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1 a novel therapeutic target for GC-resistant lymphoid malignancy.
2 l lymphocytic infiltration, enteropathy, and lymphoid malignancy.
3 s associated with a 5-fold increased risk of lymphoid malignancy.
4 enic mice, all of which developed aggressive lymphoid malignancy.
5 major role in the molecular pathogenesis of lymphoid malignancy.
6 eage cells contributes to the development of lymphoid malignancy.
7 ecular milieu which initiates and sustains a lymphoid malignancy.
8 nes potentially relevant to the induction of lymphoid malignancy.
9 athogenesis and treatment of this aggressive lymphoid malignancy.
10 e when analysis was applied to patients with lymphoid malignancy.
11 een, and liver with features of a high-grade lymphoid malignancy.
12 ombocytopenia, eczema, and a tendency toward lymphoid malignancy.
13 , immune deficiency, and a proclivity toward lymphoid malignancy.
14 se deregulation of specific genes leading to lymphoid malignancy.
15 genes have been observed in several forms of lymphoid malignancy.
16 ements and risk (at the population level) of lymphoid malignancy.
17 levated IL-10 expression and the presence of lymphoid malignancy.
18 ource of new treatments for autoimmunity and lymphoid malignancy.
19 upports that it has a key role in preventing lymphoid malignancy.
20 emergence of dominant B-cell clones and even lymphoid malignancy.
21 addition, are hypothesized to predispose to lymphoid malignancy.
22 in inhibitors showed preferential benefit in lymphoid malignancies.
23 effective treatment option for patients with lymphoid malignancies.
24 r genes and oncogenes are a hallmark of many lymphoid malignancies.
25 K6 as a specific therapeutic target in human lymphoid malignancies.
26 oexpressed with LMP2A in many EBV-associated lymphoid malignancies.
27 hich occur recurrently in a variety of human lymphoid malignancies.
28 peutic targets in a subset of EBV-associated lymphoid malignancies.
29 and oncogenes are frequently associated with lymphoid malignancies.
30 own-regulated in certain myeloid and early B-lymphoid malignancies.
31 factor, has been implicated in several human lymphoid malignancies.
32 is also unclear how the mutation may lead to lymphoid malignancies.
33 or hemizygous have an increased incidence of lymphoid malignancies.
34 aB pathway, which is frequently activated in lymphoid malignancies.
35 kappaB2 gene is recurrently mutated in human lymphoid malignancies.
36 ransplant outcomes were observed in pts with lymphoid malignancies.
37 apoptotic pathway in previously untreatable lymphoid malignancies.
38 an antiapoptotic protein also implicated in lymphoid malignancies.
39 ions, lymphoproliferative disorders, and non-lymphoid malignancies.
40 and chronic myeloid malignancies but not in lymphoid malignancies.
41 d signal transduction and the development of lymphoid malignancies.
42 therapeutic effects in solid tumors than in lymphoid malignancies.
43 s makes them effective therapeutics for many lymphoid malignancies.
44 can lead to lymphoproliferative disorders or lymphoid malignancies.
45 umor for the immunotherapy of both solid and lymphoid malignancies.
46 to genome instability and the development of lymphoid malignancies.
47 umab in patients with relapsed or refractory lymphoid malignancies.
48 MH, CMC-544, targeted to CD22 expressed by B-lymphoid malignancies.
49 nical evaluation as a treatment option for B-lymphoid malignancies.
50 combination with ionizing radiation to treat lymphoid malignancies.
51 acute lymphoblastic leukemia (ALL) and other lymphoid malignancies.
52 ing mutations in a wide range of myeloid and lymphoid malignancies.
53 perties that may be of use in the therapy of lymphoid malignancies.
54 xpressed on activated T and B cells and some lymphoid malignancies.
55 odeficiency, and increased susceptibility to lymphoid malignancies.
56 gnaling are an important advance in managing lymphoid malignancies.
57 There is relatively little data on indolent lymphoid malignancies.
58 ated low-grade and select intermediate-grade lymphoid malignancies.
59 vide evidence of altered TRAF1 expression in lymphoid malignancies.
60 eceptor loci and increased susceptibility to lymphoid malignancies.
61 ia (A-T) have an increased susceptibility to lymphoid malignancies.
62 ts affecting BCL7B or BCL7C were detected in lymphoid malignancies.
63 e the future design of immunotherapy against lymphoid malignancies.
64 a cell abnormalities, as well as myeloid and lymphoid malignancies.
65 a cell lines, suggesting an association with lymphoid malignancies.
66 gimen to produce engraftment and GVL against lymphoid malignancies.
67 of ubiquitination in the genesis of diverse lymphoid malignancies.
68 eful as an agent in the treatment of chronic lymphoid malignancies.
69 e in BCL-6-deficient mice and participate in lymphoid malignancies.
70 nt to inflammatory tissues and metastasis of lymphoid malignancies.
71 erexpression of Mer has been associated with lymphoid malignancies.
72 y of patients who underwent HDT and ABMT for lymphoid malignancies.
73 e NR4A1 and NR4A3 expression and function in lymphoid malignancies.
74 s complete tumor regression in patients with lymphoid malignancies.
75 l conditions, such as agammaglobulinemia and lymphoid malignancies.
76 sis plays a role in normal lymphopoiesis and lymphoid malignancies.
77 munity, but also a risk for autoimmunity and lymphoid malignancies.
78 encouraging clinical activity in a range of lymphoid malignancies.
79 uently is overexpressed in several solid and lymphoid malignancies.
80 nvolving antigen receptor loci are common in lymphoid malignancies.
81 ous neoplasms and represent about 12% of all lymphoid malignancies.
82 nes and clinical samples representing divers lymphoid malignancies.
83 hese compounds can be optimized for treating lymphoid malignancies.
84 proliferative and antiapoptotic signaling in lymphoid malignancies.
85 to RIC-alloHSCT in patients with aggressive lymphoid malignancies.
86 sents a potential new treatment strategy for lymphoid malignancies.
87 ral of which are already showing activity in lymphoid malignancies.
88 howing considerable promise, particularly in lymphoid malignancies.
89 he onset of T cell development and developed lymphoid malignancies.
90 ave been implicated in the genesis of select lymphoid malignancies.
91 virus (EBV) is associated with a variety of lymphoid malignancies.
92 y as a potential therapeutic target in human lymphoid malignancies.
93 cations of microRNA (miRNA) dysregulation in lymphoid malignancies.
94 tamin D also was not associated with risk of lymphoid malignancies.
95 e commonly used in the treatment of indolent lymphoid malignancies.
96 ribine's potency across the full spectrum of lymphoid malignancies.
97 of the lung, breast, colon, and a subset of lymphoid malignancies.
98 le progression and is overexpressed in human lymphoid malignancies.
99 icient mice and humans to the development of lymphoid malignancies.
100 is constitutively phosphorylated in several lymphoid malignancies.
101 in B-ALL with these rearrangements or other lymphoid malignancies.
102 derstanding of immunodeficiency diseases and lymphoid malignancies.
103 the study of alpha4beta1 expression in human lymphoid malignancies.
104 and holds promise for imaging and therapy in lymphoid malignancies, 6 LLP2A derivatives, as LLP2A-1,4
105 r lymphocyte infusion (DLI) in patients with lymphoid malignancy after failure of autologous SCT.
106 was observed in all of the malignancies, but lymphoid malignancies also exhibited hypermethylation, p
107 Some cell lines derived from adult-type lymphoid malignancies also show sensitivity to this trea
108 nt place in the treatment of certain, mainly lymphoid, malignancies, although tumors of nonhemopoieti
109 istance, and poor prognosis in patients with lymphoid malignancies and can occur in approximately 50%
110 both exhibit major activity against indolent lymphoid malignancies and have different mechanisms of a
112 anley to standardize response assessments in lymphoid malignancies and how this was adapted in the Wo
114 raft-versus-malignancy effect in myeloid and lymphoid malignancies and in metastatic renal cell cance
116 ovel epigenetic event in the pathogenesis of lymphoid malignancies and may contribute to a more aggre
118 iscuss the emerging body of clinical data in lymphoid malignancies and present future directions for
119 for the different effects of UV radiation on lymphoid malignancies and, in addition, that p53 is not
120 nslocations that underlie the development of lymphoid malignancies, and our findings highlight regula
125 g rexinoids with IL-2R-targeted therapies in lymphoid malignancies as well as possibly in autoimmune
126 at potential for improving the monitoring of lymphoid malignancies, assessing immune reconstitution a
128 ndard chemotherapy regimen for patients with lymphoid malignancies being considered for reduced-inten
129 s well established for the follow-up of many lymphoid malignancies but not for chronic lymphocytic le
130 w insight into the survival roles of mTOR in lymphoid malignancies, but also identify alterations tha
131 lterations of INK4A are commonly observed in lymphoid malignancies, but are consistently absent in pr
132 gehog (HH) signaling is activated in various lymphoid malignancies, but conflicting results exist abo
133 antation (HCT) can be curative treatment for lymphoid malignancies, but it has been characterized by
134 ne copy of the wild-type allele also develop lymphoid malignancies, but with a much lower frequency a
135 the genesis of chromosomal translocations in lymphoid malignancy, but also in translocations found in
136 radiation might influence the development of lymphoid malignancies by means of its immunosuppressive
137 ackground, the RAG-2(T490A) mutation induced lymphoid malignancies characterized by clonal chromosoma
139 ed agents for the treatment of patients with lymphoid malignancies comes the promise of safe and effe
142 n our understanding of the role of miRNAs in lymphoid malignancies demonstrate that miRNAs can effect
143 egy for targeting multiple myeloma and other lymphoid malignancies dependent on the IRF4 network.
145 oclax, has shown a high therapeutic index in lymphoid malignancies; developing a predictive marker fo
146 mutations in normal GC B-lymphocytes and in lymphoid malignancies displaying GC/post-GC phenotype.
147 less extensive than that on other myeloid or lymphoid malignancies due to low mitotic activity of pla
148 prehensively define the genetic basis of all lymphoid malignancies, examine the relative roles of ger
149 process is not always benign, since certain lymphoid malignancies exhibit recurrent chromosomal abno
152 d Hodgkin's lymphomas and that patients with lymphoid malignancies frequently had anti-HIP1 antibodie
154 , whereas patients with advanced myeloid and lymphoid malignancies had high relapse rates after nonmy
155 contrast, patients with advanced myeloid and lymphoid malignancies had rates of more than 0.52 (high
156 Our understanding of the pathogenesis of lymphoid malignancies has been transformed by next-gener
161 inhibitors may be an effective treatment for lymphoid malignancies in humans that are associated with
163 c-Abl activated by SH3 deletion induced only lymphoid malignancies in mice and did not stimulate the
164 fect of UV irradiation on the development of lymphoid malignancies in mice with no or only one functi
167 ved strategies for treating both myeloid and lymphoid malignancies in this high-risk population.
168 cal for immunosurveillance of epithelial and lymphoid malignancies in two transgenic models of de nov
171 rge B-cell lymphoma (DLBCL), the most common lymphoid malignancy in adults, is curable in less than 5
175 ic T cells is the extraordinary incidence of lymphoid malignancy in the many types of primary immunod
177 ymphocyte survival and are over-expressed in lymphoid malignancies, including chronic lymphocytic leu
178 iated with the pathogenesis of several human lymphoid malignancies, including Hodgkin's lymphoma.
179 been implicated in tumorigenesis in several lymphoid malignancies, including non-Hodgkin's and Hodgk
181 has been associated with the development of lymphoid malignancies mainly of B-cell lineage, although
182 while most NF-kappaB activating mutations in lymphoid malignancies occur in upstream signaling compon
183 mmunomodulatory drug (IMiD) with activity in lymphoid malignancies occurring primarily through immune
186 on-self or neo-epitopes, many tumors such as lymphoid malignancies or cancers induced by oncogenic vi
190 d in the treatment of patients with indolent lymphoid malignancies such as chronic lymphocytic leukem
191 ated (ATM) gene is frequently inactivated in lymphoid malignancies such as chronic lymphocytic leukem
192 genesis because IL-7 transgenic mice develop lymphoid malignancies, suggesting that IL-7 may regulate
193 volvement of Notch as an oncogene in several lymphoid malignancies (T-ALL, B-chronic lymphocytic leuk
195 on profiling in defining subtypes within the lymphoid malignancies that are molecularly and clinicall
196 mary effusion lymphoma (PEL) and myeloma are lymphoid malignancies that arise from terminally differe
197 These data identify HIP1 as a new marker of lymphoid malignancies that contributes to the transforma
199 recent major genetic advances in myeloid and lymphoid malignancies, the impact of these findings on p
200 ect and their ability to induce apoptosis in lymphoid malignancies through the glucocorticoid recepto
201 stered in 15 patients with refractory EBV(+) lymphoid malignancies to evaluate the drug combination f
202 we review specific use cases in myeloid and lymphoid malignancies to highlight the utility of single
204 leukemia (T-PLL) is a rare and aggressive T-lymphoid malignancy usually refractory to current treatm
205 aviolet radiation (UVR) exposure and risk of lymphoid malignancies, we examined the association of pr
206 m and iron and the use of (67)Ga scanning in lymphoid malignancies, we examined the effect of HFE exp
207 to study the role of BCL3 overexpression in lymphoid malignancies, we generated five lines of E mu-B
208 deeper insight into the function of Dnmt1 in lymphoid malignancies, we genetically inactivated Dnmt1
209 ged >/=18 years) with relapsed or refractory lymphoid malignancies were enrolled and treated at seven
210 nificant biologic activity in vivo in EBV(+) lymphoid malignancies which are refractory to other regi
211 e to solar UV radiation and the incidence of lymphoid malignancies, which has increased substantially
212 e rare and have been identified only in some lymphoid malignancies, while most NF-kappaB activating m
213 ation in an in vivo mouse model and in human lymphoid malignancies, while suggesting mechanisms for P
214 f the c-rel protooncogene is associated with lymphoid malignancy, while c-rel deletion produces sever
215 ronic lymphocytic leukemia (B-CLL), a common lymphoid malignancy whose molecular etiology remains lar
216 Approximately 60% of E2A-HLF mice developed lymphoid malignancies with a mean latency of 10 months.
217 ediastinal large B-cell lymphoma (MLBCL) are lymphoid malignancies with certain shared clinical, hist
218 phocytic leukemia (PLL) are rare, aggressive lymphoid malignancies with characteristic morphologic, i
219 stability and an increased predisposition to lymphoid malignancies with chromosomal translocations in
220 oring of treatment response in ALL and other lymphoid malignancies with great sensitivity and precisi
221 l in the treatment of DLBCL and additional B-lymphoid malignancies with increased PDE4B expression.
225 highlight recent progress in selected common lymphoid malignancies, with a focus on the genetic alter
226 in-Barr virus (EBV) has been associated with lymphoid malignancies, yet collaborative roles between M
227 t common human chromosomal translocations in lymphoid malignancies, yet the mechanism of how breaks o
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