Effect of hematopoietic-specific heterozygous loss of Dnmt3a on the molecular pathophysiology of colitis-associated colon cancer (CAC) in a mouse model

To model clonal hematopoiesis driven by DNMT3A loss-of-function, bone marrow chimerae with Dnmt3a(+/-) (experiment) or Dnmt3a(+/+) (control) were established in C57BL6/J wt mice, followed by standard CAC induction by AOM/DSS Overall design: Colon tumors were dissected, and whole tumor transcriptomes were compared by RNA-seq (polyA) between Dnmt3a(+/-)-CH (n=4) and control Dnmt3a(+/+)-transplanted (n=3) animals from two independent experiments