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1 ic leukemia (CLL), mantle cell lymphoma, and Waldenstrom macroglobulinemia.
2 from patients with mantle cell lymphoma and Waldenstrom macroglobulinemia.
3 ificance, smoldering plasma cell myeloma, or Waldenstrom macroglobulinemia.
4 of MyD88, which is mutated in a fraction of Waldenstrom macroglobulinemia.
5 ght-chain amyloidosis, multiple myeloma, and Waldenstrom macroglobulinemia.
6 as splenic marginal zone B-cell lymphoma or Waldenstrom macroglobulinemia.
7 the advances observed in the pathogenesis of Waldenstrom macroglobulinemia.
8 ironment) that regulate tumor progression in Waldenstrom macroglobulinemia.
9 rapeutic targeting, such as interleukin-6 in Waldenstrom macroglobulinemia.
10 patients with heavily pretreated MM (22) or Waldenstrom macroglobulinemia (3) were administered seli
11 ymphoma overall, and a 3-fold higher risk of Waldenstrom macroglobulinemia, a low-grade lymphoma.
14 with splenic marginal zone lymphoma, 29 with Waldenstrom macroglobulinemia, and 57 with B-cell chroni
16 ell lymphoma, diffuse large B-cell lymphoma, Waldenstroms macroglobulinemia, chronic lymphocytic leuk
17 Adjusted P values for non-Hodgkin lymphoma, Waldenstrom macroglobulinemia, cryoglobulinemia, and thy
18 early universal in multiple myeloma, whereas Waldenstrom macroglobulinemia generally does not harbor
19 enetic abnormalities in multiple myeloma and Waldenstrom macroglobulinemia have implications for dise
21 d in 17 patients (relative risk [RR], 14.8), Waldenstrom macroglobulinemia in 6 (RR, 262), primary am
24 = 2.9; 1.9-4.3), lymphoplasmacytic lymphoma/Waldenstrom macroglobulinemia (LPL/WM; RR = 4.0; 1.5-11)
25 ype diffuse large B-cell lymphoma and 90% of Waldenstrom macroglobulinemia, making it conceptually at
27 Risks for non-Hodgkin lymphoma (n = 1359), Waldenstrom macroglobulinemia (n = 165), and cryoglobuli
28 ic leukemia (Richter transformation; n = 7), Waldenstrom macroglobulinemia (n = 4), and marginal zone
32 B-cell morphology revealed that plasma cell Waldenstrom macroglobulinemia samples most closely resem
34 en with systemic treatment of the underlying Waldenstrom macroglobulinemia, the visual prognosis was
35 he bone marrow biopsy specimen, diagnosis of Waldenstrom macroglobulinemia was established, and compu
36 cil to Fludarabine in Patients With Advanced Waldenstrom Macroglobulinemia) was undertaken in 101 cen
37 (IgM) class, which progresses to lymphoma or Waldenstrom macroglobulinemia, whereas IgA and IgG MGUS
38 ell lymphoproliferative disorders, including Waldenstrom macroglobulinemia (WM) and chronic lymphocyt
40 both in the understanding of the biology of Waldenstrom macroglobulinemia (WM) and in therapeutic op
41 significance (MGUS), multiple myeloma (MM), Waldenstrom macroglobulinemia (WM) and light chain AL am
42 YD88 L265P somatic mutation in patients with Waldenstrom macroglobulinemia (WM) and provide insight i
44 265P somatic mutation is highly prevalent in Waldenstrom macroglobulinemia (WM) and supports malignan
47 mbination led to synergistic cytotoxicity in Waldenstrom macroglobulinemia (WM) cells that was mediat
48 cal evaluation of investigational agents for Waldenstrom macroglobulinemia (WM) has been limited by t
49 ormation about the molecular pathogenesis of Waldenstrom macroglobulinemia (WM) has significantly adv
50 elated clones in the blood of a patient with Waldenstrom macroglobulinemia (WM) indicates the functio
68 ing thalidomide and rituximab in symptomatic Waldenstrom macroglobulinemia (WM) patients naive to eit
70 nical models, the role of these molecules in Waldenstrom macroglobulinemia (WM) remains poorly unders
72 4 years), 34 (71%) progressed to symptomatic Waldenstrom macroglobulinemia (WM) requiring treatment,
74 igh response rates and durable remissions in Waldenstrom macroglobulinemia (WM) that are impacted by
76 gnificance of IL-21 has not been examined in Waldenstrom macroglobulinemia (WM), a B-cell lymphoma ch
79 portant information on the cell of origin in Waldenstrom macroglobulinemia (WM), a longstanding puzzl
80 ed as appropriate agents in the treatment of Waldenstrom macroglobulinemia (WM), a lymphoplasmacytic
81 hemokine receptor type 4 (CXCR4) mutation in Waldenstrom macroglobulinemia (WM), a marker of tumor ag
83 resent in approximately 95% of patients with Waldenstrom macroglobulinemia (WM), as well as other B-c
84 eviously untreated symptomatic patients with Waldenstrom macroglobulinemia (WM), most of which were o
85 derstand the molecular changes that occur in Waldenstrom macroglobulinemia (WM), we employed antibody
86 r approach and its use has been validated in Waldenstrom macroglobulinemia (WM), where bortezomib has
87 ic of several B cell malignancies, including Waldenstrom macroglobulinemia (WM), where elevated IgM i
103 of patients with lymphoplasmacytic lymphoma (Waldenstrom macroglobulinemia [WM]), being either absent
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