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Hormone-Driven Growth Signaling as a Therapeutic Target in Acute Myeloid Leukemia: Implications for Drug-Resistant

Joel Costoya1, Joaquin J Jimenez1,2

  • 1Department of Biochemistry and Molecular Biology, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.

Journal of Personalized Medicine
|June 25, 2026
PubMed

Insights

Growth hormone-releasing hormone (GHRH) antagonists show promise in treating acute myeloid leukemia (AML). MIA-602, a GHRH antagonist, reduced leukemia growth, suggesting potential against drug-resistant AML.

Area of Science:

  • Oncology
  • Molecular Biology
  • Hematology

Background:

  • Growth hormone-releasing hormone (GHRH) antagonists exhibit anti-neoplastic effects in various cancers.
  • GHRH receptors are present in experimental acute myeloid leukemia (AML) models, including drug-resistant ones.
  • Therapeutic resistance is a significant challenge in AML, despite advances in targeted therapies.

Purpose of the Study:

  • To investigate the efficacy of GHRH antagonism in acute myeloid leukemia (AML).
  • To explore the potential of GHRH receptor (GHRH-R) antagonism as a therapeutic strategy for AML, particularly in the context of drug resistance.

Main Methods:

  • In vitro and in vivo studies using xenografted tumors in nude mice.
  • Treatment with MIA-602, a GHRH antagonist, was assessed for its effect on leukemic growth.
  • Exploration of GHRH-R expression in AML models, including drug-resistant sublines.

Main Results:

  • MIA-602 demonstrated significant time- and dose-dependent reduction in leukemic cell growth both in vitro and in vivo.
  • GHRH receptor (GHRH-R) expression was observed in experimental AML models.
  • The study highlights the potential for GHRH-R antagonism to impact signaling pathways involved in therapeutic resistance in AML.

Conclusions:

  • GHRH antagonism, exemplified by MIA-602, shows therapeutic potential against acute myeloid leukemia (AML).
  • Further research is warranted to understand the mechanisms underlying GHRH antagonism's effects in AML and its potential to overcome therapeutic resistance.
  • Investigating GHRH-R expression and antagonism in relation to specific AML genetic profiles, such as FLT3 status, is crucial.
Keywords:
AMLFLT3GHRH antagonismMIA-602drug-resistance

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