Research projects in the laboratory rely on a variety of cellular, molecular, biochemical, and mouse genetic approaches to evaluate novel genes and singling pathways implicated in MDS and AML. Dr. Starczynowski recently identified that deletion of a microRNA (miR-146a) in MDS results in increased TRAF6 activation, and that overexpression of TRAF6 results in a mouse phenotype resembling human MDS. TRAF6 is an E3 ubiquitin ligase and signaling molecule within the innate immune signaling pathway. Although TRAF6 and innate immune pathway activation are implicated in MDS, the consequences of its activation and the mechanism(s) by which it is activated in MDS or AML are not known. Therefore, one of the main objectives of Dr. Starczynowski’s research program is to evaluate the role of the innate immune pathway in normal HSC and in MDS. Broader initiatives involve characterizing novel candidate genes (including miRNAs) relevant to MDS, dissecting molecular and cellular alterations in MDS (and related hematologic malignancies), and attempting to identify novel therapeutics.

Current projects in the lab include:

  • Examining the role of innate immune pathway effectors and miRNAs in normal hematopoiesis and myeloid malignancies.
  • Characterizing the HSC in MDS.
  • Establishing novel mouse models of MDS.
  • Identifying novel treatments for usage in MDS and related myeloid malignancies.