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.
Original language | English (US) |
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Pages (from-to) | 555-557 |
Number of pages | 3 |
Journal | Cancer Cell |
Volume | 25 |
Issue number | 5 |
DOIs | |
State | Published - May 12 2014 |
ASJC Scopus subject areas
- Oncology
- Cell Biology
- Cancer Research