Abstract
Heterozygous deletions of chromosome 7 are frequent in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). In this issue of Cancer Cell, Chen and colleagues identify MLL3 as a novel haplo-insufficient tumor suppressor on 7q that, in combination with NF1 suppression and TP53 deficiency, mediates MDS and AML phenotypes in mouse and human systems.
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