Ashish R Kumar
Affiliation: Cincinnati Children's Hospital Medical Center
- t(4;11) leukemias display addiction to MLL-AF4 but not to AF4-MLLAshish R Kumar
Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA
Leuk Res 35:305-9. 2011..Overall, these results demonstrate that in t(4;11) leukemia, the MLL-AF4 fusion protein is critical for leukemia cell proliferation and survival while the AF4-MLL fusion product is dispensable...
- A role for MEIS1 in MLL-fusion gene leukemiaAshish R Kumar
Masonic Cancer Center, Minneapolis, MN 55455, USA
Blood 113:1756-8. 2009..Targeting MEIS1 may have therapeutic potential for treating leukemias expressing this transcription factor...
- Malignant transformation initiated by Mll-AF9: gene dosage and critical target cellsWeili Chen
University of Minnesota Cancer Center, University of Minnesota, 420 Delaware Street S E, Minneapolis, MN 55455, USA
Cancer Cell 13:432-40. 2008..Mll-AF9 upregulated expression of 192 genes in both LSK and progenitor cells, but to higher levels in LSKs than in committed myeloid progenitors...
- Hoxa9 influences the phenotype but not the incidence of Mll-AF9 fusion gene leukemiaAshish R Kumar
Department of Pediatrics, University of Minnesota, Minneapolis, USA
Blood 103:1823-8. 2004..Instead, we propose that the "Hox code" minimally defined by the Hoxa5-a9 cluster is central to MLL leukemogenesis...
- FLT3 expressing leukemias are selectively sensitive to inhibitors of the molecular chaperone heat shock protein 90 through destabilization of signal transduction-associated kinasesQing Yao
University of Minnesota Cancer Center, Minneapolis, Minnesota 55455, USA
Clin Cancer Res 9:4483-93. 2003..We conducted studies to evaluate the hypothesis that FLT3 is a client of heat shock protein (Hsp) 90 and inhibitors of Hsp90 may be useful for therapy of leukemia...