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Opinion Statement: Cytogenetics and mutation identification in acute myeloid leukemia have allowed for more targeted therapy. Many therapies have been approved by the FDA in the last 3 years including gilteritinib and azacitidine but the overall survival has remained stagnant at 25%. The inability to achieve complete remission was related to the residual leukemic stem cells (LSCs). Thus, the relationship between bone marrow niche and LSCs must be further explored to prevent treatment relapse/resistance. The development of immunotherapy and nanotechnology may play a role in future therapy to achieve the complete remission. Nano-encapsulation of drugs can improve drugs' bioavailability, help drugs evade resistance, and provide combination therapy directly to the cancer cells. Studies indicate targeting surface antigens such as CLL1 and CD123 using chimeric antibody receptor T cells can improve survival outcomes. Finally, new discoveries indicate that inhibiting integrin αvβ3 and acid ceramidase may prove to be efficacious.

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.