Evidence map›Paper›PMID 10077643›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Inhibition of growth, production of insulin-like growth factor-II (IGF-II), and expression of IGF-II mRNA of human cancer cell lines by antagonistic analogs of growth hormone-releasing hormone in vitro.

V J Csernus, A V Schally, H Kiaris, P Armatis

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. 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
7.5field-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, 78 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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
  11. 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
    Article
  12. Article
  13. Article
  14. 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
  15. 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
  16. 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
  17. Article
  18. Antitumorigenic actions of growth hormone-releasing hormone antagonists.Proceedings of the National Academy of Sciences of the United States of America · 2000
    Article
  19. Growth hormone-releasing hormone: an autocrine growth factor for small cell lung carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 1999
    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 1 institution in 1 country.

V J CsernusEndocrine, Polypeptide, and Cancer Institute, Veterans Affairs Medical Center, New Orleans, LA 70112-1262, USA.
A V Schally
H Kiaris
P Armatis
Tulane University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antagonistic analogs of growth hormone-releasing hormone (GHRH) suppress growth of various tumors in vivo. This effect is exerted in part through inhibition of the GHRH-GH-insulin-like growth factor (IGF)-I axis. Nevertheless, because autocrine/paracrine control of proliferation by IGF-II also is a major factor in many tumors, the interference with this growth-stimulating pathway would offer another approach to tumor control. We thus investigated whether GHRH antagonists MZ-4-71 and MZ-5-156 also act on the tumor cells directly by blocking the production of IGF-II. An increase in the IGF-II concentration in the media during culture was found in 13 of 26 human cancer cell lines tested. Reverse transcription-PCR studies on 8 of these cell lines showed that they also expressed IGF-II mRNA. Antagonists of GHRH significantly inhibited the rate of proliferation of mammary (MDA-MB-468 and ZR-75-1), prostatic (PC-3 and DU-145), and pancreatic (MiaPaCa-2, SW-1990, and Capan-2) cancer cell lines as shown by colorimetric and [3H]thymidine incorporation tests and reduced the expression of IGF-II mRNA in the cells and the concentration of IGF-II secreted into the culture medium. Growth and IGF-II production of lung (H-23 and H-69) and ovarian (OV-1063) cancer cells that express mRNA for IGF-II and excrete large quantities of IGF-II also was marginally suppressed by the antagonists. These findings suggest that antagonistic analogs of GHRH can inhibit growth of certain tumors not only by inhibiting the GHRH-GH-IGF-I axis, but also by reducing the IGF-II production and by interfering with the autocrine regulatory pathway.

Indexed as

NeoplasmsCell DivisionGene Expression Regulation, NeoplasticGrowth Hormone-Releasing HormoneHormone AntagonistsHumansInsulin-Like Growth Factor IIRNA, MessengerSermorelinTumor Cells, CulturedGrowth Hormone-Releasing HormoneHormone AntagonistsInsulin-Like Growth Factor IIMZ 4-71MZ 5-156RNA, MessengerSermorelin

Identifiers

PMID10077643
PMCPMC15901
OpenAlexW2037861236

What OpenQuestion holds

Texttitle and abstract
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.