Evon Wang
Program: Unspecified
Current advisor:
Undergraduate university: Tufts University
Research summary
Current literature has shown that deletion of MLL3 in healthy hematopoietic stem
cell (HSC) results in enhanced self renewal and reduced differentiation. MLL3 belongs to a large family of SET methyltransferases called COMPASS. It is known as a tumor suppressor gene on chromosome 7 that is frequently mutated in many cancer types. Established literature has shown that Mll3 is a haploinsufficient 7q tumor suppressor in acute myeloid leukemia and deletion of Mll3 in healthy HSC results in enhanced self renewal and reduced differentiation. However, little is known about how MLL3 regulates this balance in diseases, particularly in the setting of CH and MDS driven by other epigenetic regulators such as TET2. My rotation project used a transplant cohort with mice with a Cre-Lox system expressing Tet2, Mll3 or Tet2/Mll3 alleles to characterize changes in the bone marrow. We used flow cytometry to analyze hematopoiesis and assess whether the differentiation blockage in HSC is further exacerbated in the double mutant mice. We also performed CITE seq and scATAC seq on harvested bone marrow to examine mRNA expression, surface protein expressions and chromatin accessibility changes across different HSC populations to determine how MLL3 loss modifies the transcriptional and epigenetic programs in TET2 deficiency.
Graduate publications