Evidence map›Paper›PMID 24395797›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Preclinical efficacy of growth hormone-releasing hormone antagonists for androgen-dependent and castration-resistant human prostate cancer.

Cale D Fahrenholtz, Ferenc G Rick, Maria I Garcia, Marta Zarandi, Ren-Zhi Cai, Norman L Block, Andrew V Schally, Kerry L Burnstein

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 57 citations in OpenAlex.

  1. Effects of GHRH and its analogues on the Vascular System.Reviews in endocrine & metabolic disorders · 2025
    Review
  2. GHRH and the prostate.Reviews in endocrine & metabolic disorders · 2025
    Review
  3. Review
  4. Review
  5. Review
  6. Growth hormone-releasing hormone and cancer.Reviews in endocrine & metabolic disorders · 2025
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
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  15. Review
  16. Article
  17. 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
  18. Article
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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

8 authors at 2 institutions in 1 country.

Cale D FahrenholtzDepartment of Molecular and Cellular Pharmacology, Miller School of Medicine, University of Miami, Miami, FL 33136.
Ferenc G Rick
Maria I Garcia
Marta Zarandi
Ren-Zhi Cai
Norman L Block
Andrew V Schally
Kerry L Burnstein
South Florida Veterans Affairs Foundation for Research and Education · USUniversity of Miami · US

Funding

TRAINING PROGRAMS IN CARDIOVASCULAR PHARMACOLOGYT32HL007188 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SZCZESNA-CORDARY, DANUTA · 1985 to 2011
$3.8M
Vav3 Oncogene Potentiation of Androgen Receptor Signaling in Prostate Cancer.R01CA132200 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BURNSTEIN, KERRY L · 2009 to 2013
$1.6M
NCI NIH HHS CA132200NCI NIH HHS R01 CA132200NHLBI NIH HHS T32 HL007188NHLBI NIH HHS T32-HL007188
6 · The paper itself

Abstract

Advanced hormone-sensitive prostate cancer responds to androgen-deprivation therapy (ADT); however, therapeutic options for recurrent castration-resistant disease are limited. Because growth hormone-releasing hormone (GHRH) and GHRH receptor (GHRH-R) are regulated in an autocrine fashion in prostate cancer, inhibition of GHRH-R represents a compelling approach to treatment. We investigated the effects of the latest series of improved, highly potent GHRH antagonists--MIA-602, MIA-606, and MIA-690--on the growth of androgen-dependent as well as castration-resistant prostate cancer (CRPC) cells in vitro and in vivo. GHRH-R and its splice variant, SV1, were present in 22Rv1, LNCaP, and VCaP human prostate cancer cell lines. Androgen-dependent LNCaP and VCaP cells expressed higher levels of GHRH-R protein compared with castration-resistant 22Rv1 cells; however, 22Rv1 expressed higher levels of SV1. In vitro, MIA-602 decreased cell proliferation of 22Rv1, LNCaP, and VCaP prostate cancer cell lines by 70%, 61%, and 20%, respectively (all P < 0.05), indicating direct effects of MIA-602. In vivo, MIA-602 was more effective than MIA-606 and MIA-690 and decreased 22Rv1 xenograft tumor volumes in mice by 63% after 3 wk (P < 0.05). No noticeable untoward effects or changes in body weight occurred. In vitro, the VCaP cell line was minimally inhibited by MIA-602, but in vivo, this line showed a substantial reduction in growth of xenografts in response to MIA-602, indicating both direct and systemic inhibitory effects. MIA-602 also further inhibited VCaP xenografts when combined with ADT. This study demonstrates the preclinical efficacy of the GHRH antagonist MIA-602 for treatment of both androgen-dependent and CRPC.

Indexed as

AndrogensAnimalsBody WeightCell Line, TumorCell ProliferationDrug Screening Assays, AntitumorGrowth Hormone-Releasing HormoneHumansHypothalamusLigandsMaleMiceMice, NudeNeoplasm TransplantationProstate-Specific AntigenProstatic NeoplasmsAndrogensGrowth Hormone-Releasing HormoneLigandsProstate-Specific AntigenReceptors, G-Protein-Coupledandrogen-independentG protein-coupled receptorhypothalamic neurohormoneneuropeptidetargeted therapy

Identifiers

PMID24395797
PMCPMC3903215
OpenAlexW2081201545

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.