Evidence map›Paper›PMID 10962030›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Human renal cell carcinoma expresses distinct binding sites for growth hormone-releasing hormone.

G Halmos, A V Schally, J L Varga, A Plonowski, Z Rekasi, T Czompoly

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

21 citing papers in PubMed, 86 citations in OpenAlex.

  1. Growth hormone-releasing hormone receptor (GHRH-R) and its signaling.Reviews in endocrine & metabolic disorders · 2025
    Review
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  12. Effective treatment of experimental human non-Hodgkin's lymphomas with antagonists of growth hormone-releasing hormone.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
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  16. Increased activity of antagonists of growth hormone-releasing hormone substituted at positions 8, 9, and 10.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  17. Article
  18. Ligand-dependent and -independent effects of splice variant 1 of growth hormone-releasing hormone receptor.Proceedings of the National Academy of Sciences of the United States of America · 2003
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  19. Article
  20. 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
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

6 authors at 1 institution in 1 country.

G HalmosEndocrine, Polypeptide and Cancer Institute, Veterans Affairs Medical Center and Department of Medicine, Tulane University School of Medicine, New Orleans, LA 70112-2699, USA.
A V Schally
J L Varga
A Plonowski
Z Rekasi
T Czompoly
Tulane University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antagonists of growth hormone-releasing hormone (GHRH) inhibit the proliferation of various human cancers in vitro and in vivo by mechanisms that include apparent direct effects through specific binding sites expressed on tumors and that differ from pituitary human GHRH (hGHRH) receptors. In this study, GHRH antagonist JV-1-38 (20 microgram/day per animal s.c.) inhibited the growth of orthotopic CAKI-1 human renal cell carcinoma (RCC) by 83% and inhibited the development of metastases to lung and lymph nodes. Using ligand competition assays with (125)I-labeled GHRH antagonist JV-1-42, we demonstrated the presence of specific high-affinity (K(d) = 0.25 +/- 0.03 nM) binding sites for GHRH with a maximal binding capacity (B(max)) of 70.2 +/- 4.1 fmol/mg of membrane protein in CAKI-1 tumors. These receptors bind GHRH antagonists preferentially and display a lower affinity for hGHRH. The binding of (125)I-JV-1-42 is not inhibited by vasoactive intestinal peptide (VIP)-related peptides sharing structural homology with hGHRH. The receptors for GHRH antagonists on CAKI-1 tumors are distinct from binding sites detected with (125)I-VIP (K(d) = 0.89 +/- 0.14 nM; B(max) = 183.5 +/- 2.6 fmol/mg of protein) and also have different characteristics from GHRH receptors on rat pituitary as documented by the insignificant binding of [His(1),(125)I-Tyr(10), Nle(27)]hGHRH(1-32)NH(2). Reverse transcription-PCR revealed the expression of splice variants of hGHRH receptor in CAKI-1 RCC. Biodistribution studies demonstrate an in vivo uptake of (125)I-JV-1-42 by the RCC tumor tissue. The presence of specific receptor proteins that bind GHRH antagonists in CAKI-1 RCC supports the view that distinct binding sites that mediate the inhibitory effect of GHRH antagonists are present on various human cancers.

Indexed as

Binding SitesCarcinoma, Renal CellCell DivisionGrowth Hormone-Releasing HormoneHumansIodine RadioisotopesKidney NeoplasmsNeoplasm MetastasisReceptors, NeuropeptideReceptors, Pituitary Hormone-Regulating HormoneReceptors, Vasoactive Intestinal PeptideRNA, MessengerTissue DistributionGrowth Hormone-Releasing HormoneIodine RadioisotopesReceptors, NeuropeptideReceptors, Pituitary Hormone-Regulating HormoneReceptors, Vasoactive Intestinal PeptideRNA, Messengersomatotropin releasing hormone receptor

Identifiers

PMID10962030
PMCPMC27063
OpenAlexW2149609035

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.