Evidence map›Paper›PMID 21971318›Full record

ReviewNature reviews. Urology2011

Prolactin regulation of the prostate gland: a female player in a male game.

Vincent Goffin, David T Hoang, Roman L Bogorad, Marja T Nevalainen

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Urology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

41 citing papers in PubMed, 88 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Stat5 induces androgen receptor (Science advances · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. The Involvement of Prolactin in Stress-Related Disorders.International journal of environmental research and public health · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. COX-2 mediates tumor-stromal prolactin signaling to initiate tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  19. Article
  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 4 institutions in 2 countries.

Vincent GoffinInserm, Unit 845, Research Center Growth and Signaling, Prolactin/GH Pathophysiology Laboratory, University Paris Descartes, Sorbonne Paris Cité, Faculty of Medicine, Necker site, Paris F-75015, France. vincent.goffin@inserm.fr
David T Hoang
Roman L Bogorad
Marja T Nevalainen
Inserm · FRSidney Kimmel Cancer Center · USSorbonne Paris Cité · FRThomas Jefferson University · US

Funding

Stat5 in Progression of Prostate CancerR01CA113580 · NCI · THOMAS JEFFERSON UNIVERSITY · PI NEVALAINEN, MARJA T · 2006 to 2015
$2.7M
Novel Strategy to Sensitize Prostate Cancer Cells to RadiationR21CA178755 · NCI · THOMAS JEFFERSON UNIVERSITY · PI NEVALAINEN, MARJA T · 2013 to 2014
$365k
NCI NIH HHS 1R01CA113580‑01A1NCI NIH HHS R01 CA113580NCI NIH HHS R21 CA178755
6 · The paper itself

Abstract

Prolactin is best known for its actions on the mammary gland. However, circulating prolactin is also detected in males and its receptor (PRLR) is expressed in the prostate, suggesting that the prostate is a target of prolactin. Germline knockout of prolactin or its receptor has failed to reveal a key role for prolactin signaling in mouse prostate physiology. However, several studies involving rodent models and human prostate cell lines and specimens have supported the contribution of the canonical PRLR-Jak2-Stat5a/b pathway to prostate cancer tumorigenesis and progression. Increased expression of prolactin in the prostate itself (rather than changes in circulating prolactin levels) and crosstalk with androgen receptor (AR) signaling are potential mechanisms for increased Stat5a/b signaling in prostate cancer. In the mouse prostate, prolactin overexpression results in disorganized expansion of the basal/stem cell compartment, which has been proposed to house putative prostate tumor-initiating cells. These findings provide new insight into the molecular and cellular targets by which locally produced prolactin could contribute to prostate cancer initiation and progression. A number of pharmacological inhibitors targeting various levels of the PRLR-Jak2-Stat5a/b pathway have been developed and are entering clinical trials for advanced prostate cancer.

Indexed as

AnimalsAntineoplastic AgentsFemaleGene TargetingHumansMaleProlactinProstateProstatic NeoplasmsReceptors, ProlactinSignal TransductionAntineoplastic AgentsProlactinReceptors, Prolactin

Identifiers

PMID21971318
PMCPMC6035044
OpenAlexW1972677695

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.