Evidence map›Paper›PMID 10935510›Full record

ArticleNeoplasia (New York, N.Y.)

Antagonists of growth hormone-releasing hormone inhibit the growth of U-87MG human glioblastoma in nude mice.

H Kiaris, A V Schally, J L Varga

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.). 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, 57 citations in OpenAlex.

  1. GHRH and the prostate.Reviews in endocrine & metabolic disorders · 2025
    Review
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  7. Simultaneous reconstruction of multiple signaling pathways via the prize-collecting steiner forest problem.Journal of computational biology : a journal of computational molecular cell biology · 2013
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  14. Potentiation of mammary cancer inhibition by combination of antagonists of growth hormone-releasing hormone with docetaxel.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
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  18. Expression of a splice variant of the receptor for GHRH in 3T3 fibroblasts activates cell proliferation responses to GHRH analogs.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  19. Isolation and sequencing of cDNAs for splice variants of growth hormone-releasing hormone receptors from human cancers.Proceedings of the National Academy of Sciences of the United States of America · 2000
    Article
  20. Human renal cell carcinoma expresses distinct binding sites for growth hormone-releasing hormone.Proceedings of the National Academy of Sciences of the United States of America · 2000
    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

3 authors at 1 institution in 1 country.

H KiarisEndocrine, Polypeptide and Cancer Institute, Veterans Affairs Medical Center, Department of Medicine, Tulane University School of Medicine, New Orleans, LA 70112-1262, USA.
A V Schally
J L Varga
Tulane University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antagonists of growth hormone-releasing hormone(GH-RH)inhibit the growth of various cancers by mechanisms that involve the suppression of the insulin-like growth factor (IGF)-I and/or IGF-II. In view of the importance of the IGF system in glioma tumorigenesis, the effects of GH-RH antagonists MZ-5-156 and JV-1-36 were investigated in nude mice bearing subcutaneous and orthotopic xenografts of U-87MG human glioblastomas. After 4 weeks of therapy with MZ-5-156 or JV-1 -36 at the dose of 20 microg/day per animal, the final volume of subcutaneous U-87MG tumors was significantly (P < .01) decreased by 84% and 76%, respectively, as compared with controls. Treatment with GH-RH antagonists also reduced tumor weight and the levels of mRNA for IGF receptor type I (IGFR-I). A reduction in the mRNA levels for IGF-II was found in tumors of mice treated with MZ-5-156. Treatment with MZ-5-156 or JV-1 -36 also extended the survival of nude mice implanted orthotopically with U-87MG glioblastomas by 81% (P < .005) and 18%, respectively, as compared with the controls. Exposure in vitro to GH-RH antagonists MZ-5-156 or JV-1 -36 at 1 microM concentration for 24 hours decreased the tumorigenicity of U-87MG cells in nude mice by 10% to 30% and extended the latency period for the development of subcutaneous palpable tumors by 31% to 56%, as compared with the controls. Exposure of U-87MG cells to GH-RH antagonists in vitro also resulted in a time-dependent increase in the mRNA levels of IGFR-II or a decrease in the mRNA levels of IGFR-I. mRNA for GH-RH was detected in U-87MG cells and xenografts implying that GH-RH may play a role in the pathogenesis of this tumor. Our results suggest that GH-RH antagonists MZ-5-156 and JV-1-36 inhibit the growth of U-87MG human glioblastoma by mechanisms that involve the suppression of IGF system. Antagonistic analogs of GH-RH merit further development for the treatment of malignant glioblastoma.

Indexed as

AnimalsGlioblastomaGrowth Hormone-Releasing HormoneHumansMaleMiceMice, NudeNeoplasm TransplantationReceptors, SomatomedinRNA, MessengerSermorelinSomatomedinsTransplantation, HeterologousTumor Cells, CulturedGrowth Hormone-Releasing HormoneJV 1-36MZ 5-156Receptors, SomatomedinRNA, MessengerSermorelinSomatomedins

Identifiers

PMID10935510
PMCPMC1507563
OpenAlexW2050730054

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.