287 results on '"Hunter, Zachary R"'
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2. BTKCys481Ser drives ibrutinib resistance via ERK1/2 and protects BTKwild-type MYD88-mutated cells by a paracrine mechanism
3. Extracellular vesicle–mediated transfer of constitutively active MyD88L265P engages MyD88wt and activates signaling
4. Acquired mutations associated with ibrutinib resistance in Waldenström macroglobulinemia
5. Transcriptome sequencing reveals a profile that corresponds to genomic variants in Waldenström macroglobulinemia
6. HCK is a survival determinant transactivated by mutated MYD88, and a direct target of ibrutinib
7. The ERK1/2 Regulator WNK2 Shows Novel Alternative Splicing Aberrations That Support Tumor Growth in MYD88 Mutated Waldenström's Macroglobulinemia
8. Identification of Robust Predictors for Ibrutinib Response By Multi-Omic Genomics in MYD88 Mutated Waldenstrom's Macroglobulinemia
9. Clinical Effectiveness and Long-Term Serologic Responses of COVID-19 Vaccination in Patients with Multiple Myeloma and Waldenström Macroglobulinemia
10. Ibrutinib and Venetoclax in Previously Untreated Waldenström Macroglobulinemia
11. Multi-Omic Analysis of 253 Untreated Patients with Waldenström's Macroglobulinemia Reveals Clinically and Genomically Distinct Disease Subtypes and a Model for Disease Progression
12. Somatic mutations in MYD88 and CXCR4 are determinants of clinical presentation and overall survival in Waldenström macroglobulinemia
13. The genomic landscape of Waldenström macroglobulinemia is characterized by highly recurring MYD88 and WHIM-like CXCR4 mutations, and small somatic deletions associated with B-cell lymphomagenesis
14. MYD88 L265P in Waldenström macroglobulinemia, immunoglobulin M monoclonal gammopathy, and other B-cell lymphoproliferative disorders using conventional and quantitative allele-specific polymerase chain reaction
15. Long-term follow-up of symptomatic patients with lymphoplasmacytic lymphoma/Waldenström macroglobulinemia treated with the anti-CD52 monoclonal antibody alemtuzumab
16. Hyperphosphorylated paratarg-7: a new molecularly defined risk factor for monoclonal gammopathy of undetermined significance of the IgM type and Waldenström macroglobulinemia
17. The HCK/BTK inhibitor KIN-8194 is active in MYD88-driven lymphomas and overcomes mutated BTKCys481 ibrutinib resistance
18. The ERK1/2 Regulator WNK2 Shows Differential Expression and Isoform Usage, Primarily Driven By Aberrant Methylation, in MYD88 Mutated Waldenström's Macroglobulinemia
19. A New Role for the SRC Family Member HCK As a Driver of BCR/SYK Signaling in MYD88 Mutated Lymphomas
20. COVID-19 Vaccine Responsiveness in Patients with Multiple Myeloma and Waldenström Macroglobulinemia
21. Pirtobrutinib (LOXO-305) Is Active and Overcomes ERK Related Pro-Survival Signaling in Ibrutinib Resistant, BTK Cys481 Mutant Expressing WM and ABC DLBCL Lymphoma Cells Driven By Activating MYD88 Mutations
22. Phase 1 study of ibrutinib and the CXCR4 antagonist ulocuplumab in CXCR4-mutated Waldenström macroglobulinemia
23. Endoplasmic reticulum stress is a target for therapy in Waldenstrom macroglobulinemia
24. Aberrant Expression of Spliced WNK2 Is an Early Event in MYD88 Mutated WM That Activates ERK1/2 and Supports Tumor Growth
25. Novel Isoforms Identified By Isoseq Analysis Drive Expression Differences in Key Genes That Delineate the Subtypes of Waldenstrom's Macroglobulinemia
26. Ibrutinib and Venetoclax in Symptomatic, Treatment-Naive Patients with Waldenström Macroglobulinemia
27. Atypical Stem Cell, Pre-B-Cell, T-Cell and Myeloid Gene Expression Characterizes Early Waldenstrom's Macroglobulinemia Clones Which Diminishes with Advancing Disease and Has Therapeutic Implications
28. Changes in Methylation and Chromatin Accessibility Underlie Subtype Classification and Disease Evolution in Waldenström's Macroglobulinemia
29. Novel Protacs Demonstrate Dual Kinase Inhibition and Degradation of HCK and BTK, and Are Highly Active in MYD88 Mutated WM and ABC DLBCL Cells
30. Early Subclones Showing Aberrant Co-Expression of Stem Cell, T Cell and Myeloid Genes Can be Detected By Flow Cytometry in MYD88 Mutated Waldenström's Macroglobulinemia Patients
31. Quantitative MYD88 L265P Analysis Represents a Powerful Tool for Assessing Disease Response and Evaluating Clinical Trial Performance in Waldenstrom's Macroglobulinemia
32. CD27-CD70 interactions in the pathogenesis of Waldenström macroglobulinemia
33. Thalidomide and rituximab in Waldenstrom macroglobulinemia
34. Genomic and Transcriptomic Characterization of IgM Multiple Myeloma Identifies a Pre-Germinal Center Plasma Cell Disorder with Immature B-Cell Transcription-Factor Signature
35. Epigenomics in Waldenström macroglobulinemia
36. CXCR4 Mutational Status Does Not Impact Outcomes in Patients with Waldenstrom Macroglobulinemia Treated with Proteasome Inhibitors
37. Mutated MYD88 Regulates HCK Pro-Survival Signaling through JunB in MYD88 Mutated B-Lymphoma Cells
38. Clinical and Genomic Factors Are Predictive of Response and Prognostic of Progression-Free Survival in Patients with Waldenström Macroglobulinemia Treated with Ibrutinib
39. High-Dimensional Heterogeneity of Waldenström Macroglobulinemia within Its Immune Tumor Microenvironment
40. A Novel HCK and BTK Dual Inhibitor Kin-8194 Shows Superior Activity over Ibrutinib and Overcomes BTKC481S Mediated Ibrutinib Resistance in Vitro and In Vivo in MYD88 Mutated B-Cell Lymphomas
41. Myeloma Heterogeneity within Its Complex Immune Ecosystem
42. Ibrutinib Dose Reduction Does Not Affect Progression-Free Survival in Patients with Waldenstrom Macroglobulinemia
43. Non-IgM Secreting Lymphoplasmacytic Lymphoma - Experience of a Reference Center for Waldenstrom Macroglobulinemia
44. Comprehensive Integration of Whole Genome, Transcriptome and Methylation Profiling Reveals Novel Gene Dysregulation Including IL15, SOCS6 and CARD11 Associated with MYD88 and CXCR4 Genotype Status in WM
45. Genomic Analysis of Ibrutinib Resistance in Waldenstrom Macroglobulinemia
46. Alternative Mutations and Isoform Dysregulation in MYD88 in Waldenstrom's Macroglobulinemia
47. Deepening of Response after Completing Rituximab-Containing Primary Therapy in Patients with Waldenstrom Macroglobulinemia
48. Multicenter Prospective Phase II Study of Venetoclax in Patients with Previously Treated Waldenstrom Macroglobulinemia
49. MYD88 Triggered SYK Activation Promotes BCR Cross-Talk, and Identifies SYK As a Novel Therapeutic Target of Mutated MYD88 Signaling
50. A Novel HCK Inhibitor Kin-8193 Blocks BTK Activity in BTKCys481 Mutated Ibrutinib Resistant B-Cell Lymphomas Driven By Mutated MYD88
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