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Loss of Mll3Catalytic FunctionPromotes AberrantMyelopoiesis Kelly M. ArcipowskiMarinka BulicSandeep Gurbuxani2016 год

Loss of Mll3 Catalytic Function Promotes Aberrant Myelopoiesis
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Аннотация: Two of the most common myeloid malignancies, myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), are associated with exceedingly low survival rates despite recent therapeutic advances. While their etiology is not completely understood, evidence suggests that certain chromosomal abnormalities contribute to MDS and AML progression. Among the most frequent chromosomal abnormalities in these disorders are alterations of chromosome 7: either complete loss of one copy of chromosome 7 (-7) or partial deletion of 7q (del(7q)), both of which increase the risk of progression from MDS to AML and are associated with chemoresistance. Notably, 7q36.1, a critical minimally deleted region in 7q, includes the gene encoding the histone methyltransferase mixed-lineage leukemia 3 (MLL3), which is also mutated in a small percentage of AML patients. However, the mechanisms by which MLL3 loss contributes to malignancy are unknown. Using an engineered mouse model expressing a catalytically inactive form of Mll3, we found a significant shift in hematopoiesis toward the granulocyte/macrophage lineage, correlating with myeloid infiltration and enlargement of secondary lymphoid organs. Therefore, we propose that MLL3 loss in patients may contribute to the progression of MDS and AML by promoting myelopoiesis.
Год издания: 2016
Авторы: Kelly M. Arcipowski, Marinka Bulic, Sandeep Gurbuxani, Jonathan D. Licht
Издательство: Public Library of Science
Источник: PLoS ONE
Ключевые слова: Acute Myeloid Leukemia Research, Epigenetics and DNA Methylation, Chronic Myeloid Leukemia Treatments
Другие ссылки: PLoS ONE (PDF)
PLoS ONE (HTML)
DOAJ (DOAJ: Directory of Open Access Journals) (HTML)
Europe PMC (PubMed Central) (PDF)
Europe PMC (PubMed Central) (HTML)
PubMed Central (HTML)
INDIGO (University of Illinois at Chicago) (PDF)
INDIGO (University of Illinois at Chicago) (HTML)
PubMed (HTML)