Deletions in BCP-ALL result in a TAD more FLT3

Abstract

The molecular consequences of coding mutations can often be predicted simply from their effect on a gene’s sequence. Noncoding mutations require more work. In this issue of Blood, Yang and colleagues1 use 3D genomics to make an important contribution to the list of functional noncoding mutations in cancer. They show that microdeletions at 13q12.2 in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) eliminate the boundary of a topologically associated domain (TAD) at the FLT3 locus, which results in higher expression of FLT3, an important driver gene in acute leukemias.