Evidence map›Paper›PMID 34439107›Full record

ArticleCancers2021

Antagonists of Growth Hormone-Releasing Hormone Inhibit the Growth of Pituitary Adenoma Cells by Hampering Oncogenic Pathways and Promoting Apoptotic Signaling.

Iacopo Gesmundo, Giuseppina Granato, Antonio C Fuentes-Fayos, Clara V Alvarez, Carlos Dieguez, Maria Chiara Zatelli, Noemi Congiusta, Dana Banfi, Nunzia Prencipe, Sheila Leone and 8 more

Abstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Growth hormone-releasing hormone and cancer.Reviews in endocrine & metabolic disorders · 2025
    Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Alleviation of LPS-induced Endothelial Injury due to GHRH Antagonist Treatment.International journal of peptide research and therapeutics · 2024
    Article
  7. Article
  8. Article
  9. 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

18 authors.

Iacopo GesmundoDivision of Endocrinology, Diabetes and Metabolism, Department of Medical Science, University of Turin, 10126 Turin, Italy.
Giuseppina GranatoDivision of Endocrinology, Diabetes and Metabolism, Department of Medical Science, University of Turin, 10126 Turin, Italy.
Antonio C Fuentes-FayosMaimonides Institute for Biomedical Research of Córdoba (IMIBIC), Department of Cell Biology, Physiology and Immunology, University of Córdoba and Reina Sofia University Hospital, 14004 Córdoba, Spain.ORCID 0000-0003-2069-4823
Clara V AlvarezCentro de Investigaciones Médicas (CIMUS) e Instituto de Investigaciones Sanitarias, University of Santiago de Compostela and Complexo Hospitalario Universitario of Santiago de Compostela, 14004 Santiago de Compostela, Spain.ORCID 0000-0003-1500-4058
Carlos DieguezCentro de Investigaciones Médicas (CIMUS) e Instituto de Investigaciones Sanitarias, University of Santiago de Compostela and Complexo Hospitalario Universitario of Santiago de Compostela, 14004 Santiago de Compostela, Spain.
Maria Chiara ZatelliSection of Endocrinology and Internal Medicine, Department of Medical Sciences, University of Ferrara, 15706 Ferrara, Italy.
Noemi CongiustaDivision of Endocrinology, Diabetes and Metabolism, Department of Medical Science, University of Turin, 10126 Turin, Italy.
Dana BanfiDivision of Endocrinology, Diabetes and Metabolism, Department of Medical Science, University of Turin, 10126 Turin, Italy.
Nunzia PrencipeDivision of Endocrinology, Diabetes and Metabolism, Department of Medical Science, University of Turin, 10126 Turin, Italy.
Sheila LeoneDepartment of Pharmacy, G. d'Annunzio University of Chieti-Pescara, 66100 Chieti, Italy.
Luigi BrunettiDepartment of Pharmacy, G. d'Annunzio University of Chieti-Pescara, 66100 Chieti, Italy.
Justo P CastañoMaimonides Institute for Biomedical Research of Córdoba (IMIBIC), Department of Cell Biology, Physiology and Immunology, University of Córdoba and Reina Sofia University Hospital, 14004 Córdoba, Spain.ORCID 0000-0002-3145-7287
Raúl M LuqueMaimonides Institute for Biomedical Research of Córdoba (IMIBIC), Department of Cell Biology, Physiology and Immunology, University of Córdoba and Reina Sofia University Hospital, 14004 Córdoba, Spain.
Renzhi CaiDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Wei ShaDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.ORCID 0000-0003-4740-2325
Ezio GhigoDivision of Endocrinology, Diabetes and Metabolism, Department of Medical Science, University of Turin, 10126 Turin, Italy.
Andrew V SchallyDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Riccarda GranataDivision of Endocrinology, Diabetes and Metabolism, Department of Medical Science, University of Turin, 10126 Turin, Italy.ORCID 0000-0003-4164-7313

Funding

Italian Ministry of Instruction and Research PRIN 2017 2017S55RXB_002Italian Ministry of Instruction and Research PRIN 2017 (to RG) 2017HRTZYASpanish Ministry of Science, Innovation and Universities to ACF, JPC and RML PID2019-105564RB-I00
6 · The paper itself

Abstract

Pituitary adenomas (PAs) are intracranial tumors, often associated with excessive hormonal secretion and severe comorbidities. Some patients are resistant to medical therapies; therefore, novel treatment options are needed. Antagonists of growth hormone-releasing hormone (GHRH) exert potent anticancer effects, and early GHRH antagonists were found to inhibit GHRH-induced secretion of pituitary GH in vitro and in vivo. However, the antitumor role of GHRH antagonists in PAs is largely unknown. Here, we show that the GHRH antagonists of MIAMI class, MIA-602 and MIA-690, inhibited cell viability and growth and promoted apoptosis in GH/prolactin-secreting GH3 PA cells transfected with human GHRH receptor (GH3-GHRHR), and in adrenocorticotropic hormone ACTH-secreting AtT20 PA cells. GHRH antagonists also reduced the expression of proteins involved in tumorigenesis and cancer progression, upregulated proapoptotic molecules, and lowered GHRH receptor levels. The combination of MIA-690 with temozolomide synergistically blunted the viability of GH3-GHRHR and AtT20 cells. Moreover, MIA-690 reduced both basal and GHRH-induced secretion of GH and intracellular cAMP levels. Finally, GHRH antagonists inhibited cell viability in human primary GH- and ACTH-PA cell cultures. Overall, our results suggest that GHRH antagonists, either alone or in combination with pharmacological treatments, may be considered for further development as therapy for PAs.

Indexed as

ACTH-secreting pituitary adenomasapoptosiscell viabilityGHRHGH-secreting pituitary adenoma

Identifiers

PMID34439107
PMCPMC8393969

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Registered trials

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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.