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1 nderstanding of the biology and treatment of B cell chronic lymphocytic leukemia.
2 with "low-grade" non-Hodgkin's lymphoma and B-cell chronic lymphocytic leukemia.
3 recurrent chromosomal abnormalities in human B-cell chronic lymphocytic leukemia.
4 n T-cell lymphoblastic leukemia/lymphoma and B-cell chronic lymphocytic leukemia.
5 ssion down-regulation in lung carcinomas and B-cell chronic lymphocytic leukemia.
6 of miR-15b/16-2 loss in the pathogenesis of B-cell chronic lymphocytic leukemia.
7 leted and/or down-regulated in patients with B cell chronic lymphocytic leukemia, a disorder characte
8 ulin VH gene that is frequently expressed in B cell chronic lymphocytic leukemia and early in B cell
9 useful in the treatment of some cancers like B-cell chronic lymphocytic leukemia and Hodgkin's diseas
11 -GC B cells and post-GC neoplasms, including B-cell chronic lymphocytic leukemia and multiple myeloma
12 with relapsed/refractory leukemias (n = 24, B-cell chronic lymphocytic leukemia and n = 11, T-cell p
13 a breakpoint junction in some cases of human B-cell chronic lymphocytic leukemia and that it is highl
14 ciated lymphoid tissue non-Hodgkin lymphoma, B-cell chronic lymphocytic leukemia, and mantle cell lym
15 actors that contribute to the development of B cell chronic lymphocytic leukemia (B-CLL) are unknown,
17 ve molecule CD200 as up-regulated on primary B cell chronic lymphocytic leukemia (B-CLL) cells and de
20 to its relatively slow clinical progression, B cell chronic lymphocytic leukemia (B-CLL) is classical
23 d by leukemic lymphocytes from patients with B cell chronic lymphocytic leukemia (B-CLL) suggest that
27 13q14 chromosome region are associated with B-cell chronic lymphocytic leukemia (B-CLL) and several
28 ntracellular cAMP levels induce apoptosis in B-cell chronic lymphocytic leukemia (B-CLL) but not in T
29 ocytic cell line (JVM-2), an EBV-transformed B-cell chronic lymphocytic leukemia (B-CLL) cell line (I
30 a novel Epstein-Barr virus-negative (EBV(-)) B-cell chronic lymphocytic leukemia (B-CLL) cell line (W
33 (UCN-01) were examined for their effects on B-cell chronic lymphocytic leukemia (B-CLL) cells in vit
34 protein complex and constitutively active in B-cell chronic lymphocytic leukemia (B-CLL) cells, resul
36 An understanding of the molecular biology of B-cell chronic lymphocytic leukemia (B-CLL) has led to t
37 However, its potential as a treatment for B-cell chronic lymphocytic leukemia (B-CLL) has not been
45 from the peripheral blood lymphocytes of one B-cell chronic lymphocytic leukemia (B-CLL) patient usin
46 ave been detected in the peripheral blood of B-cell chronic lymphocytic leukemia (B-CLL) patients, bu
47 on of bcl-2 and bax proteins in B-cells from B-cell chronic lymphocytic leukemia (B-CLL) patients.
48 G-136 in primary tumor cells derived from 34 B-cell chronic lymphocytic leukemia (B-CLL) patients.
52 tients with small lymphocytic lymphoma (SLL)/B-cell chronic lymphocytic leukemia (B-CLL) treated at S
53 of non-Hodgkin's lymphoma, its subtypes, and B-cell chronic lymphocytic leukemia (B-CLL) were evaluat
54 e t(12;14)(q23;q32) breakpoints in a case of B-cell chronic lymphocytic leukemia (B-CLL) were mapped
55 nesis and or progression of more than 40% of B-cell chronic lymphocytic leukemia (B-CLL), a common ly
56 indicator of clinical course and outcome in B-cell chronic lymphocytic leukemia (B-CLL), although th
57 was identified as a highly expressed gene in B-cell chronic lymphocytic leukemia (B-CLL), but not nor
58 n adenine nucleoside analog with efficacy in B-cell chronic lymphocytic leukemia (B-CLL), has also be
59 us deletions in chromosome region 13q14.3 in B-cell chronic lymphocytic leukemia (B-CLL), suggesting
62 d anti-CD52 antibody licensed for refractory B-cell chronic lymphocytic leukemia (B-CLL), when given
72 ripheral blood of individuals diagnosed with B-cell chronic lymphocytic leukemia (B-CLL; n = 70) or f
73 n the ATM gene have been previously found in B-cell chronic lymphocytic leukemias (B-CLLs) but their
75 ells similar to the aggressive form of human B-cell chronic lymphocytic leukemia, B220(+) CD43(+) B1-
76 LI1 directly interacted with the oncoprotein B cell chronic lymphocytic leukemia (BCL6) and induced l
77 ) diffuse large B-cell lymphoma (DLBCL), (2) B-cell chronic lymphocytic leukemia (BCLL) and (3) folli
78 equence from the minimally deleted region in B-cell chronic lymphocytic leukemia (BCLL), we have iden
79 iffuse Large B-cell Lymphoma (DLBCLL) versus B-cell Chronic Lymphocytic Leukemia (BCLL); (4) normal v
81 sively demonstrated, with over two-thirds of B-cell chronic lymphocytic leukemia characterized by the
82 wide expression profiling of miRNAs in human B cell chronic lymphocytic leukemia (CLL) by using a mic
86 surface-associated proteins overexpressed on B cell chronic lymphocytic leukemia (CLL) to use as ther
87 ells from previously untreated patients with B cell chronic lymphocytic leukemia (CLL) with those fro
92 pite having several characteristics of naive B cells, chronic lymphocytic leukemia (CLL) cells have b
94 vestigations of gene expression profiling of B-cell chronic lymphocytic leukemia (CLL) and normal B c
99 segment of chromosome 13 (13q14) in cases of B-cell chronic lymphocytic leukemia (CLL) have suggested
109 emonstrate that MVs circulating in plasma of B-cell chronic lymphocytic leukemia (CLL) patients exhib
110 noassay, we measured cellular VEGF levels in B-cell chronic lymphocytic leukemia (CLL) samples from 2
111 A subset of blood cells from patients with B-cell chronic lymphocytic leukemia (CLL) spontaneously
112 ectors for the transduction of primary human B-cell chronic lymphocytic leukemia (CLL) was explored.
113 e monoclonal antibody in single-agent use in B-cell chronic lymphocytic leukemia (CLL) with reported
115 (HD) occasionally develops in patients with B-cell chronic lymphocytic leukemia (CLL), and has been
116 AP-70 are both useful prognostic markers for B-cell chronic lymphocytic leukemia (CLL), but are varia
117 darabine, the current standard treatment for B-cell chronic lymphocytic leukemia (CLL), can induce ap
123 1H) for patients with relapsed or refractory B-cell chronic lymphocytic leukemia exposed to alkylatin
126 fter infection, and requires Ca(2+) flux and B cell chronic lymphocytic leukemia/lymphoma 2-associate
127 ndrial Ca(2+) loading, and is independent of B cell chronic lymphocytic leukemia/lymphoma translocati
128 c T lymphocyte-associated antigen 4 (CTLA4), B-cell chronic lymphocytic leukemia/lymphoma 10 (BCL10),
129 ecruitment domain family, member 11 (CARD11)-B-cell chronic lymphocytic leukemia/lymphoma 10 (BCL10)-
130 ed that XIAP deficiency selectively impaired B-cell chronic lymphocytic leukemia/lymphoma 10 (BCL10)-
132 ested compounds, including topoisomerase II, B-cell chronic lymphocytic leukemia/lymphoma 2 (BCL2), a
134 in multiple hematologic malignancies such as B cell chronic lymphocytic leukemia, multiple myeloma, a
135 oplasms which are dominated by CD5+ B cells (B cell chronic lymphocytic leukemia) or plasma cells (mu
136 pression signature was also detected in p53- B-cell chronic lymphocytic leukemia patients displaying
138 (13%) B-NHLs arising from pregerminal center B cells (chronic lymphocytic leukemia/small lymphocytic
139 ge B-cell lymphoma, follicular lymphoma, and B-cell chronic lymphocytic leukemia/small lymphocytic ly
140 ein levels were also elevated in circulating B cell chronic lymphocytic leukemia specimens (n = 49) c
141 acute lymphoblastic leukemias and aggressive B-cell chronic lymphocytic leukemias that occur in the g
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