320 results on '"Famulare, Christopher"'
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52. Despite High Rates of Remission, Treatment of IDH-Mutant AML with Hypomethylating Agents and Venetoclax Is Associated with Frequent Treatment Delays, Modifications, and Transfusions
53. TP53 Y220C Mutations in Patients with Myeloid Malignancies
54. MPN Transformation Is Characterized By Heterogeneous Shifts in Lineage Character
55. LKB1/STK11 Is a Tumor Suppressor in the Progression of Myeloproliferative Neoplasms
56. Immunophenotypic Lineage Assessment By Multiparameter Flow Cytometry Provides More Precise MDS Prognosis
57. Clinical Outcomes of Acute Myeloid Leukemia Patients Bridged to Allogeneic Stem Cell Transplant By Venetoclax Combination Therapy
58. Venetoclax Therapy for Relapsed and Treatment Refractory AML: Clinical Outcomes and Molecular Predictors
59. Loss of LKB1/STK11 Facilitates Leukemic Progression of the Myeloproliferative Neoplasms
60. Leukemia Cell of Origin Influences Apoptotic Priming and Sensitivity to LSD1 Inhibition
61. Plasmacytoid dendritic cell expansion defines a distinct subset of RUNX1 mutated acute myeloid leukemia
62. Multicenter evaluation of efficacy and toxicity of venetoclax‐based combinations in patients with accelerated and blast phase myeloproliferative neoplasms.
63. Single cell mutational profiling delineates clonal trajectories in myeloid malignancies
64. Combined Venetoclax and Hypomethylating Agent (HMA) Therapy Induces High Response Rates in Patients with Myelodysplastic Syndrome Including Patients Previously Failing HMA
65. Overcoming Adaptive Therapy Resistance in AML By Targeting Immune Response Pathways
66. RAS Mutations Are Independently Associated with Decreased Overall Survival and Event-Free Survival in Patients with AML Receiving Induction Chemotherapy
67. Acute Leukemia with Lineage Infidelity: Mixed Phenotype AML Exhibits a Distinct Immunophenotype with Clinical Features Overlapping Mixed Phenotype Acute Leukemia
68. Single Cell DNA Sequencing Identifies Combinatorial Mutation Patterns and Clonal Architecture in Myeloid Malignancies
69. Landscape of TP53 Mutations in MPN
70. The Genetic Architecture of Myeloproliferative Neoplasms-Blast Phase (MPN-BP) Stem Cells
71. Leukemia Cell of Origin Influences p53 Activity and Therapeutic Sensitivity Via an Evi1-Dependent Mechanism
72. Stability and uniqueness of clonal immunoglobulin CDR3 sequences for MRD tracking in multiple myeloma
73. Prognostic impact of RAS-pathway mutations in patients with myelofibrosis
74. Overcoming adaptive therapy resistance in AML by targeting immune response pathways
75. Aurora Kinase A Inhibition Provides Clinical Benefit, Normalizes Megakaryocytes, and Reduces Bone Marrow Fibrosis in Patients with Myelofibrosis: A Phase I Trial
76. Safety and Efficacy of CPX-351 in Younger Patients < 60 Years Old with Secondary Acute Myeloid Leukemia: An Updated Analysis
77. Loss of plasmacytoid dendritic cell differentiation is highly predictive for post-induction measurable residual disease and inferior outcomes in acute myeloid leukemia
78. Isoform Switching as a Mechanism of Acquired Resistance to Mutant Isocitrate Dehydrogenase Inhibition
79. Acute Myeloid Leukemia with Plasmacytoid Dendritic Cell Differentiation: Predominantly Secondary AML, Enriched for RUNX1 Mutations, Frequent Cross-Lineage Antigen Expression and Poor Prognosis
80. Myeloproliferative Neoplasm (MPN) Blastic Transformation Occurs at the Level of Hematopoietic Stem Cells
81. Small-Molecule Targeting of Musashi RNA-Binding Activity in Acute Myeloid Leukemia
82. TP53 Mutations Predict Poorer Responses to CPX-351 in Acute Myeloid Leukemia
83. Molecular Predictors and Current Management of Minimal Residual Disease (MRD) Following Induction Chemotherapy for Acute Myeloid Leukemia (AML)
84. Prognostic Impact of Activating Mutations of the NRAS/KRAS Genes in Patients with Primary and Post-Essential Thrombocythemia (ET)/Polycythemia Vera (PV) Myelofibrosis (MF)
85. A Novel Prognostic Model Including Cytogenetic and Molecular Data in Patients with Primary and Post-Essential Thrombocythemia (ET)/Polycythemia Vera (PV) Myelofibrosis (MF)
86. Alisertib (MLN8237), an Oral Selective Inhibitor of Aurora Kinase a, Has Clinical Activity and Restores GATA1 Expression in Patients with Myelofibrosis
87. Genomic Landscape Impacts Induction Outcome with CPX-351 in Patients with Acute Myeloid Leukemia
88. AML with Mutations in IDH1 and DNMT3A Exhibits a Distinct Epigenetic Signature with Poorer Overall Survival
89. Loss of Plasmacytoid Dendritic Cell Differentiation Is Highly Predictive for Persistent Measurable Residual Disease and Poor Outcomes in Acute Myeloid Leukemia
90. PHF6 Mutations Are Mutually Exclusive to TP53 Mutations, and Define a Distinct Subgroup of Secondary Acute Myeloid Leukemia Associated with a Primitive Stem/Progenitor Immunophenotype, Absent Complex Karyotype and Relatively Better Outcomes
91. Comparison of Induction Strategies and Responses for Acute Myeloid Leukemia Patients after Resistance to Hypomethylating Agents for Antecedent Myeloid Malignancy
92. Isoform switching as a mechanism of acquired resistance to isocitrate dehydrogenase inhibition
93. Small-molecule targeting of MUSASHI RNA-binding activity in acute myeloid leukemia
94. m6a Regulates Differentiation State and mRNA Translation in Myeloid Leukemia
95. Functional screen of MSI2 interactors identifies an essential role for SYNCRIP in myeloid leukemia stem cells
96. MSI2 is required for maintaining activated myelodysplastic syndrome stem cells
97. Molecular Profiling in Extramedullary Acute Myeloid Leukemia Reveals Distinct Subgroups Defined By Mutations in KIT and RUNX1
98. Clinical and Pathological Features of B-Cell Acute Lymphoblastic Leukemia Following Maintenance Treatment with Lenalidomide for Multiple Myeloma
99. SETBP1 and NRAS Mutations Are Frequent Events in Post-Myeloproliferative Neoplasm Acute Myeloid Leukemia (post-MPN AML) Lacking JAK-STAT Activating Mutations
100. PHF6and DNMT3Amutations are enriched in distinct subgroups of mixed phenotype acute leukemia with T-lineage differentiation
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