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1 K2gamma antagonizes mTORC1 activation during hepatocarcinogenesis.
2 ational spectra (HRMS) during the process of hepatocarcinogenesis.
3 ein kinases II gamma isoform (CAMK2gamma) in hepatocarcinogenesis.
4 y loss of SIRT6 possess oncogenic effects in hepatocarcinogenesis.
5 pa B (NF-kappaB) pathways that contribute to hepatocarcinogenesis.
6 on in the context of the immune responses in hepatocarcinogenesis.
7 he coagulation pathway to augment aggressive hepatocarcinogenesis.
8 ional and post-transcriptional regulation of hepatocarcinogenesis.
9 nt pathways in mediating AKT and Ras induced hepatocarcinogenesis.
10 /beta-catenin signaling that is critical for hepatocarcinogenesis.
11 icient mice after diethylnitrosamine-induced hepatocarcinogenesis.
12 ndent functions of RIPK1 promote DEN-induced hepatocarcinogenesis.
13 HCC of F344 rats, genetically susceptible to hepatocarcinogenesis.
14 signaling, in this model of insulin-induced hepatocarcinogenesis.
15 mechanism for the androgen pathway in early hepatocarcinogenesis.
16 reconstruct the molecular etiology of human hepatocarcinogenesis.
17 roach to effectively inhibit insulin-induced hepatocarcinogenesis.
18 2; these processes appeared to contribute to hepatocarcinogenesis.
19 deregulation and diabetes mellitus in human hepatocarcinogenesis.
20 lopment of nonalcoholic steatohepatitis, and hepatocarcinogenesis.
21 parallels progressive stages of intranodular hepatocarcinogenesis.
22 el cellular target for combating HCV-induced hepatocarcinogenesis.
23 V X (HBx) gene, which has been implicated in hepatocarcinogenesis.
24 vated gene-1 (AEG-1) plays a seminal role in hepatocarcinogenesis.
25 nterrogated mechanisms of insulin-associated hepatocarcinogenesis.
26 increased RISC activity might contribute to hepatocarcinogenesis.
27 e (NAFLD) occurs and progresses sometimes to hepatocarcinogenesis.
28 liferation culminating in the development of hepatocarcinogenesis.
29 , thus revealing a potential role of SND1 in hepatocarcinogenesis.
30 dules suggesting that loss of MT accelerates hepatocarcinogenesis.
31 anism for control of hepatic cell growth and hepatocarcinogenesis.
32 atrix production, stem cell homeostasis, and hepatocarcinogenesis.
33 activation of ERK and AKT pathways in human hepatocarcinogenesis.
34 n expression has a more critical function in hepatocarcinogenesis.
35 lays important roles in liver physiology and hepatocarcinogenesis.
36 e occur at early stages of CDAA diet-induced hepatocarcinogenesis.
37 ntracellular signaling pathways during human hepatocarcinogenesis.
38 nt liver-specific miR-122 at early stages of hepatocarcinogenesis.
39 s acting as a weak oncogene or a cofactor in hepatocarcinogenesis.
40 t early stages of feeding CDAA diet promotes hepatocarcinogenesis.
41 ated liver cancer, significantly accelerates hepatocarcinogenesis.
42 with carcinogen, we examined the AR roles in hepatocarcinogenesis.
43 AzaC-treated HCC cells suggest their role in hepatocarcinogenesis.
44 f FXR in hepatoprotection and suppression of hepatocarcinogenesis.
45 e apoptosis determine and predict subsequent hepatocarcinogenesis.
46 than suppressed the early stages of chemical hepatocarcinogenesis.
47 ch also protected male mice from DEN-induced hepatocarcinogenesis.
48 iguing link between metabolic regulation and hepatocarcinogenesis.
49 arly stages of N-nitrosodiethylamine-induced hepatocarcinogenesis.
50 generation, induction of hepatotoxicity, and hepatocarcinogenesis.
51 C/EBPalpha in regulation of MT expression in hepatocarcinogenesis.
52 K1 were much less susceptible to DEN-induced hepatocarcinogenesis.
53 ceptible to diethylnitrosamine (DEN)-induced hepatocarcinogenesis.
54 initiate HCC and suggest novel mechanisms in hepatocarcinogenesis.
55 n of the IGF-I/ERK/MAPK pathway during human hepatocarcinogenesis.
56 e identified at an early dysplastic stage of hepatocarcinogenesis.
57 (EGFR) pathway during liver regeneration and hepatocarcinogenesis.
58 may shed additional light on the process of hepatocarcinogenesis.
59 -promoting signaling that may play a role in hepatocarcinogenesis.
60 gration, which may contribute importantly to hepatocarcinogenesis.
61 poietic-derived cells that promotes chemical hepatocarcinogenesis.
62 e contribution of HCV structural proteins to hepatocarcinogenesis.
63 us may play a key role in ethanol-associated hepatocarcinogenesis.
64 y and high levels of Se compounds suppressed hepatocarcinogenesis.
65 ting that these markers may reflect stepwise hepatocarcinogenesis.
66 gh shared steps in the multistage process of hepatocarcinogenesis.
67 ent in HCC and may play an important role in hepatocarcinogenesis.
68 ly methylated or amplified during multistage hepatocarcinogenesis.
69 ocellular carcinoma (HCC) in mouse models of hepatocarcinogenesis.
70 le mouse model may provide new insights into hepatocarcinogenesis.
71 ying an important role in the suppression of hepatocarcinogenesis.
72 e liver confers intrinsic resistance to AFB1 hepatocarcinogenesis.
73 ed for the high susceptibility of BR mice to hepatocarcinogenesis.
74 and HBV X protein (HBx) acts as cofactor in hepatocarcinogenesis.
75 oid insufficiency is an early event in human hepatocarcinogenesis.
76 proliferation and apoptosis increase during hepatocarcinogenesis.
77 dicates a reciprocal control of NQO genes in hepatocarcinogenesis.
78 es mellitus may suggest a common pathway for hepatocarcinogenesis.
79 useful model for studying the progression of hepatocarcinogenesis.
80 ryotyping, to be an initial episode in human hepatocarcinogenesis.
81 alcohol and to choline-deficiency models of hepatocarcinogenesis.
82 n using the folate/methyl-deficient model of hepatocarcinogenesis.
83 sis are operative but at different stages of hepatocarcinogenesis.
84 X protein-driven transgenic mouse models of hepatocarcinogenesis.
85 sm between MeIQx and c-myc overexpression in hepatocarcinogenesis.
86 thylation may be important in the process of hepatocarcinogenesis.
87 he pathogenesis of hepatic wound healing and hepatocarcinogenesis.
88 of TNFR1-mediated inflammation, resulting in hepatocarcinogenesis.
89 for preferential site of genetic changes in hepatocarcinogenesis.
90 ontribute to epigenetic dysregulation during hepatocarcinogenesis.
91 CD8(+) T lymphocytes, leading to accelerated hepatocarcinogenesis.
92 bile acid signaling, inhibits NAFLD-induced hepatocarcinogenesis.
93 quired for liver regeneration, survival, and hepatocarcinogenesis.
94 abolism, as well as promotes cell growth and hepatocarcinogenesis.
95 EBP1, significantly delayed, AKT/Ras-induced hepatocarcinogenesis.
96 wo oncogenes and other molecules involved in hepatocarcinogenesis.
97 g as a highly oncogenic driver mechanism for hepatocarcinogenesis.
98 ) and diethylnitrosamine (DEN)-induced mouse hepatocarcinogenesis.
99 ays a critical role in viral replication and hepatocarcinogenesis.
100 odel enables the dissection of all stages of hepatocarcinogenesis.
101 ak is required for c-Met/beta-catenin-driven hepatocarcinogenesis.
102 cin and 4EBP1A4 completely inhibited AKT/Ras hepatocarcinogenesis.
103 exhibits important yet opposing functions in hepatocarcinogenesis.
104 iliary compartment and hepatocytes in murine hepatocarcinogenesis.
105 an, Meg-3, and Mirg, which are implicated in hepatocarcinogenesis.
106 molecular interplay between HSC biology and hepatocarcinogenesis.
107 nct roles and are both necessary for AKT/Ras hepatocarcinogenesis.
108 bed HOX genes deregulation to be involved in hepatocarcinogenesis.
109 f mice lacking the AEG-1 gene to DEN-induced hepatocarcinogenesis.
110 n as to why autophagy is required to promote hepatocarcinogenesis.
111 novel mechanistic insights into PB-mediated hepatocarcinogenesis.
112 aberrantly activated at the initial stage of hepatocarcinogenesis.
113 e, we further demonstrate that Gab2 mediates hepatocarcinogenesis.
114 s a central and ancestry-independent node of hepatocarcinogenesis.
115 53's ability to control tumor cell growth in hepatocarcinogenesis.
116 und in HCC occur in the very early stages of hepatocarcinogenesis.
117 of RXR and RXR/RAR that might contribute to hepatocarcinogenesis.
118 e (CCl(4)), and to dimethylnitrosamine (DEN) hepatocarcinogenesis; 2) the ductular "bipolar" progenit
120 ce our understanding of the role of AEG-1 in hepatocarcinogenesis, a transgenic mouse with hepatocyte
122 miRNAs have recently been implicated in hepatocarcinogenesis, although the actions and mechanism
124 e role of c-MYC as a master regulator during hepatocarcinogenesis and establish a new gatekeeper role
125 the notion that Dlc-1 protein is involved in hepatocarcinogenesis and has oncosuppressive activity in
126 cle, a mechanistic link between HBx-mediated hepatocarcinogenesis and host cell DNA replication remai
127 r the TAL-mediated branch of the PPP against hepatocarcinogenesis and identify NAC as a promising tre
129 ) is one of the major factors in HBV-induced hepatocarcinogenesis and is essential for the establishm
130 n performed to evaluate the role of SALL4 in hepatocarcinogenesis and its potential as a molecular ta
131 the incidence of diethylnitrosamine-induced hepatocarcinogenesis and malignant progression are suppr
132 contradiction underscores the complexity of hepatocarcinogenesis and predicts uncertainty in targeti
133 ral and molecular mechanisms responsible for hepatocarcinogenesis and should have substantial value f
134 targets implicate their role in NASH-induced hepatocarcinogenesis and suggest their use in the diagno
135 bserved during the early dysplastic stage of hepatocarcinogenesis and the stable deletions of chromos
136 V1 on human outcomes and experimental murine hepatocarcinogenesis and to elucidate its mechanism of a
137 del to scrutinize the molecular mechanism of hepatocarcinogenesis and to evaluate the efficacy of nov
138 al cross talks among multiple pathways along hepatocarcinogenesis and to test the therapeutic potenti
141 can provide insight into the role of HCV in hepatocarcinogenesis and, conversely, the effect of HCC
142 1q, 8p, 8q, and 17p occur as early events in hepatocarcinogenesis, and 12q, 17q25 and 20q occur as la
143 are resistant to diethylnitrosamine-induced hepatocarcinogenesis, and Akt2(-/-) mice display a high
145 el insights on the function of lncRNA-driven hepatocarcinogenesis, and paves the way for further inve
146 -1 is essential for NF-kappaB activation and hepatocarcinogenesis, and they reveal new roles for AEG-
147 ain insight into the molecular mechanisms of hepatocarcinogenesis, and to identify potential HCC mark
148 ibited, and to N-2-acetylaminofluorene (AAF) hepatocarcinogenesis; and 3) the putative periductular s
149 (miRNA) dysregulation in the early stages of hepatocarcinogenesis are hampered by the difficulty of d
152 ults established the iAST model of inducible hepatocarcinogenesis as a robust and versatile preclinic
153 nisms involved in obesity- and NAFLD-induced hepatocarcinogenesis as well as potential early markers
154 sed diethylnitrosamine-induced (DEN-induced) hepatocarcinogenesis, as an increased number of large tu
155 tools for models of cellular plasticity and hepatocarcinogenesis, as well as lines for use in cellul
156 f GCIP in mouse liver suppressed DEN-induced hepatocarcinogenesis at an early stage of tumor developm
157 ports the hypothesis that HBx contributes to hepatocarcinogenesis, at least in part, by promoting cha
158 with beta-catenin mutations contributing to hepatocarcinogenesis, AXIN1 and AXIN2 mutations appear t
159 tations were highly related to the step-wise hepatocarcinogenesis because mutations were identified i
160 the rates of chromosomal aberrations during hepatocarcinogenesis, but only telomerase-proficient mic
163 cooperation of AEG-1 and c-Myc in promoting hepatocarcinogenesis by analyzing hepatocyte-specific tr
164 a potential new marker for HCC and regulates hepatocarcinogenesis by directly targeting CDKN1A/p21 ex
165 Down-regulation of hSulf1 contributes to hepatocarcinogenesis by enhancing heparin-binding growth
167 fibrosis in the liver, but also to suppress hepatocarcinogenesis by inhibiting EGFR-dependent hepato
168 ively, these results show that NEMO prevents hepatocarcinogenesis by inhibiting RIPK1 kinase activity
169 F)-alpha dramatically enhances c-myc-induced hepatocarcinogenesis by promoting proliferation and surv
170 1 (PITX1) functions as a tumor suppressor in hepatocarcinogenesis by regulating the expression level
173 able to reduce HCC incidence; nevertheless, hepatocarcinogenesis can occur in the absence of active
174 ltahep) mice) exhibited a marked increase in hepatocarcinogenesis caused by diethylnitrosamine (DEN).
175 nsive chromosomal damage and acceleration of hepatocarcinogenesis characteristic for TGFalpha/c-myc m
176 displayed severely enhanced chemical-induced hepatocarcinogenesis compared with wild-type controls.
177 it results in the development of HCC tumors (hepatocarcinogenesis) concomitantly with liver cirrhosis
178 malignant transformation and progression in hepatocarcinogenesis, consequences of c-MYC activation f
179 ts considered immune tolerant indicated that hepatocarcinogenesis could be underway-even in patients
182 chemical (DEN treatment) and genetic-induced hepatocarcinogenesis (disruptions in LKB1, p53, MST1/2,
183 from animals modeling HBx- and HBV-mediated hepatocarcinogenesis, downregulation of chromatin regula
185 chanistic studies suggested that accelerated hepatocarcinogenesis driven by AKT and N-Ras resulted fr
186 arly and sensitive biomarker for TAA-induced hepatocarcinogenesis due to its consistent elevation dur
187 ges in hepatic gene expression that underlie hepatocarcinogenesis following hepatitis C virus (HCV) i
189 that the altered LAT1 expression observed in hepatocarcinogenesis gives cells a growth or survival ad
190 altered TA1 expression is an early event in hepatocarcinogenesis giving neoplastic cells a growth or
191 atocellular carcinoma (HCC), and spontaneous hepatocarcinogenesis has been observed in FXR-null mice.
192 ver, the contribution of these two routes to hepatocarcinogenesis has not been determined, partly bec
194 at in a rat model of inflammation-associated hepatocarcinogenesis, heterozygous deficiency of p53 res
195 We focus on the role of these pathways in hepatocarcinogenesis, how they are altered, and the cons
199 wn to be an effective inhibitor of aflatoxin hepatocarcinogenesis in animal models by blocking carcin
200 so suppressed spontaneous liver fibrosis and hepatocarcinogenesis in animals with hepatocyte-specific
201 s idea, we recently demonstrated that during hepatocarcinogenesis in c-myc/TGFalpha double transgenic
205 ther increased susceptibility to DEN-induced hepatocarcinogenesis in Ikkbeta(Deltahep) mice requires
206 vely studied the extent of liver disease and hepatocarcinogenesis in immunocompromised versus immunoc
209 stsurgical mechanisms that drive accelerated hepatocarcinogenesis in Mdr2(-/-) mice by perioperative
210 R-122 depletion facilitates cystogenesis and hepatocarcinogenesis in mice on DEN challenge by up-regu
211 ne expression patterns in liver cells during hepatocarcinogenesis in mice with homozygous, heterozygo
214 androgen receptor (AR) was increased during hepatocarcinogenesis in normal female or male mice, resp
215 ) is induced during early stages of chemical hepatocarcinogenesis in parenchymal cells of Fischer 344
216 t that rs738409 exerts a marked influence on hepatocarcinogenesis in patients with cirrhosis of Europ
218 first report addressing the role of a MMP in hepatocarcinogenesis in the corresponding genetic mouse
219 rm of Spry2 cooperates with c-Met to promote hepatocarcinogenesis in the mouse liver by sustaining pr
220 an approach to the study of the promotion of hepatocarcinogenesis in the presence of a transgene regu
221 events involved in the multistep process of hepatocarcinogenesis in the resistant-hepatocyte rat mod
222 xamined the relationship of gamma-OHPdG with hepatocarcinogenesis in two animal models and its potent
228 atitis B virus X protein (pX), implicated in hepatocarcinogenesis, induces DNA damage because of re-r
234 These findings suggest that MeIQx-induced hepatocarcinogenesis is associated with MeIQx-induced mu
235 Furthermore, the role of Bid in promoting hepatocarcinogenesis is in contrast to its reported role
237 chanisms of hepatitis B virus (HBV)-mediated hepatocarcinogenesis is needed to gain insights into the
244 genetic variants associated with HBV-related hepatocarcinogenesis may already play an important role
245 , experimental models of liver injury and of hepatocarcinogenesis may call forth a cellular response
246 The foci of the Solt-Farber experimental hepatocarcinogenesis model have identical morphological
247 approach has been applied to an experimental hepatocarcinogenesis model to discover early individual
249 of liver damage; in the case of HBsAg-driven hepatocarcinogenesis, NF-kappaB in hepatocytes acts as a
250 virus (HBV) X protein (pX) is implicated in hepatocarcinogenesis of chronic HBV patients by an unkno
251 virus (HBV) X protein (pX) is implicated in hepatocarcinogenesis of chronically infected HBV patient
253 ive stimulation and/or a growth advantage in hepatocarcinogenesis of woodchucks with chronic WHV infe
254 were linked to early genomic alterations in hepatocarcinogenesis, particularly gains of 1q and 8q.
255 esults demonstrate a direct role of HBV in a hepatocarcinogenesis pathway that involves the interacti
256 ignaling and Smad adaptor ELF suppress human hepatocarcinogenesis, potentially through cyclin D1 dere
257 rlying molecular mechanisms leading to human hepatocarcinogenesis, providing the scientific rationale
258 t sterilization restricted to late stages of hepatocarcinogenesis reduced HCC, suggesting that the in
259 ptible to spontaneous and chemically induced hepatocarcinogenesis relative to females of other inbred
266 ogenic pathway is significantly modulated in hepatocarcinogenesis, resulting in altered levels of glu
268 level increased in male liver tissues during hepatocarcinogenesis, starting from the precancerous sta
269 t therapy inhibits or delays immune-mediated hepatocarcinogenesis suggests that platelets may be key
271 tudy the transporter proteins in 2 models of hepatocarcinogenesis, the chemically induced Solt and Fa
272 ion links partial hepatectomy to accelerated hepatocarcinogenesis; this suggests a new therapeutic ap
273 1/PUMA-dependent apoptosis promotes chemical hepatocarcinogenesis through compensatory proliferation,
274 reduced the N-nitrosodiethylamine-initiated hepatocarcinogenesis to the levels of Cre-Ctrl mice.
276 quirement of lipogenesis in AKT/c-Met driven hepatocarcinogenesis using conditional Fatty Acid Syntha
277 e we examine androgen receptor (AR) roles in hepatocarcinogenesis using mice lacking AR in hepatocyte
278 ivation of the c-Met protooncogene to induce hepatocarcinogenesis via in vitro and in vivo approaches
279 stic dissection suggests that AR may promote hepatocarcinogenesis via increased cellular oxidative st
282 nexpectedly, however, liver regeneration and hepatocarcinogenesis was impaired in p21-deficient mice
286 n the diethylnitrosamine (DEN)-induced mouse hepatocarcinogenesis, we demonstrated that overexpressio
287 ution of additional Wnt pathway molecules to hepatocarcinogenesis, we examined beta-catenin, AXIN1 an
288 ole in hepatocyte growth, proliferation, and hepatocarcinogenesis, we generated transgenic mice with
289 urther understand the molecular mechanism of hepatocarcinogenesis, we have investigated the promoter
290 of mature TGF-beta1 from the early stages of hepatocarcinogenesis, we have now assessed whether impai
291 mediator of c-Met- and beta-catenin-induced hepatocarcinogenesis, we investigated the genetic intera
292 uppressor gene candidates relevant for human hepatocarcinogenesis, we performed genome-wide methylati
293 RNAs (miRNAs) that may have a causal role in hepatocarcinogenesis, we used an animal model in which C
294 investigate the involvement of this gene in hepatocarcinogenesis, we used several transgenic mouse m
296 act telomeres, p53 mutation had no effect on hepatocarcinogenesis, whereas in the setting of telomere
297 as up-regulated in the early stages of E2F-1 hepatocarcinogenesis, whereas p53 was overexpressed in t
298 tanding on the molecular mechanisms inducing hepatocarcinogenesis, which almost never occurs in healt
300 e proliferation and define a murine model of hepatocarcinogenesis with direct relevance to human HCC.
301 es 63 and 73 impedes inflammation-associated hepatocarcinogenesis, yet deleting c-Jun only in hepatoc
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