Combinatorial haplo-deficient tumor suppression in 7q-deficient myelodysplastic syndrome and acute myeloid leukemia.
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.
Department of Cell Biology, Albert Einstein College of Medicine/Montefiore Medical Center, New York, NY 10461, USA; Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine/Montefiore Medical Center, New York, NY 10461, USA.
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Department of Cell Biology, Albert Einstein College of Medicine/Montefiore Medical Center, New York, NY 10461, USA; Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine/Montefiore Medical Center, New York, NY 10461, USA; Division of Hematologic Malignancies, Department of Medicine (Oncology), Albert Einstein College of Medicine/Montefiore Medical Center, New York, NY 10461, USA; Albert Einstein Cancer Center, Albert Einstein College of Medicine/Montefiore Medical Center, New York, NY 10461, USA. Electronic address: ulrich.steidl@einstein.yu.edu.
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D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D011495:Histone-Lysine N-Methyltransferase / Q000235:genetics*; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000235:genetics*; D025521:Tumor Suppressor Proteins / Q000235:genetics*; D004268:DNA-Binding Proteins
D011495:Histone-Lysine N-Methyltransferase; D025521:Tumor Suppressor Proteins; C510652:Kmt2c protein, mouse; D004268:DNA-Binding Proteins