39 results on '"Demos, Maria G"'
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2. Ixazomib, dexamethasone, and rituximab in treatment-naive patients with Waldenström macroglobulinemia: long-term follow-up
3. Expression of the prosurvival kinase HCK requires PAX5 and mutated MYD88 signaling in MYD88-driven B-cell lymphomas
4. Human MYD88L265P is insufficient by itself to drive neoplastic transformation in mature mouse B cells
5. CXCR4S338X clonality is an important determinant of ibrutinib outcomes in patients with Waldenström macroglobulinemia
6. BTKCys481Ser drives ibrutinib resistance via ERK1/2 and protects BTKwild-type MYD88-mutated cells by a paracrine mechanism
7. SYK is activated by mutated MYD88 and drives pro-survival signaling in MYD88 driven B-cell lymphomas
8. Venetoclax in Previously Treated Waldenström Macroglobulinemia
9. The HCK/BTK inhibitor KIN-8194 is active in MYD88-driven lymphomas and overcomes mutated BTKCys481 ibrutinib resistance
10. The ERK1/2 Regulator WNK2 Shows Differential Expression and Isoform Usage, Primarily Driven By Aberrant Methylation, in MYD88 Mutated Waldenström's Macroglobulinemia
11. A New Role for the SRC Family Member HCK As a Driver of BCR/SYK Signaling in MYD88 Mutated Lymphomas
12. Phase 1 study of ibrutinib and the CXCR4 antagonist ulocuplumab in CXCR4-mutated Waldenström macroglobulinemia
13. Long-term follow-up of ibrutinib monotherapy in treatment-naive patients with Waldenstrom macroglobulinemia
14. Diagnostic Next-generation Sequencing Frequently Fails to Detect MYD88L265P in Waldenström Macroglobulinemia
15. Cell‐free DNA analysis for detection ofMYD88 L265PandCXCR4 S338Xmutations in W aldenström macroglobulinemia
16. Partial response or better at six months is prognostic of superior progression‐free survival in Waldenström macroglobulinaemia patients treated with ibrutinib
17. Comparative genomics of CXCR4MUT and CXCR4WT single cells in Waldenström’s macroglobulinemia
18. Response and Survival Outcomes to Ibrutinib Monotherapy for Patients With Waldenström Macroglobulinemia on and off Clinical Trials
19. Genomic evolution of ibrutinib‐resistant clones in Waldenström macroglobulinaemia
20. A matched case-control study comparing features, treatment and outcomes between patients with non-IgM lymphoplasmacytic lymphoma and Waldenström macroglobulinemia
21. CXCR4 mutational status does not impact outcomes in patients with W aldenström macroglobulinemia treated with proteasome inhibitors
22. Deepening of response after completing rituximab‐containing therapy in patients with Waldenstrom macroglobulinemia
23. Cell‐free DNA analysis for detection of MYD88L265P and CXCR4S338X mutations in Waldenström macroglobulinemia.
24. CXCR4 S338X clonality is an important determinant of ibrutinib outcomes in patients with Waldenström macroglobulinemia
25. CXCR4 mutation subtypes impact response and survival outcomes in patients with Waldenström macroglobulinaemia treated with ibrutinib
26. Partial response or better at six months is prognostic of superior progression‐free survival in Waldenström macroglobulinaemia patients treated with ibrutinib.
27. CXCR4 mutational status does not impact outcomes in patients with Waldenström macroglobulinemia treated with proteasome inhibitors.
28. Insights into the genomic landscape of MYD88 wild-type Waldenström macroglobulinemia
29. TP53mutations are associated with mutatedMYD88andCXCR4, and confer an adverse outcome in Waldenström macroglobulinaemia
30. Spotting the elusive Siberian tiger: Complete response to ibrutinib in a patient with Waldenström macroglobulinemia
31. Comparative genomics of CXCR4MUTand CXCR4WTsingle cells in Waldenström's macroglobulinemia
32. TP53 mutations are associated with mutated MYD88 and CXCR4, and confer an adverse outcome in Waldenström macroglobulinaemia.
33. Human MYD88L265Pis insufficient by itself to drive neoplastic transformation in mature mouse B cells
34. CXCR4S338Xclonality is an important determinant of ibrutinib outcomes in patients with Waldenström macroglobulinemia
35. BTKCys481Serdrives ibrutinib resistance via ERK1/2 and protects BTKwild-typeMYD88-mutated cells by a paracrine mechanism
36. The HCK/BTK inhibitor KIN-8194 is active in MYD88 driven lymphomas and overcomes mutated BTKCys481ibrutinib resistance.
37. BTKCys481Ser drives ibrutinib resistance via ERK1/2 and protects BTKwild-type MYD88-mutated cells by a paracrine mechanism.
38. Diagnostic Next-generation Sequencing Frequently Fails to Detect MYD88 L265P in Waldenström Macroglobulinemia.
39. Cell-free DNA analysis for detection of MYD88 L265P and CXCR4 S338X mutations in Waldenström macroglobulinemia.
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