Evidence map›Paper›PMID 28824547›Full record

ReviewFrontiers in endocrinology2017

The Role of Gonadotropin-Releasing Hormone in Cancer Cell Proliferation and Metastasis.

Carsten Gründker, Günter Emons

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05247268 (Gonadotropin-releasing Hormone Agonist Combined With Letrozole Compared With Megestrol Acetate or Medroxyprogesterone Acetate Alone as Fertility-sparing Treatment in Early Endometrial Cancer), which is not on this map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
10.6field-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.

NCT05247268 phase2recruitingnot on this mapstarted 2022, after this paper: background citation

Gonadotropin-releasing Hormone Agonist Combined With Letrozole Compared With Megestrol Acetate or Medroxyprogesterone Acetate Alone as Fertility-sparing Treatment in Early Endometrial Cancer

TypeinterventionalSponsorFudan UniversityRan2022 to 2027Enrolled104ConditionsEndometrial Neoplasm Malignant Stage IArmsMegestrol Acetate 160 MG Oral Tablet, Medroxyprogesterone Acetate 500 MG, Triprorelin Acetate, Letrozole 2.5mg
3 · Its place in the literature

Who cites it

68 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
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  9. Peptide-Drug Conjugates: A New Hope for Cancer.Journal of peptide science : an official publication of the European Peptide Society · 2025
    Review
  10. Review
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  12. Article
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  16. Prevention of prostate cancer metastasis by a CRISPR-delivering nanoplatform for interleukin-30 genome editing.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
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  18. Article
  19. Review
  20. Article

8 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

2 authors at 1 institution in 1 country.

Carsten GründkerDepartment of Gynecology and Obstetrics, Georg-August-University, Göttingen, Germany.
Günter EmonsDepartment of Gynecology and Obstetrics, Georg-August-University, Göttingen, Germany.
University of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In several human malignant tumors of the urogenital tract, including cancers of the endometrium, ovary, urinary bladder, and prostate, it has been possible to identify expression of gonadotropin-releasing hormone (GnRH) and its receptor as part of an autocrine system, which regulates cell proliferation. The expression of GnRH receptor has also been identified in breast cancers and non-reproductive cancers such as pancreatic cancers and glioblastoma. Various investigators have observed dose- and time-dependent growth inhibitory effects of GnRH agonists in cell lines derived from these cancers. GnRH antagonists have also shown marked growth inhibitory effects on most cancer cell lines. This indicates that in the GnRH system in cancer cells, there may not be a dichotomy between GnRH agonists and antagonists. The well-known signaling mechanisms of the GnRH receptor, which are present in pituitary gonadotrophs, are not involved in forwarding the antiproliferative effects of GnRH analogs in cancer cells. Instead, the GnRH receptor activates a phosphotyrosine phosphatase (PTP) and counteracts with the mitogenic signal transduction of growth factor receptors, which results in a reduction of cancer cell proliferation. The PTP activation, which is induced by GnRH, also inhibits G-protein-coupled estrogen receptor 1 (GPER), which is a membrane-bound receptor for estrogens. GPER plays an important role in breast cancers, which do not express the estrogen receptor α (ERα). In metastatic breast, ovarian, and endometrial cancer cells, GnRH reduces cell invasion

Indexed as

cancergonadotropin-releasing hormonemetastasisproliferationsignal transduction

Identifiers

PMID28824547
PMCPMC5543040
OpenAlexW2743782212

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.