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1 itical role for BCL-W in B cell survival and lymphomagenesis.
2 ssion of apoptosis with implications for EBV lymphomagenesis.
3 of IRF5, p53 and PUMA in DNA damage-induced lymphomagenesis.
4 mu-Myc mouse model, resulting in decelerated lymphomagenesis.
5 proliferation, processes fundamental to EBV lymphomagenesis.
6 id context that K171E IKKbeta contributes to lymphomagenesis.
7 r effects allowing for the oncogene to drive lymphomagenesis.
8 tors, the disruption of which contributes to lymphomagenesis.
9 on of apoptosis resistance during Myc-driven lymphomagenesis.
10 Dnmt1 in a mouse model of MYC-induced T-cell lymphomagenesis.
11 rom cell proliferation and those specific to lymphomagenesis.
12 tivation, potentially contributing to B-cell lymphomagenesis.
13 an unexpected role of the IL-10R pathway in lymphomagenesis.
14 bolic pathways that contribute to sustaining lymphomagenesis.
15 tic activation, processes fundamental to EBV lymphomagenesis.
16 r microenvironment contributes to EBV-driven lymphomagenesis.
17 guish early versus late genetic eventsduring lymphomagenesis.
18 ropose that these genes play a role in DLBCL lymphomagenesis.
19 q21 may be a critical determinant of NK cell lymphomagenesis.
20 y accelerated the rate of Myc-induced B-cell lymphomagenesis.
21 r understanding of the molecular programs of lymphomagenesis.
22 is implicated in control of GC reaction and lymphomagenesis.
23 AIP3 targeting on miR-125a/miR-125b-mediated lymphomagenesis.
24 n about the additional lesions necessary for lymphomagenesis.
25 ion promotes immune evasion and virus-driven lymphomagenesis.
26 f evidence supports a causal role of PCBs in lymphomagenesis.
27 tor (BCR) signaling by PAX5 contributes to B-lymphomagenesis.
28 t knowledge on BCL6 function and its role in lymphomagenesis.
29 cer-associated ARED genes is disabled during lymphomagenesis.
30 alone and cooperate in development of B-cell lymphomagenesis.
31 contribute to c-Myc-induced KSHV-associated lymphomagenesis.
32 The deficient mice are prone to B-cell lymphomagenesis.
33 demonstrating the oncogenic role of MALT1 in lymphomagenesis.
34 expected to be mutually exclusive events in lymphomagenesis.
35 terations targeting key loci in human T cell lymphomagenesis.
36 ism of GC selection and the role of c-Myc in lymphomagenesis.
37 cusses recent findings on the role of AID in lymphomagenesis.
38 lted in rapid, fatal lymphoproliferation and lymphomagenesis.
39 est that FOXO1 repression contributes to cHL lymphomagenesis.
40 our understanding of oncogenic mechanisms in lymphomagenesis.
41 vated Dnmt3b in a mouse model of MYC-induced lymphomagenesis.
42 ation and whose de-regulation is involved in lymphomagenesis.
43 l loss of E6AP attenuated Myc-induced B-cell lymphomagenesis.
44 to RAG-initiated genomic rearrangements and lymphomagenesis.
45 hat reduction in HAT dosage is important for lymphomagenesis.
46 llular oncogenic processes that arise during lymphomagenesis.
47 ubclinical immune system function influences lymphomagenesis.
48 regulated NF-kappaB signaling can facilitate lymphomagenesis.
49 flammation and chronic B-cell stimulation in lymphomagenesis.
50 epigenetic modifications might contribute to lymphomagenesis.
51 o-operative mutations leading to spontaneous lymphomagenesis.
52 genes might initiate genomic instability and lymphomagenesis.
53 us tumors and showed accelerated Myc-induced lymphomagenesis.
54 e to DNA damage and the suppression of early lymphomagenesis.
55 ggesting that chronic HBV infection promotes lymphomagenesis.
56 tions for understanding the role of Gfi-1 in lymphomagenesis.
57 an oncoprotein that cooperates with c-Myc in lymphomagenesis.
58 rminal center (GC) reaction and important in lymphomagenesis.
59 n in tumor-derived cells suppressed leukemia/lymphomagenesis.
60 -renewal, and differentiation while opposing lymphomagenesis.
61 uming that HIV is only indirectly related to lymphomagenesis.
62 t non-Ig genes and thereby promote GC B-cell lymphomagenesis.
63 eculation that vitamin D may protect against lymphomagenesis.
64 from a chromosomal translocation involved in lymphomagenesis.
65 ion of pre-B cells and, subsequently, during lymphomagenesis.
66 nal center (GC) B cells and is implicated in lymphomagenesis.
67 ough its ability to accelerate c-Myc-induced lymphomagenesis.
68 nce survival in a mouse model of Myc-induced lymphomagenesis.
69 ha in Notch pathway activation during T-cell lymphomagenesis.
70 er immune function, which may be relevant to lymphomagenesis.
71 have examined the role of circadian genes in lymphomagenesis.
72 in B cell development, immune function, and lymphomagenesis.
73 t regulate cell survival, proliferation, and lymphomagenesis.
74 inal center (GC) formation and implicated in lymphomagenesis.
75 erate with MYC over-expression to accelerate lymphomagenesis.
76 ear development, and has been implicated in lymphomagenesis.
77 t that blocking this pathway is critical for lymphomagenesis.
78 stream kinase ERK plays an important role in lymphomagenesis.
79 endent apoptosis, has been shown to suppress lymphomagenesis.
80 on in caspases may play an important role in lymphomagenesis.
81 3-dependent non-apoptotic pathways in B-cell lymphomagenesis.
82 into the pathways that contribute to B-cell lymphomagenesis.
83 e various B cell subsets while counteracting lymphomagenesis.
84 oncogene by cooperating with Akt2 to promote lymphomagenesis.
85 ity for non-Hodgkin lymphomas may illuminate lymphomagenesis.
86 tumors, p52 transgenic mice are not prone to lymphomagenesis.
87 ements that cooperate with activated Akt2 in lymphomagenesis.
88 ed, which could be critical for BCL6-induced lymphomagenesis.
89 tical insight into normal B-cell biology and lymphomagenesis.
90 al center (GC) reaction and is implicated in lymphomagenesis.
91 s apoptosis during the preleukemic period of lymphomagenesis.
92 repressor known to play a causative role in lymphomagenesis.
93 s are varied in their efficiency in inducing lymphomagenesis.
94 et this TCR must be downregulated for T-cell lymphomagenesis.
95 tes resulted in thymic involution instead of lymphomagenesis.
96 vivo genetic evidence for a role of MTA1 in lymphomagenesis.
97 tumor progression, loss of E2f2 accelerated lymphomagenesis.
98 n because its conditional ablation abrogates lymphomagenesis.
99 sion, resulting in an acceleration of B-cell lymphomagenesis.
100 n signaling that in turn prevent MYC-induced lymphomagenesis.
101 tations might play an important role in PTFL lymphomagenesis.
102 d NF-kappaB pathway previously implicated in lymphomagenesis.
103 es cause GC B cells to become susceptible to lymphomagenesis.
104 ay represent a novel animal model of gastric lymphomagenesis.
105 ph nodes to identify potential mechanisms of lymphomagenesis.
106 ene expression in mouse GC B cells, promotes lymphomagenesis.
107 sibility that HIV may directly contribute to lymphomagenesis.
108 null mice, show delayed onset of MYC-induced lymphomagenesis.
109 n mechanism of NF-kappaB deregulation during lymphomagenesis.
110 of malignant transformation in virus-driven lymphomagenesis.
111 ) checkpoint are required for ThPOK-mediated lymphomagenesis.
112 tential mechanism of gammaherpesvirus-driven lymphomagenesis.
113 d we add new mechanistic insight into B-cell lymphomagenesis.
114 viously unrecognized role of BRCA1 in B-cell lymphomagenesis.
115 initiate and maintain oncogenesis, including lymphomagenesis.
116 lation of epigenetic-repressive marks during lymphomagenesis.
117 hat MTHFR variants contribute to pSS-related lymphomagenesis.
118 n, tumour apoptosis and prevention of T-cell lymphomagenesis.
119 ng a critical function of PTEN in preventing lymphomagenesis.
120 t substitute for LMP1 in EBV-positive B cell lymphomagenesis.
121 novel link between ThPOK, TCR signaling, and lymphomagenesis.
122 clonogenicity, suggesting a role of vp17s in lymphomagenesis.
123 its repression by MYC contributes to B-cell lymphomagenesis.
124 establish PTPN1 mutations as new drivers in lymphomagenesis.
125 tudy the multistep transformation process in lymphomagenesis.
126 implications for the role of NF-kappaB in GC lymphomagenesis.
127 ressor function of IRF5 in IR-induced thymic lymphomagenesis.
128 function in CD40-driven B-cell expansion and lymphomagenesis.
129 with tumor suppressor properties involved in lymphomagenesis.
130 BCL6 may function in a 'hit-and-run' role in lymphomagenesis.
131 thereby contribute to B-cell homeostasis and lymphomagenesis.
132 a critical component of API2-MALT1-dependent lymphomagenesis.
133 type p53 it leads to significantly increased lymphomagenesis (56%) when compared with control mice (2
134 decreased DGK activity also promotes thymic lymphomagenesis accompanying elevated Ras and Erk1/2 act
135 on are thought to be the main drivers of HIV lymphomagenesis, although the current scenario does not
136 be an important mechanism involved in B-cell lymphomagenesis among severely immunocompromised and hea
137 ement, and restoring TTP impairs Myc-induced lymphomagenesis and abolishes maintenance of the maligna
138 transgenic mouse model of Myc-induced T cell lymphomagenesis and analyzed tumor progression in mice d
140 ir-146b significantly delayed PTEN-deficient lymphomagenesis and delayed c-myc oncogene induction, a
141 berrant transcriptional programming leads to lymphomagenesis and development of targeted antilymphoma
142 at, while loss of one copy of Rpl22 promotes lymphomagenesis and disseminated disease, loss of both c
144 on by constitutively active EZH2 facilitates lymphomagenesis and identifies EZH2 as a possible therap
145 -cell lymphoma 6 plays a fundamental role in lymphomagenesis and is an excellent therapeutic target f
146 tand the pathobiologic link of HCV in B cell lymphomagenesis and its optimal management in the oncolo
148 of NF-kappaB that are implicated in leukemia/lymphomagenesis and modulates their transcriptional and
151 ressor that directly protects against B cell lymphomagenesis and provides a strong rationale for bloc
152 Strikingly, PARP14 deficiency delayed B lymphomagenesis and reversed the block to B-cell maturat
153 etwork, we can elucidate known mechanisms of lymphomagenesis and suggest candidate tumorigenic altera
154 mor development, accelerated Emu-Myc-induced lymphomagenesis and susceptibility to carcinogenesis.
155 mouse model of Burkitt lymphoma accelerates lymphomagenesis and that approximately 75% of Emu-Myc ly
156 aneously arising tumors in a murine model of lymphomagenesis and that c-Myc is involved in their regu
157 on and subsequent induction of BCL6 promotes lymphomagenesis and that this pathway may be a potential
159 e(+)/Emicro-myc mice significantly inhibited lymphomagenesis, and all lymphomas that did arise in the
161 viral integration site in retrovirus-induced lymphomagenesis, and new, emerging data suggest a role o
162 This study implicates oncogenic NKX2-3 in lymphomagenesis, and provides a valid experimental mouse
163 as miRNAs during B-cell differentiation and lymphomagenesis, and recent advancements in targeted str
164 mor development, accelerated Emu-Myc-induced lymphomagenesis, and rendered mice susceptible to carcin
165 ng of the processes and pathways involved in lymphomagenesis, and some of the pathways mutated here m
166 3 dysfunction, recent advances implicated in lymphomagenesis, and therapeutic approaches to overcomin
168 e found that DNA methylation profiles during lymphomagenesis are largely influenced by the methylatio
173 tion of INK4 control on Cdk4 does not affect lymphomagenesis, B-cell maturation, and functions in Cdk
174 o have implications for the role of FOXO1 in lymphomagenesis because they suggest that constitutive F
175 C1, PRC2 is a tumor suppressor in Emicro-myc lymphomagenesis, because disease onset was accelerated b
176 the Rel proteins are implicated in leukemia/lymphomagenesis but the mechanism is not fully understoo
177 verses and prevents the onset of MYC-induced lymphomagenesis, but fails to reverse or prevent tumorig
178 s of Dicer function was not advantageous for lymphomagenesis, but rather, Dicer ablation was strongly
179 of just one Rpl22 allele accelerates T-cell lymphomagenesis by activating NF-kappaB and inducing the
181 ng indicates that EBV and KSHV contribute to lymphomagenesis by affecting genomic stability and by su
182 rant expression of FOXP1 might contribute to lymphomagenesis by blocking this terminal B-cell differe
183 somatic mutations of MEF2B may contribute to lymphomagenesis by deregulating BCL6 expression, and MEF
184 investigate the mechanism of Stat5-mediated lymphomagenesis by exploring the contributions of major
185 Activation-induced deaminase (AID) can drive lymphomagenesis by generating off-target DNA breaks at l
187 conditional knockout in T cells accelerated lymphomagenesis by increasing cellular proliferation, wh
188 ss all MZL subtypes, which may contribute to lymphomagenesis by inducing constitutive NF-kappaB activ
189 VEM interaction with BTLA may play a role in lymphomagenesis by interfering with Vgamma9Vdelta2 T-cel
190 the loss or activation of which may promote lymphomagenesis by leading to abnormally prolonged NF-ka
191 suppressor gene whose early loss facilitates lymphomagenesis by remodeling the epigenetic landscape o
194 e analyses demonstrate that miR-17~92 drives lymphomagenesis by suppressing the expression of multipl
199 641F) can collaborate with Myc to accelerate lymphomagenesis demonstrating a cooperative role of EZH2
200 at HIV structural proteins may contribute to lymphomagenesis directly, because they can persist long
201 ese events are not restricted to APL because lymphomagenesis driven by deletion of p53 or, to a lesse
202 mplete ablation of Hdac1 and Hdac2 abrogated lymphomagenesis due to a block in early thymic developme
203 humans and mouse models have indicated that lymphomagenesis evolves through the accumulation of mult
204 ions, opening the possibility that multi-hit lymphomagenesis gradually occurs throughout life during
205 (+/-) mice showed a dramatic acceleration of lymphomagenesis, greater even than that observed in Emic
206 role for B-cell-receptor (BCR) signalling in lymphomagenesis has been inferred by studying immunoglob
208 c fibroblasts (MEFs) and impairs Myc-induced lymphomagenesis in a transgenic mouse model of human Bur
211 the INK4-Cdk4 checkpoint can participate in lymphomagenesis in conjunction with additional alteratio
213 , genetic inactivation of Dnmt3b accelerated lymphomagenesis in Dnmt3a(Delta/Delta) mice, demonstrati
215 As such, the loss of caspase-2 enhances lymphomagenesis in Emicro-Myc transgenic mice, and caspa
216 gnaling also appears to modulate the risk of lymphomagenesis in gastric mucosa-associated lymphoid ti
217 ent promotes Epstein-Barr virus (EBV)-driven lymphomagenesis in Hodgkin lymphoma by a novel pathway i
218 the many genes whose mutation contributes to lymphomagenesis in humans, relatively little is known ab
219 vo, establish a preclinical model for B cell lymphomagenesis in immunosuppressed patients, and valida
221 omic instability and germinal center derived lymphomagenesis in mice infected with Plasmodium to recr
222 del, we observed a significant inhibition of lymphomagenesis in mice lacking one or both alleles of S
228 GCs, suggesting that S1P(2) loss may promote lymphomagenesis in part by disrupting GC B-cells homeost
229 te that BCL6 expression is maintained during lymphomagenesis in part through DNA methylation that pre
230 mechanisms underlie genomic instability and lymphomagenesis in Rag2(c/c) p53(-/-) and Atm(-/-) mice.
231 c-rel-/- mice display significantly earlier lymphomagenesis in the c-Myc driven, Emu-Myc model of B-
234 e and observed spontaneous follicular B-cell lymphomagenesis in this model to show that ING proteins
238 increased Mdm2 expression facilitated B-cell lymphomagenesis, in part, through regulation of p53 by a
239 rmore, CDK6-deficient mice were resistant to lymphomagenesis induced by active Akt, a downstream targ
240 at Src kinase is pathogenically activated in lymphomagenesis induced by FGFR1 fusion genes, implying
241 FIP200 did not further accelerate or inhibit lymphomagenesis induced by inactivation of p53 in mice.
242 en suggested as a major mechanism underlying lymphomagenesis induced by NF-kappaB2 mutations, which o
244 Previous studies have shown that MYC-driven lymphomagenesis is associated with mammalian target of r
245 involvement of paired box gene 5 (PAX5) in B-lymphomagenesis is based largely on the discovery of Pax
249 -17 approximately 92- overexpression induces lymphomagenesis/leukemogenesis, we generated a B-cell-sp
251 gest that predisposition of MIM-null mice to lymphomagenesis may involve aberrant interactions betwee
253 deletion-induced delay in Myc-driven B-cell lymphomagenesis, nor allowed a single B-cell lymphoma to
254 ding of the pathogenesis of autoimmunity and lymphomagenesis of autoimmune lymphoproliferative syndro
255 e role of specific signaling pathways in the lymphomagenesis of MCL and the biologic basis for ibruti
257 cell growth in mouse xenografts and postpone lymphomagenesis onset in murine transplantation models.
259 to reveal novel factors that participate in lymphomagenesis or to define biomarkers of onset or prog
260 V-6A genome from the telomere contributed to lymphomagenesis, or was coincidental, remains unclear bu
261 t gene results in protection from IR-induced lymphomagenesis rather than enhanced susceptibility to.
262 chd1 in Emu-Myc transgenic mice that undergo lymphomagenesis reduced disease latency by 50% relative
263 ement of lesions at the very early stages of lymphomagenesis, refines the diagnostic criteria for som
264 protein cholesterol (HDL-C) may occur during lymphomagenesis, reflecting underlying etiology such as
271 ts dysregulation, frequently associated with lymphomagenesis, requires robust dynamical modeling tech
272 penetrance and that, conversely, Myc-driven lymphomagenesis stringently requires two intact alleles
273 BCL that suppresses B-cell proliferation and lymphomagenesis, suggesting pharmaceutical targeting of
274 serial transplantation models of MYC-driven lymphomagenesis, supporting the idea that the mutational
275 Our findings identify Ment as an enhancer of lymphomagenesis that contributes to the tumor suppressor
276 ght into the role of the microenvironment in lymphomagenesis, these findings expose a unique molecula
277 7 overexpression also promotes mature B-cell lymphomagenesis; this is physiologically relevant as we
278 Constitutive expression of BCL6 mediates lymphomagenesis through aberrant proliferation, survival
280 iates the humoral immune response and drives lymphomagenesis through formation of bivalent chromatin
281 rging evidence supports a key role of AID in lymphomagenesis through genome-wide off-target induction
282 of routine residential UVR exposure against lymphomagenesis through mechanisms possibly independent
283 oes not change the overall rate, it modifies lymphomagenesis to favor mature B cell lymphomas that ar
284 port that SIRT4 represses Myc-induced B cell lymphomagenesis via inhibition of mitochondrial glutamin
285 of T-cell malignancy, and found that T-cell lymphomagenesis was accelerated in mice bearing both mut
287 role of BCR/ITAM signaling in Pax5-dependent lymphomagenesis was corroborated in Syk, an ITAM-associa
289 further characterize these EZH2 mutations in lymphomagenesis, we generated a mouse line where EZH2(Y6
290 nd the role of miRNAs in B cell function and lymphomagenesis, we generated short-RNA libraries from n
293 e p53 deficient mouse model with accelerated lymphomagenesis, we previously observed whole chromosome
294 ein synthesis and attenuation of Myc-induced lymphomagenesis, we showed that Myc-induced UPR activati
295 rts its effects and how it may contribute to lymphomagenesis, we sought to characterize the outcome o
297 e relationship between parasitic disease and lymphomagenesis, we used Plasmodium chabaudi (Pc) to pro
298 ar subsets has implications for human B cell lymphomagenesis, which originates mostly from GC B cells
299 or during the onset of Emu-myc-driven B cell lymphomagenesis, while p73 modulated tumor dissemination
300 of PTEN was found to be a powerful driver of lymphomagenesis within the thymus characterized by overe
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