36 in cancer progression, stemness, and targeting.Frontiers in cell and developmental biology · 2022
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. LXRs, SHP, and FXR in Prostate Cancer: Enemies orNuclear receptor signaling · 2018
    Review
  20. 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

4 authors at 2 institutions in 1 country.

Renea A TaylorDepartment of PhysiologyCancer Program and Obesity and Metabolic Disease Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Victoria 3800, Australia renea.taylor@monash.edu matthew.watt@monash.edu.
Jennifer LoDepartment of PhysiologyCancer Program and Obesity and Metabolic Disease Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Victoria 3800, Australia.
Natasha AscuiDepartment of PhysiologyCancer Program and Obesity and Metabolic Disease Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Victoria 3800, Australia.
Matthew J WattDepartment of PhysiologyCancer Program and Obesity and Metabolic Disease Program, Biomedicine Discovery Institute, Monash University, Wellington Road, Victoria 3800, Australia renea.taylor@monash.edu matthew.watt@monash.edu.
Monash University · AUAustralian Regenerative Medicine Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The global epidemic of obesity is closely linked to the development of serious co-morbidities, including many forms of cancer. Epidemiological evidence consistently shows that obesity is associated with a similar or mildly increased incidence of prostate cancer but, more prominently, an increased risk for aggressive prostate cancer and prostate cancer-specific mortality. Studies in mice demonstrate that obesity induced by high-fat feeding increases prostate cancer progression; however, the mechanisms underpinning this relationship remain incompletely understood. Adipose tissue expansion in obesity leads to local tissue dysfunction and is associated with low-grade inflammation, alterations in endocrine function and changes in lipolysis that result in increased delivery of fatty acids to tissues of the body. The human prostate gland is covered anteriorly by the prominent peri-prostatic adipose tissue and laterally by smaller adipose tissue depots that lie directly adjacent to the prostatic surface. We discuss how the close association between dysfunctional adipose tissue and prostate epithelial cells might result in bi-directional communication to cause increased prostate cancer aggressiveness and progression. However, the literature indicates that several 'mainstream' hypotheses regarding obesity-related drivers of prostate cancer progression are not yet supported by a solid evidence base and, in particular, are not supported by experiments using human tissue. Understanding the links between obesity and prostate cancer will have major implications for the health policy for men with prostate cancer and the development of new therapeutic or preventative strategies.

Indexed as

adipose tissueinflammationlipid metabolismobesityprostate cancer

Identifiers

PMID26581226
PMCPMC4653354
OpenAlexW2196756223

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.