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1 cells, which is the typical program seen in lymphomagenesis.
2 null mice, show delayed onset of MYC-induced lymphomagenesis.
3 n mechanism of NF-kappaB deregulation during lymphomagenesis.
4 of malignant transformation in virus-driven lymphomagenesis.
5 ) checkpoint are required for ThPOK-mediated lymphomagenesis.
6 tential mechanism of gammaherpesvirus-driven lymphomagenesis.
7 d we add new mechanistic insight into B-cell lymphomagenesis.
8 nal center B cells is thought to precipitate lymphomagenesis.
9 viously unrecognized role of BRCA1 in B-cell lymphomagenesis.
10 initiate and maintain oncogenesis, including lymphomagenesis.
11 lation of epigenetic-repressive marks during lymphomagenesis.
12 n, tumour apoptosis and prevention of T-cell lymphomagenesis.
13 ng a critical function of PTEN in preventing lymphomagenesis.
14 s is critical to understand viral-associated lymphomagenesis.
15 t substitute for LMP1 in EBV-positive B cell lymphomagenesis.
16 novel link between ThPOK, TCR signaling, and lymphomagenesis.
17 its repression by MYC contributes to B-cell lymphomagenesis.
18 establish PTPN1 mutations as new drivers in lymphomagenesis.
19 tudy the multistep transformation process in lymphomagenesis.
20 implications for the role of NF-kappaB in GC lymphomagenesis.
21 ressor function of IRF5 in IR-induced thymic lymphomagenesis.
22 function in CD40-driven B-cell expansion and lymphomagenesis.
23 with tumor suppressor properties involved in lymphomagenesis.
24 BCL6 may function in a 'hit-and-run' role in lymphomagenesis.
25 thereby contribute to B-cell homeostasis and lymphomagenesis.
26 a critical component of API2-MALT1-dependent lymphomagenesis.
27 of IRF5, p53 and PUMA in DNA damage-induced lymphomagenesis.
28 ation critically control EBV-mediated B cell lymphomagenesis.
29 mu-Myc mouse model, resulting in decelerated lymphomagenesis.
30 proliferation, processes fundamental to EBV lymphomagenesis.
31 id context that K171E IKKbeta contributes to lymphomagenesis.
32 r effects allowing for the oncogene to drive lymphomagenesis.
33 in vivo, it plays a critical role in B-cell lymphomagenesis.
34 tors, the disruption of which contributes to lymphomagenesis.
35 on of apoptosis resistance during Myc-driven lymphomagenesis.
36 Dnmt1 in a mouse model of MYC-induced T-cell lymphomagenesis.
37 rom cell proliferation and those specific to lymphomagenesis.
38 tivation, potentially contributing to B-cell lymphomagenesis.
39 an unexpected role of the IL-10R pathway in lymphomagenesis.
40 bolic pathways that contribute to sustaining lymphomagenesis.
41 tic activation, processes fundamental to EBV lymphomagenesis.
42 r microenvironment contributes to EBV-driven lymphomagenesis.
43 guish early versus late genetic eventsduring lymphomagenesis.
44 ropose that these genes play a role in DLBCL lymphomagenesis.
45 q21 may be a critical determinant of NK cell lymphomagenesis.
46 y accelerated the rate of Myc-induced B-cell lymphomagenesis.
47 r understanding of the molecular programs of lymphomagenesis.
48 is implicated in control of GC reaction and lymphomagenesis.
49 AIP3 targeting on miR-125a/miR-125b-mediated lymphomagenesis.
50 n about the additional lesions necessary for lymphomagenesis.
51 ion promotes immune evasion and virus-driven lymphomagenesis.
52 f evidence supports a causal role of PCBs in lymphomagenesis.
53 tor (BCR) signaling by PAX5 contributes to B-lymphomagenesis.
54 t knowledge on BCL6 function and its role in lymphomagenesis.
55 cer-associated ARED genes is disabled during lymphomagenesis.
56 contribute to c-Myc-induced KSHV-associated lymphomagenesis.
57 The deficient mice are prone to B-cell lymphomagenesis.
58 demonstrating the oncogenic role of MALT1 in lymphomagenesis.
59 expected to be mutually exclusive events in lymphomagenesis.
60 terations targeting key loci in human T cell lymphomagenesis.
61 ism of GC selection and the role of c-Myc in lymphomagenesis.
62 nd HIV proteins could directly contribute to lymphomagenesis.
63 cusses recent findings on the role of AID in lymphomagenesis.
64 lted in rapid, fatal lymphoproliferation and lymphomagenesis.
65 est that FOXO1 repression contributes to cHL lymphomagenesis.
66 our understanding of oncogenic mechanisms in lymphomagenesis.
67 ccelerate and enhance the dissemination of T-lymphomagenesis.
68 vated Dnmt3b in a mouse model of MYC-induced lymphomagenesis.
69 ation and whose de-regulation is involved in lymphomagenesis.
70 l loss of E6AP attenuated Myc-induced B-cell lymphomagenesis.
71 to RAG-initiated genomic rearrangements and lymphomagenesis.
72 hat reduction in HAT dosage is important for lymphomagenesis.
73 llular oncogenic processes that arise during lymphomagenesis.
74 nsights into the mechanism of viral-mediated lymphomagenesis.
75 ubclinical immune system function influences lymphomagenesis.
76 regulated NF-kappaB signaling can facilitate lymphomagenesis.
77 flammation and chronic B-cell stimulation in lymphomagenesis.
78 epigenetic modifications might contribute to lymphomagenesis.
79 genes might initiate genomic instability and lymphomagenesis.
80 us tumors and showed accelerated Myc-induced lymphomagenesis.
81 e to DNA damage and the suppression of early lymphomagenesis.
82 ggesting that chronic HBV infection promotes lymphomagenesis.
83 tions for understanding the role of Gfi-1 in lymphomagenesis.
84 an oncoprotein that cooperates with c-Myc in lymphomagenesis.
85 rminal center (GC) reaction and important in lymphomagenesis.
86 n in tumor-derived cells suppressed leukemia/lymphomagenesis.
87 -renewal, and differentiation while opposing lymphomagenesis.
88 t non-Ig genes and thereby promote GC B-cell lymphomagenesis.
89 tem, but collaborates strongly with c-Myc in lymphomagenesis.
90 eculation that vitamin D may protect against lymphomagenesis.
91 from a chromosomal translocation involved in lymphomagenesis.
92 ion of pre-B cells and, subsequently, during lymphomagenesis.
93 nal center (GC) B cells and is implicated in lymphomagenesis.
94 ough its ability to accelerate c-Myc-induced lymphomagenesis.
95 ng new strategies to inhibit MALT1-dependent lymphomagenesis.
96 nce survival in a mouse model of Myc-induced lymphomagenesis.
97 ha in Notch pathway activation during T-cell lymphomagenesis.
98 er immune function, which may be relevant to lymphomagenesis.
99 have examined the role of circadian genes in lymphomagenesis.
100 in B cell development, immune function, and lymphomagenesis.
101 ngiogenesis, thus revealing targets to block lymphomagenesis.
102 that are commonly targeted during GC B cell lymphomagenesis.
103 CD30 signaling increases the risk of B-cell lymphomagenesis.
104 f BCL6 and significantly delayed BCL6-driven lymphomagenesis.
105 underlying mechanisms of EBV-induced B-cell lymphomagenesis.
106 as a cell-extrinsic suppressor of GC B cell lymphomagenesis.
107 is on how Tfh cell signals may contribute to lymphomagenesis.
108 how their application to study clonal B-cell lymphomagenesis.
109 eir inactivation is thought to contribute to lymphomagenesis.
110 pment but completely abrogates Eu-Myc-driven lymphomagenesis.
111 ell activation is hyperactivated, leading to lymphomagenesis.
112 ed gammaherpesvirus infection and associated lymphomagenesis.
113 hypothesis that sex hormones play a role in lymphomagenesis.
114 ression that can contribute to viral-induced lymphomagenesis.
115 tion resulting from Blimp1 loss in ABC-DLBCL lymphomagenesis.
116 section of early steps in the progression to lymphomagenesis.
117 h as autoimmunity, chronic inflammation, and lymphomagenesis.
118 itical role for BCL-W in B cell survival and lymphomagenesis.
119 ssion of apoptosis with implications for EBV lymphomagenesis.
120 o-operative mutations leading to spontaneous lymphomagenesis.
121 tations might play an important role in PTFL lymphomagenesis.
122 of the tumor microenvironment that promotes lymphomagenesis.
123 ay represent a novel animal model of gastric lymphomagenesis.
124 hat MTHFR variants contribute to pSS-related lymphomagenesis.
125 clonogenicity, suggesting a role of vp17s in lymphomagenesis.
126 ied that Akt2 cooperates with Dlx5 in T-cell lymphomagenesis.
127 alone and cooperate in development of B-cell lymphomagenesis.
128 uming that HIV is only indirectly related to lymphomagenesis.
129 onal collaboration between Gfi1 and c-Myc in lymphomagenesis.
130 erate with MYC over-expression to accelerate lymphomagenesis.
131 into the pathways that contribute to B-cell lymphomagenesis.
132 al center (GC) reaction and is implicated in lymphomagenesis.
133 et this TCR must be downregulated for T-cell lymphomagenesis.
134 d NF-kappaB pathway previously implicated in lymphomagenesis.
135 es cause GC B cells to become susceptible to lymphomagenesis.
136 ph nodes to identify potential mechanisms of lymphomagenesis.
137 ene expression in mouse GC B cells, promotes lymphomagenesis.
138 sibility that HIV may directly contribute to lymphomagenesis.
139 type p53 it leads to significantly increased lymphomagenesis (56%) when compared with control mice (2
140 on are thought to be the main drivers of HIV lymphomagenesis, although the current scenario does not
141 sults reveal a pre-neoplastic stage in human lymphomagenesis and a cascade of somatic mutations leadi
142 ement, and restoring TTP impairs Myc-induced lymphomagenesis and abolishes maintenance of the maligna
143 tein-Barr virus (EBV) has been implicated in lymphomagenesis and can be found infecting tumor cells a
145 ir-146b significantly delayed PTEN-deficient lymphomagenesis and delayed c-myc oncogene induction, a
146 at, while loss of one copy of Rpl22 promotes lymphomagenesis and disseminated disease, loss of both c
148 on by constitutively active EZH2 facilitates lymphomagenesis and identifies EZH2 as a possible therap
149 tand the pathobiologic link of HCV in B cell lymphomagenesis and its optimal management in the oncolo
153 ressor that directly protects against B cell lymphomagenesis and provides a strong rationale for bloc
154 , explaining how HVEM loss contributes to GC lymphomagenesis and revealing a cell-extrinsic tumor-sup
155 Strikingly, PARP14 deficiency delayed B lymphomagenesis and reversed the block to B-cell maturat
156 etwork, we can elucidate known mechanisms of lymphomagenesis and suggest candidate tumorigenic altera
157 mor development, accelerated Emu-Myc-induced lymphomagenesis and susceptibility to carcinogenesis.
158 on and subsequent induction of BCL6 promotes lymphomagenesis and that this pathway may be a potential
160 svirus infection has been implicated in both lymphomagenesis and, somewhat controversially, autoimmun
161 e(+)/Emicro-myc mice significantly inhibited lymphomagenesis, and all lymphomas that did arise in the
162 ht a multifaceted role for TMEM30A in B-cell lymphomagenesis, and characterize intrinsic and extrinsi
164 viral integration site in retrovirus-induced lymphomagenesis, and new, emerging data suggest a role o
165 This study implicates oncogenic NKX2-3 in lymphomagenesis, and provides a valid experimental mouse
166 as miRNAs during B-cell differentiation and lymphomagenesis, and recent advancements in targeted str
167 mor development, accelerated Emu-Myc-induced lymphomagenesis, and rendered mice susceptible to carcin
168 ng of the processes and pathways involved in lymphomagenesis, and some of the pathways mutated here m
169 3 dysfunction, recent advances implicated in lymphomagenesis, and therapeutic approaches to overcomin
171 e found that DNA methylation profiles during lymphomagenesis are largely influenced by the methylatio
177 tion of INK4 control on Cdk4 does not affect lymphomagenesis, B-cell maturation, and functions in Cdk
178 o have implications for the role of FOXO1 in lymphomagenesis because they suggest that constitutive F
179 C1, PRC2 is a tumor suppressor in Emicro-myc lymphomagenesis, because disease onset was accelerated b
181 s of Dicer function was not advantageous for lymphomagenesis, but rather, Dicer ablation was strongly
182 of just one Rpl22 allele accelerates T-cell lymphomagenesis by activating NF-kappaB and inducing the
184 ng indicates that EBV and KSHV contribute to lymphomagenesis by affecting genomic stability and by su
185 rant expression of FOXP1 might contribute to lymphomagenesis by blocking this terminal B-cell differe
186 somatic mutations of MEF2B may contribute to lymphomagenesis by deregulating BCL6 expression, and MEF
187 Activation-induced deaminase (AID) can drive lymphomagenesis by generating off-target DNA breaks at l
189 conditional knockout in T cells accelerated lymphomagenesis by increasing cellular proliferation, wh
190 VEM interaction with BTLA may play a role in lymphomagenesis by interfering with Vgamma9Vdelta2 T-cel
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
196 e normal counterpart of FL and DLBCL, and in lymphomagenesis by using conditional GC-directed deletio
201 641F) can collaborate with Myc to accelerate lymphomagenesis demonstrating a cooperative role of EZH2
202 at HIV structural proteins may contribute to lymphomagenesis directly, because they can persist long
203 ese events are not restricted to APL because lymphomagenesis driven by deletion of p53 or, to a lesse
204 mplete ablation of Hdac1 and Hdac2 abrogated lymphomagenesis due to a block in early thymic developme
205 signaling in macrophages can promote B-cell lymphomagenesis during chronic Helicobacter infection.
206 er and how these mutations may contribute to lymphomagenesis, either individually or in combination.
207 humans and mouse models have indicated that lymphomagenesis evolves through the accumulation of mult
208 ions, opening the possibility that multi-hit lymphomagenesis gradually occurs throughout life during
209 (+/-) mice showed a dramatic acceleration of lymphomagenesis, greater even than that observed in Emic
211 role for B-cell-receptor (BCR) signalling in lymphomagenesis has been inferred by studying immunoglob
213 ransformation during gammaherpesvirus-driven lymphomagenesis, identification of host and viral factor
217 EBNA3A contributes to efficient EBV-induced lymphomagenesis in CBH mice.IMPORTANCE The EBV protein E
218 the INK4-Cdk4 checkpoint can participate in lymphomagenesis in conjunction with additional alteratio
220 , genetic inactivation of Dnmt3b accelerated lymphomagenesis in Dnmt3a(Delta/Delta) mice, demonstrati
222 As such, the loss of caspase-2 enhances lymphomagenesis in Emicro-Myc transgenic mice, and caspa
223 gnaling also appears to modulate the risk of lymphomagenesis in gastric mucosa-associated lymphoid ti
224 behind the possible different mechanisms of lymphomagenesis in HIV-associated Burkitt lymphoma and e
225 ent promotes Epstein-Barr virus (EBV)-driven lymphomagenesis in Hodgkin lymphoma by a novel pathway i
226 the many genes whose mutation contributes to lymphomagenesis in humans, relatively little is known ab
228 vo, establish a preclinical model for B cell lymphomagenesis in immunosuppressed patients, and valida
230 omic instability and germinal center derived lymphomagenesis in mice infected with Plasmodium to recr
231 del, we observed a significant inhibition of lymphomagenesis in mice lacking one or both alleles of S
237 te that BCL6 expression is maintained during lymphomagenesis in part through DNA methylation that pre
238 mechanisms underlie genomic instability and lymphomagenesis in Rag2(c/c) p53(-/-) and Atm(-/-) mice.
239 c-rel-/- mice display significantly earlier lymphomagenesis in the c-Myc driven, Emu-Myc model of B-
245 at Src kinase is pathogenically activated in lymphomagenesis induced by FGFR1 fusion genes, implying
247 Previous studies have shown that MYC-driven lymphomagenesis is associated with mammalian target of r
253 -17 approximately 92- overexpression induces lymphomagenesis/leukemogenesis, we generated a B-cell-sp
254 gest that predisposition of MIM-null mice to lymphomagenesis may involve aberrant interactions betwee
257 deletion-induced delay in Myc-driven B-cell lymphomagenesis, nor allowed a single B-cell lymphoma to
258 ding of the pathogenesis of autoimmunity and lymphomagenesis of autoimmune lymphoproliferative syndro
259 e role of specific signaling pathways in the lymphomagenesis of MCL and the biologic basis for ibruti
261 cell growth in mouse xenografts and postpone lymphomagenesis onset in murine transplantation models.
263 to reveal novel factors that participate in lymphomagenesis or to define biomarkers of onset or prog
264 V-6A genome from the telomere contributed to lymphomagenesis, or was coincidental, remains unclear bu
265 t gene results in protection from IR-induced lymphomagenesis rather than enhanced susceptibility to.
266 chd1 in Emu-Myc transgenic mice that undergo lymphomagenesis reduced disease latency by 50% relative
267 ement of lesions at the very early stages of lymphomagenesis, refines the diagnostic criteria for som
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
279 iates the humoral immune response and drives lymphomagenesis through formation of bivalent chromatin
280 rging evidence supports a key role of AID in lymphomagenesis through genome-wide off-target induction
281 of routine residential UVR exposure against lymphomagenesis through mechanisms possibly independent
282 oes not change the overall rate, it modifies lymphomagenesis to favor mature B cell lymphomas that ar
283 port that SIRT4 represses Myc-induced B cell lymphomagenesis via inhibition of mitochondrial glutamin
284 of T-cell malignancy, and found that T-cell lymphomagenesis was accelerated in mice bearing both mut
287 further characterize these EZH2 mutations in lymphomagenesis, we generated a mouse line where EZH2(Y6
288 nd the role of miRNAs in B cell function and lymphomagenesis, we generated short-RNA libraries from n
291 e p53 deficient mouse model with accelerated lymphomagenesis, we previously observed whole chromosome
292 ein synthesis and attenuation of Myc-induced lymphomagenesis, we showed that Myc-induced UPR activati
293 rts its effects and how it may contribute to lymphomagenesis, we sought to characterize the outcome o
294 e relationship between parasitic disease and lymphomagenesis, we used Plasmodium chabaudi (Pc) to pro
295 P1 together with LMP2A, EBNA3A only promotes lymphomagenesis when the EBNA2 target Myc is also overex
296 ficiency of Smarcal1 resulted in accelerated lymphomagenesis, whereas haploinsufficiency of Zranb3 in
297 ar subsets has implications for human B cell lymphomagenesis, which originates mostly from GC B cells
298 or during the onset of Emu-myc-driven B cell lymphomagenesis, while p73 modulated tumor dissemination
299 of PTEN was found to be a powerful driver of lymphomagenesis within the thymus characterized by overe
300 s a layer of Myc autoregulation critical for lymphomagenesis yet partly dispensable for normal develo