Evidence map›Paper›PMID 12186980›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

The expression of growth hormone-releasing hormone (GHRH) and splice variants of its receptor in human gastroenteropancreatic carcinomas.

Rebeca Busto, Andrew V Schally, Jozsef L Varga, M Olga Garcia-Fernandez, Kate Groot, Patricia Armatis, Karoly Szepeshazi

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. Growth hormone-releasing hormone and cancer.Reviews in endocrine & metabolic disorders · 2025
    Review
  3. Review
  4. Effects of GHRH and its analogues on the Vascular System.Reviews in endocrine & metabolic disorders · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Constitutive signal bias mediated by the human GHRHR splice variant 1.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Beneficial effects of growth hormone-releasing hormone agonists on rat INS-1 cells and on streptozotocin-induced NOD/SCID mice.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  17. Article
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  19. Review
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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

7 authors at 1 institution in 1 country.

Rebeca BustoEndocrine, Polypeptide, and Cancer Institute, Veterans Affairs Medical Center, and Section of Experimental Medicine, Department of Medicine, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Andrew V Schally
Jozsef L Varga
M Olga Garcia-Fernandez
Kate Groot
Patricia Armatis
Karoly Szepeshazi
Tulane University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Splice variants (SVs) of receptors for growth hormone-releasing hormone (GHRH) have been found in primary human prostate cancers and diverse human cancer cell lines. GHRH antagonists inhibit growth of various experimental human cancers, including pancreatic and colorectal, xenografted into nude mice or cultured in vitro, and their antiproliferative action could be mediated in part through SVs of GHRH receptors. In this study we examined the expression of mRNA for GHRH and for SVs of its receptors in tumors of human pancreatic, colorectal, and gastric cancer cell lines grown in nude mice. mRNA for both GHRH and SV(1) isoform of GHRH receptors was expressed in tumors of pancreatic (SW1990, PANC-1, MIA PaCa-2, Capan-1, Capan-2, and CFPAC1), colonic (COLO 320DM and HT-29), and gastric (NCI-N87, HS746T, and AGS) cancer cell lines; mRNA for SV(2) was also present in Capan-1, Capan-2, CFPAC1, HT-29, and NCI-N87 tumors. In proliferation studies in vitro, the growth of pancreatic, colonic, and gastric cancer cells was stimulated by GHRH(1-29)NH(2) and inhibited by GHRH antagonist JV-1-38. The stimulation of some gastroenteropancreatic cancer cells by GHRH was followed by an increase in cAMP production, and GHRH antagonist JV-1-38 competitively inhibited this effect. Our study indicates the presence of an autocrine/paracrine stimulatory loop based on GHRH and SV(1) of GHRH receptors in human pancreatic, colorectal, and gastric cancers. The finding of SV(1) receptor in human cancers provides an approach to an antitumor therapy based on the blockade of this receptor by specific GHRH antagonists.

Indexed as

RNA SplicingAnimalsBase SequenceCyclic AMPDNA PrimersGastrointestinal NeoplasmsGrowth Hormone-Releasing HormoneHumansMaleMiceMice, NudeReceptors, NeuropeptideReceptors, Pituitary Hormone-Regulating HormoneReverse Transcriptase Polymerase Chain ReactionRNA, MessengerTumor Cells, CulturedCyclic AMPDNA PrimersGrowth Hormone-Releasing HormoneJV 1-38Receptors, NeuropeptideReceptors, Pituitary Hormone-Regulating HormoneRNA, Messengersomatotropin releasing hormone receptor

Identifiers

PMID12186980
PMCPMC129360
OpenAlexW2043392177

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.