604. Molecular Pharmacology and Drug Resistance: Myeloid Neoplasms: Poster II
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Anti-Leukemia Combinatorial Efficacy of ABBV155, a B7H3-BCL-XL Inhibitor Antibody-Drug Conjugate, in Combination with Venetoclax through BCL-XL/BIM and BCL-2/BIM Complex Dissociations
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Anti-Leukemia Combinatorial Efficacy of ABBV155, a B7H3-BCL-XL Inhibitor Antibody-Drug Conjugate, in Combination with Venetoclax through BCL-XL/BIM and BCL-2/BIM Complex Dissociations
BVX001, a Bispecific ADC Targeting CD7-Positive AML with Favorable Toxicity Profile, Exhibits Significant Efficacy in Primary Patient Samples and PDX-Models
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BVX001, a Bispecific ADC Targeting CD7-Positive AML with Favorable Toxicity Profile, Exhibits Significant Efficacy in Primary Patient Samples and PDX-Models
Combined CXCR-4 Inhibition with Novel Agent GPC-100 (burixafor) and Beta 2 Adrenergic Receptor Blockade Enhances Cytarabine Response for Acute Myeloid Leukemia Blasts on Stroma
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Combined CXCR-4 Inhibition with Novel Agent GPC-100 (burixafor) and Beta 2 Adrenergic Receptor Blockade Enhances Cytarabine Response for Acute Myeloid Leukemia Blasts on Stroma
Combined Use of Ziftomenib and Selinexor Is Effective in NPM1 Mutant Acute Myeloid Leukemia
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Combined Use of Ziftomenib and Selinexor Is Effective in NPM1 Mutant Acute Myeloid Leukemia
ERK1/2 Inhibition Mediates Bax Dependent Proteolysis of OPA1 and Induces Mitochondrial Cristae Remodeling to Overcome Resistance to Venetoclax
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ERK1/2 Inhibition Mediates Bax Dependent Proteolysis of OPA1 and Induces Mitochondrial Cristae Remodeling to Overcome Resistance to Venetoclax
Efficacy of a Novel BCL-XL Degrader, DT2216, in Preclinical Models of Post-Myeloproliferative Neoplasm Secondary AML
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Efficacy of a Novel BCL-XL Degrader, DT2216, in Preclinical Models of Post-Myeloproliferative Neoplasm Secondary AML
Elucidating Transcriptional Heterogeneity in Venetoclax Resistant AMLs
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Elucidating Transcriptional Heterogeneity in Venetoclax Resistant AMLs
HPK1 Inhibition and Venetoclax Combination Suppressed AML By Enhancing Cytotoxic T-Cell Response to Leukaemia
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HPK1 Inhibition and Venetoclax Combination Suppressed AML By Enhancing Cytotoxic T-Cell Response to Leukaemia
Integrative Analysis of Transcriptomic and Proteomic Data Identifies Patterns of Primary Resistance to Venetoclax-Azacitidine and Reveals Targetable Vulnerabilities in Acute Myeloid Leukemia (AML)
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Integrative Analysis of Transcriptomic and Proteomic Data Identifies Patterns of Primary Resistance to Venetoclax-Azacitidine and Reveals Targetable Vulnerabilities in Acute Myeloid Leukemia (AML)
M2-like Macrophages Transfer Mitochondria to Acute Myeloid Leukaemia Cells Via Tunnelling Nanotubes Promoting Therapy Resistance
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M2-like Macrophages Transfer Mitochondria to Acute Myeloid Leukaemia Cells Via Tunnelling Nanotubes Promoting Therapy Resistance
Molecular Mechanisms Associated with Autophagy Inhibition to Overcome Resistance to FLT3 Inhibitors
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Molecular Mechanisms Associated with Autophagy Inhibition to Overcome Resistance to FLT3 Inhibitors
PTPN12 Is Targetable and Context-Specific TSG in -7/del7q Myeloid Neoplasia
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PTPN12 Is Targetable and Context-Specific TSG in -7/del7q Myeloid Neoplasia
Plinabulin and Selumetinib Enhance M1 Macrophage Traits and Trigger Cell Death in AML
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Plinabulin and Selumetinib Enhance M1 Macrophage Traits and Trigger Cell Death in AML
Preclinical Activity of RAS(ON) Multi-Selective Inhibitor RMC-7977 and Therapeutic Combinations in AML with Signaling Mutations
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Preclinical Activity of RAS(ON) Multi-Selective Inhibitor RMC-7977 and Therapeutic Combinations in AML with Signaling Mutations
Preclinical Characterization of the Anti-Leukemia Activity of the CD123 Antibody-Drug Conjugate, Pivekimab Sunirine (IMGN632)
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Preclinical Characterization of the Anti-Leukemia Activity of the CD123 Antibody-Drug Conjugate, Pivekimab Sunirine (IMGN632)
Selective SMARCA2 Degradation Promotes Leukemic Differentiation and Synergizes with CDK9 Inhibition to Potently Induce Death in Pre-Clinical Models of Acute Myeloid Leukemia
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Selective SMARCA2 Degradation Promotes Leukemic Differentiation and Synergizes with CDK9 Inhibition to Potently Induce Death in Pre-Clinical Models of Acute Myeloid Leukemia
Targeting Co-Regulatory Feedback Loop of MYC and GSPT1 By MYC/GSPT1 Dual Degradation Is Synthetic Lethal in Combination with Ven/Aza in TP53 Mutant Acute Myeloid Leukemia Stem and Progenitor Cells
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Targeting Co-Regulatory Feedback Loop of MYC and GSPT1 By MYC/GSPT1 Dual Degradation Is Synthetic Lethal in Combination with Ven/Aza in TP53 Mutant Acute Myeloid Leukemia Stem and Progenitor Cells
The Mitochondrial Unfolded Protein Response (UPRmt) Is Upregulated in Acute Myeloid Leukemia (AML) and Inhibiting the UPRmt Protease, LONP1, Leads to Mitochondrial Protein Aggregation and Cell Death Selectively in AML
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The Mitochondrial Unfolded Protein Response (UPRmt) Is Upregulated in Acute Myeloid Leukemia (AML) and Inhibiting the UPRmt Protease, LONP1, Leads to Mitochondrial Protein Aggregation and Cell Death Selectively in AML
The Transcription Factor IRF8 Regulates the Sensitivity of AML Cells to LSD1 Inhibition and All-Trans Retinoic Acid
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The Transcription Factor IRF8 Regulates the Sensitivity of AML Cells to LSD1 Inhibition and All-Trans Retinoic Acid
Unraveling How Treatment Shapes Clonal Evolution and Resistance in Murine KMT2A-Rearranged Leukemia with Subclonal KrasG12D
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Unraveling How Treatment Shapes Clonal Evolution and Resistance in Murine KMT2A-Rearranged Leukemia with Subclonal KrasG12D