26 results on '"Choi, Kwangmin"'
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2. A Circulating Microbial Metabolite Drives the Clonal Expansion of Pre-Leukemic Cells
3. IRAK1 Contributes to IRAK4 Inhibitor Resistance Via Non-Canonical Signaling Mechanisms in MDS/AML
4. UBE2N Regulates Oncoprotein Networks in Myeloid Malignancies
5. Targeting CREB-Binding Protein (CREBBP) Overcomes Resistance to Azacitidine and Venetoclax Therapy in Acute Myeloid Leukemia (AML)
6. The Zymogen Form of Caspase-1 Is Required to Fine Tune Excessive Cell-Intrinsic Inflammation in Acute Myeloid Leukemia
7. Synthetic Lethal Interactions with IRAK4 Inhibition in Myeloid Malignancies
8. Defective Necroptosis Mediates Chemotherapy Resistance in AML
9. Regulation of Metabolic Homeostasis By TRAF6 Contributes to the Leukemia Progression
10. UBE2N Is a Druggable Target and an Essential Ubiquitin-Conjugating Enzyme in Myeloid Malignancies
11. Cell-Intrinsic Inflammation Drives Progression from Myelodysplastic Syndromes to Leukemia
12. Innate Immune Signaling Suppresses Acute Leukemia By Modifying MYC Oncogenic Activity
13. Overcoming Adaptive Therapy Resistance in AML By Targeting Immune Response Pathways
14. The Inherited MDS Gene DDX41 Is Required for Ribosome Biogenesis and Cell Viability
15. Genomic Landscape of Sex Disparities in Multiple Myeloma
16. Genomic Landscape of Multiple Myeloma with Elevated Lactate Dehydrogenase
17. TNF-α-Induced Bone Marrow Stromal Progenitor Alterations Enhance Leukemic Stem Cell Growth and Treatment Resistance Via Increased CXCL1-CXCR2 Signaling
18. Clinical Outcomes of Newly Diagnosed Multiple Myeloma Patients with Elevated Lactate Dehydrogenase Who Underwent Autologous Hematopoietic Stem Cell Transplantation
19. Therapeutic Targeting of the Ubiquitin Conjugating Enzyme UBE2N in Myeloid Malignancies
20. Splicesome Mutant MDS and AML Cells Activate Innate Immune Signaling By Regulating the Expression of Therapeutically Targetable IRAK4 Isoforms
21. Alternative Splice Variants of IRAK4 That Activate Innate Immune Signaling Are Associated with U2AF1 Mutations in Myelodysplastic Syndrome and Acute Myeloid Leukemia
22. Molecular Analysis and In Vivo Efficacy Studies on a Novel Chemical-Series of FLT3 Inhibitors in Human FLT3-ITD AML
23. HIF-1a Pathway, As a Signal Funnel for Genetic, Epigenetic, and Metabolic Aberrations, Is Sufficient and Essential for MDS Development
24. The Mechanism of Therapy Resistance By Lineage Plasticity in AML and How to Overcome It
25. TNF-a-Induced Bone Marrow Stromal Progenitor Alterations Enhance Leukemic Stem Cell Growth and Treatment Resistance Via Increased CXCL1-CXCR2 Signaling
26. Tifab Deficiency Protects Against Stress-Induced Bone Marrow Failure at the Expense of Pre-Leukemic Selection
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