Current and Future Molecular Targets for Acute Myeloid Leukemia Therapy

  • Shaheedul A. Sami
  • Noureldien H. E. Darwish
  • Amanda N. M. Barile
  • Shaker A. MousaEmail author
Leukemia (PH Wiernik, Section Editor)
Part of the following topical collections:
  1. Topical Collection on Leukemia

Opinion statement

Acute myeloid leukemia (AML) disease prognosis is poor and there is a high risk of chemo-resistant relapse for both young and old patients. Thus, there is a demand for alternative and target-specific drugs to improve the 5-year survival rate. Current treatment mainstays include chemotherapy, or mutation-specific targeting molecules including FLT3 inhibitors, IDH inhibitors, and monoclonal antibodies. Efforts to devise new, targeted therapy have included recent advances in methods for high-throughput genomic screening and the availability of computer-assisted techniques for the design of novel agents predicted to specifically inhibit mutant molecules involved in leukemogenesis. Crosstalk between the leukemia cells and the bone marrow microenvironment through cell surface molecules, such as the integrins αvβ3 and αvβ5, might influence drug response and AML progression. This review article focuses on current AML treatment options, new AML targeted therapies, the role of integrins in AML progression, and a potential therapeutic agent—integrin αvβ3 antagonist.


B-cell lymphoma gene 2 FMS-like tyrosine kinase 3 Isocitrate dehydrogenase Nano-diamino-tetrac l-Thyroxine tetraiodothyroacetic acid 



Acute myeloid leukemia


B-cell lymphoma gene 2


Chick egg chorioallantoic membrane


Cyclin-dependent kinase


C-kit is a type of receptor tyrosine kinase, also called CD117


Proto-oncogene that codes for the MCSF (CSF1) receptor


Epidermal growth factor


EGF receptor


Epithelial–mesenchymal transition


Focal adhesion kinase


Basic fibroblast growth factor


FMS-like tyrosine kinase 3


Isocitrate dehydrogenase


Janus kinase-2


Lysine-specific demethylase


Mitogen-activated protein kinase


Mouse double minute chromosome 2






Nuclear factor kappa-light-chain-enhancer of activated B cells




Polyethylene glycol (PEG) covalently bonded with two bi-tri-azole tetraiodothyroacetic acid molecules


Programmed cell death protein 1


Programmed death-ligand 1


Platelet-derived growth factor


Polyethylene glycol


Phosphatidylinositol 3-kinase


Signal transducer and activator of transcription


Tetraiodothyroacetic acid


Transforming growth factor β


Tyrosine kinase





There is no funding to report.

Compliance with Ethical Standards

Conflict of Interest

Shaheedul A. Sami declares that he has no conflict of interest.

Noureldien H. E. Darwish declares that he has no conflict of interest.

Amanda N. M. Barile declares that she has no conflict of interest.

Shaker A. Mousa was issued a patent that is owned by NanoPharmaceuticals LLC, and he owns stock in NanoPharmaceuticals LLC, which is developing anticancer drugs.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

References and Recommended Reading

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2020

Authors and Affiliations

  1. 1.Pharmaceutical Research InstituteAlbany College of Pharmacy and Health SciencesRensselaerUSA
  2. 2.Hematology Unit, Clinical Pathology Department, Mansoura Faculty of MedicineMansoura UniversityMansouraEgypt

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