Characterization of miR-106a in inv(3)/t(3;3) AML and its exploitation as an avenue for treatment

• Applicant: Amanda Amoah, Ph.D.
• Subject Area: Hematology, Oncology ; Cell Biology
• Term: since 2023
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 515956783

In acute myeloid leukemia (AML), cyto- and molecular genetics and karyotype are one of the strongest prognostic factors for treatment outcomes. In Germany and Canada, patients with acute myeloid leukemia (AML) have an average 5 year (5y) relative survival (RS) of 22.8% and 21% respectively. Whereas patients with favorable genetics exhibit a 5y RS of 60-90%, adverse risk cytogenetics such as inv(3)/t(3;3) confer a RS of <10%. The host lab pioneered in identifying microRNAs (miRNAs) that play a role in leukemogenesis by regulating leukemic stem cell activity. Their recent data show that the miR-106-363 cluster, specifically miR-106a, is elevated in primitive AML cells and its over-expression in a murine leukemia model results in a decrease in overall survival by impacting mitochondria function. An assessment of miR-106-363 expression and cytogenetic risk stratification in public datasets, points to a strong association with poor outcomes. Interestingly, miR-106a expression was significantly elevated in inv(3)/t(3;3) AML patients in comparison to the normal karyotype, indicating that miR-106a might play a unique role in disease progression and outcomes. Here, I suggest exploring the role of miR-106a in inv(3)/t(3;3) AML patients to better understand its molecular mechanism and function in leukemogenesis. Hitherto, interventions targeted at miR106a could serve as avenues for new treatment therapies.

• DFG Programme: WBP Fellowship
• International Connection: Canada
• Host: Dr. Florian Kuchenbauer