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2. LEF-1 drives aberrant β-catenin nuclear localization in myeloid leukemia cells

8. Supplemental Methods, Fig S1, Fig S2, Fig S3, Fig S4, Fig S5, Fig S6, Fig S7, Fig S8, Fig S9, Fig S10, Fig S11, Fig S12. from Reactive Oxygen Species Drive Proliferation in Acute Myeloid Leukemia via the Glycolytic Regulator PFKFB3

10. Nuclear factor I-C overexpression promotes monocytic development and cell survival in acute myeloid leukemia

12. Protein Kinase C Epsilon Overexpression Is Associated With Poor Patient Outcomes in AML and Promotes Daunorubicin Resistance Through p-Glycoprotein-Mediated Drug Efflux

14. Crosstalk between β-catenin and WT1 signaling activity in acute myeloid leukemia

28. Integrated nuclear proteomics and transcriptomics identifies S100A4 as a therapeutic target in acute myeloid leukemia

31. Use of an anti‐CD200‐blocking antibody improves immune responses to AML in vitro and in vivo.

34. A sub-population of primary AML blasts shows resistance to oxidative stress and reduced p38MAPK activation

35. Cord blood-derived quiescent CD34+ cells are more transcriptionally matched to AML blasts than cytokine-induced normal human hematopoietic CD34+ cells

36. Targeting the Ataxia Telangiectasia Mutated-null Phenotype in Chronic Lymphocytic Leukemia with Pro-oxidants

40. A Subpopulation of Blasts with Attenuated p38MAPK Response Is Seen in Virtually All AML Patients and AML Cell Lines and Is Defined By Cells with Augmented Lipid-Associated Anti-Oxidant Defense

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