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1 th treatment-naive, or relapse or refractory Waldenstrom macroglobulinemia.
2 a, 2 had classic Hodgkin lymphoma, and 2 had Waldenstrom macroglobulinemia.
3 ght-chain amyloidosis, multiple myeloma, and Waldenstrom macroglobulinemia.
4 ic leukemia (CLL), mantle cell lymphoma, and Waldenstrom macroglobulinemia.
5 from patients with mantle cell lymphoma and Waldenstrom macroglobulinemia.
6 ificance, smoldering plasma cell myeloma, or Waldenstrom macroglobulinemia.
7 of MyD88, which is mutated in a fraction of Waldenstrom macroglobulinemia.
8 and safety of acalabrutinib in patients with Waldenstrom macroglobulinemia.
9 as splenic marginal zone B-cell lymphoma or Waldenstrom macroglobulinemia.
10 the advances observed in the pathogenesis of Waldenstrom macroglobulinemia.
11 ironment) that regulate tumor progression in Waldenstrom macroglobulinemia.
12 rapeutic targeting, such as interleukin-6 in Waldenstrom macroglobulinemia.
13 patients with heavily pretreated MM (22) or Waldenstrom macroglobulinemia (3) were administered seli
14 ymphoma overall, and a 3-fold higher risk of Waldenstrom macroglobulinemia, a low-grade lymphoma.
17 with splenic marginal zone lymphoma, 29 with Waldenstrom macroglobulinemia, and 57 with B-cell chroni
19 ell lymphoma, diffuse large B-cell lymphoma, Waldenstroms macroglobulinemia, chronic lymphocytic leuk
20 Adjusted P values for non-Hodgkin lymphoma, Waldenstrom macroglobulinemia, cryoglobulinemia, and thy
21 early universal in multiple myeloma, whereas Waldenstrom macroglobulinemia generally does not harbor
22 enetic abnormalities in multiple myeloma and Waldenstrom macroglobulinemia have implications for dise
24 cally the standard of care for patients with Waldenstrom macroglobulinemia; however, infectious and h
26 d in 17 patients (relative risk [RR], 14.8), Waldenstrom macroglobulinemia in 6 (RR, 262), primary am
30 ording to the 6th International Workshop for Waldenstrom Macroglobulinemia (IWWM) and the modified 3r
31 = 2.9; 1.9-4.3), lymphoplasmacytic lymphoma/Waldenstrom macroglobulinemia (LPL/WM; RR = 4.0; 1.5-11)
32 ype diffuse large B-cell lymphoma and 90% of Waldenstrom macroglobulinemia, making it conceptually at
33 ies, including chronic lymphocytic leukemia, Waldenstrom macroglobulinemia, mantle cell lymphoma, and
35 Risks for non-Hodgkin lymphoma (n = 1359), Waldenstrom macroglobulinemia (n = 165), and cryoglobuli
36 ic leukemia (Richter transformation; n = 7), Waldenstrom macroglobulinemia (n = 4), and marginal zone
41 B-cell morphology revealed that plasma cell Waldenstrom macroglobulinemia samples most closely resem
43 r refractory (at least one previous therapy) Waldenstrom macroglobulinemia that required treatment, a
44 en with systemic treatment of the underlying Waldenstrom macroglobulinemia, the visual prognosis was
45 tients with iNHL (follicular, marginal zone, Waldenstrom macroglobulinemia) treated with chemotherapy
46 he bone marrow biopsy specimen, diagnosis of Waldenstrom macroglobulinemia was established, and compu
47 cil to Fludarabine in Patients With Advanced Waldenstrom Macroglobulinemia) was undertaken in 101 cen
48 tions, and myelokathexis (WHIM) syndrome and Waldenstrom macroglobulinemia, we demonstrated that muta
49 (IgM) class, which progresses to lymphoma or Waldenstrom macroglobulinemia, whereas IgA and IgG MGUS
51 ell lymphoproliferative disorders, including Waldenstrom macroglobulinemia (WM) and chronic lymphocyt
53 both in the understanding of the biology of Waldenstrom macroglobulinemia (WM) and in therapeutic op
54 significance (MGUS), multiple myeloma (MM), Waldenstrom macroglobulinemia (WM) and light chain AL am
55 YD88 L265P somatic mutation in patients with Waldenstrom macroglobulinemia (WM) and provide insight i
57 265P somatic mutation is highly prevalent in Waldenstrom macroglobulinemia (WM) and supports malignan
60 mbination led to synergistic cytotoxicity in Waldenstrom macroglobulinemia (WM) cells that was mediat
61 cal evaluation of investigational agents for Waldenstrom macroglobulinemia (WM) has been limited by t
62 rom other IgM-producing gammopathies such as Waldenstrom macroglobulinemia (WM) has not been well cha
63 ormation about the molecular pathogenesis of Waldenstrom macroglobulinemia (WM) has significantly adv
65 elated clones in the blood of a patient with Waldenstrom macroglobulinemia (WM) indicates the functio
86 tiomic analysis on a series of MYD88-mutated Waldenstrom macroglobulinemia (WM) patients and identifi
87 ing thalidomide and rituximab in symptomatic Waldenstrom macroglobulinemia (WM) patients naive to eit
89 nical models, the role of these molecules in Waldenstrom macroglobulinemia (WM) remains poorly unders
91 4 years), 34 (71%) progressed to symptomatic Waldenstrom macroglobulinemia (WM) requiring treatment,
93 igh response rates and durable remissions in Waldenstrom macroglobulinemia (WM) that are impacted by
95 large B-cell lymphoma (ABC DLBCL) and BCWM.1 Waldenstrom macroglobulinemia (WM) xenografted mice with
96 gnificance of IL-21 has not been examined in Waldenstrom macroglobulinemia (WM), a B-cell lymphoma ch
99 portant information on the cell of origin in Waldenstrom macroglobulinemia (WM), a longstanding puzzl
100 ed as appropriate agents in the treatment of Waldenstrom macroglobulinemia (WM), a lymphoplasmacytic
101 hemokine receptor type 4 (CXCR4) mutation in Waldenstrom macroglobulinemia (WM), a marker of tumor ag
103 resent in approximately 95% of patients with Waldenstrom macroglobulinemia (WM), as well as other B-c
104 phoma (MZL), Mantle Cell Lymphoma (MCL), and Waldenstrom macroglobulinemia (WM), between 01-Jan-2008
105 has revealed recurring somatic mutations in Waldenstrom macroglobulinemia (WM), including MYD88 (95%
106 eviously untreated symptomatic patients with Waldenstrom macroglobulinemia (WM), most of which were o
107 derstand the molecular changes that occur in Waldenstrom macroglobulinemia (WM), we employed antibody
108 r approach and its use has been validated in Waldenstrom macroglobulinemia (WM), where bortezomib has
109 ic of several B cell malignancies, including Waldenstrom macroglobulinemia (WM), where elevated IgM i
133 ned significance (IgM-MGUS) and asymptomatic Waldenstrom macroglobulinemia (WM; aWM) are precursor co
134 of patients with lymphoplasmacytic lymphoma (Waldenstrom macroglobulinemia [WM]), being either absent
135 xome sequencing data in 34 subjects (23 with Waldenstrom macroglobulinemia [WM], 6 with IgM monoclona