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1 addition, are hypothesized to predispose to lymphoid malignancy.
2 a novel therapeutic target for GC-resistant lymphoid malignancy.
3 l lymphocytic infiltration, enteropathy, and lymphoid malignancy.
4 s associated with a 5-fold increased risk of lymphoid malignancy.
5 enic mice, all of which developed aggressive lymphoid malignancy.
6 major role in the molecular pathogenesis of lymphoid malignancy.
7 eage cells contributes to the development of lymphoid malignancy.
8 ecular milieu which initiates and sustains a lymphoid malignancy.
9 nes potentially relevant to the induction of 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 recently identified as drivers of peripheral lymphoid malignancy.
19 athogenesis and treatment of this aggressive lymphoid malignancy.
20 ource of new treatments for autoimmunity and lymphoid malignancy.
21 upports that it has a key role in preventing lymphoid malignancy.
22 emergence of dominant B-cell clones and even lymphoid malignancy.
23 ribine's potency across the full spectrum of lymphoid malignancies.
24 of the lung, breast, colon, and a subset of lymphoid malignancies.
25 le progression and is overexpressed in human lymphoid malignancies.
26 icient mice and humans to the development of lymphoid malignancies.
27 een DNMT3A and TET2 mutations in myeloid and lymphoid malignancies.
28 is constitutively phosphorylated in several lymphoid malignancies.
29 in B-ALL with these rearrangements or other lymphoid malignancies.
30 derstanding of immunodeficiency diseases and lymphoid malignancies.
31 the study of alpha4beta1 expression in human lymphoid malignancies.
32 effective treatment option for patients with lymphoid malignancies.
33 r genes and oncogenes are a hallmark of many lymphoid malignancies.
34 K6 as a specific therapeutic target in human lymphoid malignancies.
35 oexpressed with LMP2A in many EBV-associated lymphoid malignancies.
36 ibitors, which are used for the treatment of lymphoid malignancies.
37 hich occur recurrently in a variety of human lymphoid malignancies.
38 peutic targets in a subset of EBV-associated lymphoid malignancies.
39 and oncogenes are frequently associated with lymphoid malignancies.
40 own-regulated in certain myeloid and early B-lymphoid malignancies.
41 factor, has been implicated in several human lymphoid malignancies.
42 is also unclear how the mutation may lead to lymphoid malignancies.
43 or hemizygous have an increased incidence of lymphoid malignancies.
44 aB pathway, which is frequently activated in lymphoid malignancies.
45 kappaB2 gene is recurrently mutated in human lymphoid malignancies.
46 ransplant outcomes were observed in pts with lymphoid malignancies.
47 an antiapoptotic protein also implicated in lymphoid malignancies.
48 ions, lymphoproliferative disorders, and non-lymphoid malignancies.
49 and chronic myeloid malignancies but not in lymphoid malignancies.
50 in inhibitors showed preferential benefit in lymphoid malignancies.
51 d signal transduction and the development of lymphoid malignancies.
52 s makes them effective therapeutics for many lymphoid malignancies.
53 can lead to lymphoproliferative disorders or lymphoid malignancies.
54 umor for the immunotherapy of both solid and lymphoid malignancies.
55 to genome instability and the development of lymphoid malignancies.
56 umab in patients with relapsed or refractory lymphoid malignancies.
57 MH, CMC-544, targeted to CD22 expressed by B-lymphoid malignancies.
58 nical evaluation as a treatment option for B-lymphoid malignancies.
59 combination with ionizing radiation to treat lymphoid malignancies.
60 munity, but also a risk for autoimmunity and lymphoid malignancies.
61 acute lymphoblastic leukemia (ALL) and other lymphoid malignancies.
62 perties that may be of use in the therapy of lymphoid malignancies.
63 xpressed on activated T and B cells and some lymphoid malignancies.
64 odeficiency, and increased susceptibility to lymphoid malignancies.
65 There is relatively little data on indolent lymphoid malignancies.
66 ated low-grade and select intermediate-grade lymphoid malignancies.
67 vide evidence of altered TRAF1 expression in lymphoid malignancies.
68 eceptor loci and increased susceptibility to lymphoid malignancies.
69 ia (A-T) have an increased susceptibility to lymphoid malignancies.
70 ts affecting BCL7B or BCL7C were detected in lymphoid malignancies.
71 e the future design of immunotherapy against lymphoid malignancies.
72 a cell abnormalities, as well as myeloid and lymphoid malignancies.
73 he onset of T cell development and developed lymphoid malignancies.
74 a cell lines, suggesting an association with lymphoid malignancies.
75 gimen to produce engraftment and GVL against lymphoid malignancies.
76 eful as an agent in the treatment of chronic lymphoid malignancies.
77 e in BCL-6-deficient mice and participate in lymphoid malignancies.
78 nt to inflammatory tissues and metastasis of lymphoid malignancies.
79 erexpression of Mer has been associated with lymphoid malignancies.
80 y of patients who underwent HDT and ABMT for lymphoid malignancies.
81 ecreasing pattern through quartiles for many lymphoid malignancies.
82 hematological cancers with two-thirds being lymphoid malignancies.
83 6 with RAIRDs, and 5227 (79.3%) of 6593 with lymphoid malignancies.
84 unodeficiency and greatly increased risk for lymphoid malignancies.
85 , which is associated with predisposition to lymphoid malignancies.
86 NK cells in heavily pretreated patients with lymphoid malignancies.
87 to stratify the risk of incident myeloid and lymphoid malignancies.
88 so operate in suppressing the development of lymphoid malignancies.
89 ith LC-MBL have a fourfold increased risk of lymphoid malignancies.
90 autoimmune rheumatic diseases (RAIRDs), and lymphoid malignancies.
91 apoptotic pathway in previously untreatable lymphoid malignancies.
92 he clustering patterns of haematopoietic and lymphoid malignancies.
93 transformed our knowledge of the genetics of lymphoid malignancies.
94 om 55-64 years to 75 years or older, for all lymphoid malignancies.
95 in a substantial proportion of patients with lymphoid malignancies.
96 atus designation by the FDA for treatment of lymphoid malignancies.
97 alterations (mCAs) have been associated with lymphoid malignancies.
98 tion, and radiation therapy in patients with lymphoid malignancies.
99 ilitates the survival and proliferation of B-lymphoid malignancies.
100 oncogenic driver found to be deregulated in lymphoid malignancies.
101 therapeutic effects in solid tumors than in lymphoid malignancies.
102 ing mutations in a wide range of myeloid and lymphoid malignancies.
103 gnaling are an important advance in managing lymphoid malignancies.
104 of ubiquitination in the genesis of diverse lymphoid malignancies.
105 e NR4A1 and NR4A3 expression and function in lymphoid malignancies.
106 s complete tumor regression in patients with lymphoid malignancies.
107 l conditions, such as agammaglobulinemia and lymphoid malignancies.
108 sis plays a role in normal lymphopoiesis and lymphoid malignancies.
109 encouraging clinical activity in a range of lymphoid malignancies.
110 uently is overexpressed in several solid and lymphoid malignancies.
111 nvolving antigen receptor loci are common in lymphoid malignancies.
112 ainage sites for the peritoneal expansion of lymphoid malignancies.
113 ous neoplasms and represent about 12% of all lymphoid malignancies.
114 nes and clinical samples representing divers lymphoid malignancies.
115 hese compounds can be optimized for treating lymphoid malignancies.
116 proliferative and antiapoptotic signaling in lymphoid malignancies.
117 to RIC-alloHSCT in patients with aggressive lymphoid malignancies.
118 sents a potential new treatment strategy for lymphoid malignancies.
119 ral of which are already showing activity in lymphoid malignancies.
120 howing considerable promise, particularly in lymphoid malignancies.
121 ave been implicated in the genesis of select lymphoid malignancies.
122 virus (EBV) is associated with a variety of lymphoid malignancies.
123 of action of PD-1 blockade in these related lymphoid malignancies.
124 y as a potential therapeutic target in human lymphoid malignancies.
125 cations of microRNA (miRNA) dysregulation in lymphoid malignancies.
126 tamin D also was not associated with risk of lymphoid malignancies.
127 e commonly used in the treatment of indolent lymphoid malignancies.
130 tly greater than that in patients with other lymphoid malignancies (16% prevalence), myeloid disease
132 and holds promise for imaging and therapy in lymphoid malignancies, 6 LLP2A derivatives, as LLP2A-1,4
133 LC-MBL was associated with 4.3-fold risk of lymphoid malignancies (95% CI, 1.4-12.7; P = .009); HC-M
135 r lymphocyte infusion (DLI) in patients with lymphoid malignancy after failure of autologous SCT.
136 was observed in all of the malignancies, but lymphoid malignancies also exhibited hypermethylation, p
137 Some cell lines derived from adult-type lymphoid malignancies also show sensitivity to this trea
138 nt place in the treatment of certain, mainly lymphoid, malignancies, although tumors of nonhemopoieti
139 istance, and poor prognosis in patients with lymphoid malignancies and can occur in approximately 50%
140 both exhibit major activity against indolent lymphoid malignancies and have different mechanisms of a
142 anley to standardize response assessments in lymphoid malignancies and how this was adapted in the Wo
145 raft-versus-malignancy effect in myeloid and lymphoid malignancies and in metastatic renal cell cance
147 ovel epigenetic event in the pathogenesis of lymphoid malignancies and may contribute to a more aggre
149 iscuss the emerging body of clinical data in lymphoid malignancies and present future directions for
150 t on to examine samples derived from patient lymphoid malignancies and showed that beclin-1 expressio
151 for the different effects of UV radiation on lymphoid malignancies and, in addition, that p53 is not
152 nslocations that underlie the development of lymphoid malignancies, and our findings highlight regula
154 t the development of autoimmune diseases and lymphoid malignancies are based on similar sensing mecha
159 g rexinoids with IL-2R-targeted therapies in lymphoid malignancies as well as possibly in autoimmune
160 at potential for improving the monitoring of lymphoid malignancies, assessing immune reconstitution a
163 lymphoma, the most representative class for lymphoid malignancies based on the number of incident ca
164 ost common form of genetic data collected on lymphoid malignancies, because karyotyping is part of th
165 ndard chemotherapy regimen for patients with lymphoid malignancies being considered for reduced-inten
166 inhibitors have shown impressive activity in lymphoid malignancies but have been hampered by autoimmu
167 s well established for the follow-up of many lymphoid malignancies but not for chronic lymphocytic le
168 w insight into the survival roles of mTOR in lymphoid malignancies, but also identify alterations tha
169 lterations of INK4A are commonly observed in lymphoid malignancies, but are consistently absent in pr
170 gehog (HH) signaling is activated in various lymphoid malignancies, but conflicting results exist abo
171 antation (HCT) can be curative treatment for lymphoid malignancies, but it has been characterized by
172 eceptor (CAR) T cell therapy is effective in lymphoid malignancies, but there has been limited data i
173 ne copy of the wild-type allele also develop lymphoid malignancies, but with a much lower frequency a
174 the genesis of chromosomal translocations in lymphoid malignancy, but also in translocations found in
175 radiation might influence the development of lymphoid malignancies by means of its immunosuppressive
177 ackground, the RAG-2(T490A) mutation induced lymphoid malignancies characterized by clonal chromosoma
179 eous T-cell lymphoma (CTCL) is a devastating lymphoid malignancy characterized by the accumulation of
182 ed agents for the treatment of patients with lymphoid malignancies comes the promise of safe and effe
185 agnosed between 2001 and 2013 with one of 12 lymphoid malignancies defined according to International
186 n our understanding of the role of miRNAs in lymphoid malignancies demonstrate that miRNAs can effect
187 egy for targeting multiple myeloma and other lymphoid malignancies dependent on the IRF4 network.
189 oclax, has shown a high therapeutic index in lymphoid malignancies; developing a predictive marker fo
190 mutations in normal GC B-lymphocytes and in lymphoid malignancies displaying GC/post-GC phenotype.
191 less extensive than that on other myeloid or lymphoid malignancies due to low mitotic activity of pla
192 l represents a major issue for patients with lymphoid malignancies, especially those on therapy, beca
193 irus (EBV) is associated with epithelial and lymphoid malignancies, establishes latent infection in m
194 prehensively define the genetic basis of all lymphoid malignancies, examine the relative roles of ger
195 process is not always benign, since certain lymphoid malignancies exhibit recurrent chromosomal abno
198 d Hodgkin's lymphomas and that patients with lymphoid malignancies frequently had anti-HIP1 antibodie
199 novel cytogenetic patterns across different lymphoid malignancies, furthering our understanding of t
201 , whereas patients with advanced myeloid and lymphoid malignancies had high relapse rates after nonmy
202 contrast, patients with advanced myeloid and lymphoid malignancies had rates of more than 0.52 (high
203 Our understanding of the pathogenesis of lymphoid malignancies has been transformed by next-gener
205 ric antigen receptor (CAR) T-cell therapy in lymphoid malignancies has not yet been recapitulated in
208 nteractions between autoimmune disorders and lymphoid malignancies have long been recognized; for ins
211 inhibitors may be an effective treatment for lymphoid malignancies in humans that are associated with
213 c-Abl activated by SH3 deletion induced only lymphoid malignancies in mice and did not stimulate the
214 fect of UV irradiation on the development of lymphoid malignancies in mice with no or only one functi
215 Adults with HM in general and patients with lymphoid malignancies in particular have an increased ri
218 ved strategies for treating both myeloid and lymphoid malignancies in this high-risk population.
219 cal for immunosurveillance of epithelial and lymphoid malignancies in two transgenic models of de nov
222 rge B-cell lymphoma (DLBCL), the most common lymphoid malignancy in adults, is curable in less than 5
227 nalysis demonstrates a shared mechanism with lymphoid malignancy in the formation of public rheumatoi
228 ic T cells is the extraordinary incidence of lymphoid malignancy in the many types of primary immunod
231 ymphocyte survival and are over-expressed in lymphoid malignancies, including chronic lymphocytic leu
232 iated with the pathogenesis of several human lymphoid malignancies, including Hodgkin's lymphoma.
233 been implicated in tumorigenesis in several lymphoid malignancies, including non-Hodgkin's and Hodgk
235 ardiovascular complications in patients with lymphoid malignancies is awareness and preparedness acro
236 Mimicking genetic changes commonly found in lymphoid malignancies leads to immortalized growth in vi
237 has been associated with the development of lymphoid malignancies mainly of B-cell lineage, although
238 spectrum of complications that patients with lymphoid malignancies may experience, cardiovascular tox
240 while most NF-kappaB activating mutations in lymphoid malignancies occur in upstream signaling compon
241 mmunomodulatory drug (IMiD) with activity in lymphoid malignancies occurring primarily through immune
244 on-self or neo-epitopes, many tumors such as lymphoid malignancies or cancers induced by oncogenic vi
248 igen receptor (CAR)-T cell therapies against lymphoid malignancies, responses in solid tumors have be
251 d in the treatment of patients with indolent lymphoid malignancies such as chronic lymphocytic leukem
252 ated (ATM) gene is frequently inactivated in lymphoid malignancies such as chronic lymphocytic leukem
254 genesis because IL-7 transgenic mice develop lymphoid malignancies, suggesting that IL-7 may regulate
255 volvement of Notch as an oncogene in several lymphoid malignancies (T-ALL, B-chronic lymphocytic leuk
257 on profiling in defining subtypes within the lymphoid malignancies that are molecularly and clinicall
258 mary effusion lymphoma (PEL) and myeloma are lymphoid malignancies that arise from terminally differe
259 These data identify HIP1 as a new marker of lymphoid malignancies that contributes to the transforma
262 recent major genetic advances in myeloid and lymphoid malignancies, the impact of these findings on p
263 ect and their ability to induce apoptosis in lymphoid malignancies through the glucocorticoid recepto
264 stered in 15 patients with refractory EBV(+) lymphoid malignancies to evaluate the drug combination f
265 we review specific use cases in myeloid and lymphoid malignancies to highlight the utility of single
268 leukemia (T-PLL) is a rare and aggressive T-lymphoid malignancy usually refractory to current treatm
270 aviolet radiation (UVR) exposure and risk of lymphoid malignancies, we examined the association of pr
271 m and iron and the use of (67)Ga scanning in lymphoid malignancies, we examined the effect of HFE exp
272 to study the role of BCL3 overexpression in lymphoid malignancies, we generated five lines of E mu-B
273 deeper insight into the function of Dnmt1 in lymphoid malignancies, we genetically inactivated Dnmt1
274 e patients with relapsed or refractory CD37+ lymphoid malignancies were enrolled and infused with aut
275 ged >/=18 years) with relapsed or refractory lymphoid malignancies were enrolled and treated at seven
276 nificant biologic activity in vivo in EBV(+) lymphoid malignancies which are refractory to other regi
278 e to solar UV radiation and the incidence of lymphoid malignancies, which has increased substantially
279 e rare and have been identified only in some lymphoid malignancies, while most NF-kappaB activating m
280 ation in an in vivo mouse model and in human lymphoid malignancies, while suggesting mechanisms for P
281 f the c-rel protooncogene is associated with lymphoid malignancy, while c-rel deletion produces sever
282 ronic lymphocytic leukemia (B-CLL), a common lymphoid malignancy whose molecular etiology remains lar
283 Approximately 60% of E2A-HLF mice developed lymphoid malignancies with a mean latency of 10 months.
284 ediastinal large B-cell lymphoma (MLBCL) are lymphoid malignancies with certain shared clinical, hist
285 phocytic leukemia (PLL) are rare, aggressive lymphoid malignancies with characteristic morphologic, i
286 stability and an increased predisposition to lymphoid malignancies with chromosomal translocations in
287 re clinically and biologically heterogeneous lymphoid malignancies with complex microenvironments tha
288 oring of treatment response in ALL and other lymphoid malignancies with great sensitivity and precisi
289 l in the treatment of DLBCL and additional B-lymphoid malignancies with increased PDE4B expression.
291 ial apoptosis can be effectively targeted in lymphoid malignancies with the FDA-approved B cell lymph
292 ymphocytic leukemia (T-PLL) is an aggressive lymphoid malignancy with limited treatment options.
295 highlight recent progress in selected common lymphoid malignancies, with a focus on the genetic alter
297 tages of normal B-cell differentiation and B-lymphoid malignancies, with V1 and V3 being the most abu
298 is to enable the best possible therapies for lymphoid malignancies without the complications of clini
299 in-Barr virus (EBV) has been associated with lymphoid malignancies, yet collaborative roles between M
300 t common human chromosomal translocations in lymphoid malignancies, yet the mechanism of how breaks o