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1 atory liver and, if unchecked, for promoting hepatocarcinogenesis.
2 molecular interplay between HSC biology and hepatocarcinogenesis.
3 nct roles and are both necessary for AKT/Ras hepatocarcinogenesis.
4 bed HOX genes deregulation to be involved in hepatocarcinogenesis.
5 f mice lacking the AEG-1 gene to DEN-induced hepatocarcinogenesis.
6 novel mechanistic insights into PB-mediated hepatocarcinogenesis.
7 aberrantly activated at the initial stage of hepatocarcinogenesis.
8 s a central and ancestry-independent node of hepatocarcinogenesis.
9 53's ability to control tumor cell growth in hepatocarcinogenesis.
10 und in HCC occur in the very early stages of hepatocarcinogenesis.
11 of RXR and RXR/RAR that might contribute to hepatocarcinogenesis.
12 the immune response that could contribute to hepatocarcinogenesis.
13 y loss of SIRT6 possess oncogenic effects in hepatocarcinogenesis.
14 pa B (NF-kappaB) pathways that contribute to hepatocarcinogenesis.
15 he coagulation pathway to augment aggressive hepatocarcinogenesis.
16 ional and post-transcriptional regulation of hepatocarcinogenesis.
17 nt pathways in mediating AKT and Ras induced hepatocarcinogenesis.
18 /beta-catenin signaling that is critical for hepatocarcinogenesis.
19 icient mice after diethylnitrosamine-induced hepatocarcinogenesis.
20 HCC of F344 rats, genetically susceptible to hepatocarcinogenesis.
21 signaling, in this model of insulin-induced hepatocarcinogenesis.
22 mechanism for the androgen pathway in early hepatocarcinogenesis.
23 oles of CXCR6-dependent immune mechanisms in hepatocarcinogenesis.
24 roach to effectively inhibit insulin-induced hepatocarcinogenesis.
25 2; these processes appeared to contribute to hepatocarcinogenesis.
26 deregulation and diabetes mellitus in human hepatocarcinogenesis.
27 lopment of nonalcoholic steatohepatitis, and hepatocarcinogenesis.
28 parallels progressive stages of intranodular hepatocarcinogenesis.
29 el cellular target for combating HCV-induced hepatocarcinogenesis.
30 naling cascade is a key signaling pathway in hepatocarcinogenesis.
31 V X (HBx) gene, which has been implicated in hepatocarcinogenesis.
32 vated gene-1 (AEG-1) plays a seminal role in hepatocarcinogenesis.
33 nterrogated mechanisms of insulin-associated hepatocarcinogenesis.
34 increased RISC activity might contribute to hepatocarcinogenesis.
35 e (NAFLD) occurs and progresses sometimes to hepatocarcinogenesis.
36 r injury and intra-hepatic inflammation, and hepatocarcinogenesis.
37 liferation culminating in the development of hepatocarcinogenesis.
38 , thus revealing a potential role of SND1 in hepatocarcinogenesis.
39 dules suggesting that loss of MT accelerates hepatocarcinogenesis.
40 anism for control of hepatic cell growth and hepatocarcinogenesis.
41 dentified as pivotal for NASH and subsequent hepatocarcinogenesis.
42 atrix production, stem cell homeostasis, and hepatocarcinogenesis.
43 activation of ERK and AKT pathways in human hepatocarcinogenesis.
44 n expression has a more critical function in hepatocarcinogenesis.
45 lays important roles in liver physiology and hepatocarcinogenesis.
46 e occur at early stages of CDAA diet-induced hepatocarcinogenesis.
47 ntracellular signaling pathways during human hepatocarcinogenesis.
48 nt liver-specific miR-122 at early stages of hepatocarcinogenesis.
49 s acting as a weak oncogene or a cofactor in hepatocarcinogenesis.
50 t early stages of feeding CDAA diet promotes hepatocarcinogenesis.
51 with carcinogen, we examined the AR roles in hepatocarcinogenesis.
52 AzaC-treated HCC cells suggest their role in hepatocarcinogenesis.
53 f FXR in hepatoprotection and suppression of hepatocarcinogenesis.
54 correlated and can concur in the process of hepatocarcinogenesis.
55 than suppressed the early stages of chemical hepatocarcinogenesis.
56 ch also protected male mice from DEN-induced hepatocarcinogenesis.
57 iguing link between metabolic regulation and hepatocarcinogenesis.
58 arly stages of N-nitrosodiethylamine-induced hepatocarcinogenesis.
59 generation, induction of hepatotoxicity, and hepatocarcinogenesis.
60 s among these features, possibly involved in hepatocarcinogenesis.
61 C/EBPalpha in regulation of MT expression in hepatocarcinogenesis.
62 K1 were much less susceptible to DEN-induced hepatocarcinogenesis.
63 ceptible to diethylnitrosamine (DEN)-induced hepatocarcinogenesis.
64 initiate HCC and suggest novel mechanisms in hepatocarcinogenesis.
65 n of the IGF-I/ERK/MAPK pathway during human hepatocarcinogenesis.
66 e identified at an early dysplastic stage of hepatocarcinogenesis.
67 ponse, should be tested for their effects on hepatocarcinogenesis.
68 may shed additional light on the process of hepatocarcinogenesis.
69 -promoting signaling that may play a role in hepatocarcinogenesis.
70 gration, which may contribute importantly to hepatocarcinogenesis.
71 poietic-derived cells that promotes chemical hepatocarcinogenesis.
72 e contribution of HCV structural proteins to hepatocarcinogenesis.
73 us may play a key role in ethanol-associated hepatocarcinogenesis.
74 y and high levels of Se compounds suppressed hepatocarcinogenesis.
75 ting that these markers may reflect stepwise hepatocarcinogenesis.
76 gh shared steps in the multistage process of hepatocarcinogenesis.
77 ent in HCC and may play an important role in hepatocarcinogenesis.
78 ly methylated or amplified during multistage hepatocarcinogenesis.
79 ocellular carcinoma (HCC) in mouse models of hepatocarcinogenesis.
80 le mouse model may provide new insights into hepatocarcinogenesis.
81 ying an important role in the suppression of hepatocarcinogenesis.
82 e liver confers intrinsic resistance to AFB1 hepatocarcinogenesis.
83 ed for the high susceptibility of BR mice to hepatocarcinogenesis.
84 oid insufficiency is an early event in human hepatocarcinogenesis.
85 proliferation and apoptosis increase during hepatocarcinogenesis.
86 dicates a reciprocal control of NQO genes in hepatocarcinogenesis.
87 es mellitus may suggest a common pathway for hepatocarcinogenesis.
88 hepatocyte proliferation, thereby promoting hepatocarcinogenesis.
89 K2gamma antagonizes mTORC1 activation during hepatocarcinogenesis.
90 ational spectra (HRMS) during the process of hepatocarcinogenesis.
91 e apoptosis determine and predict subsequent hepatocarcinogenesis.
92 of TNFR1-mediated inflammation, resulting in hepatocarcinogenesis.
93 ays a critical role in viral replication and hepatocarcinogenesis.
94 n as to why autophagy is required to promote hepatocarcinogenesis.
95 e, we further demonstrate that Gab2 mediates hepatocarcinogenesis.
96 ression and protected against obese/diabetic hepatocarcinogenesis.
97 ein kinases II gamma isoform (CAMK2gamma) in hepatocarcinogenesis.
98 on in the context of the immune responses in hepatocarcinogenesis.
99 ndent functions of RIPK1 promote DEN-induced hepatocarcinogenesis.
100 reconstruct the molecular etiology of human hepatocarcinogenesis.
101 ated liver cancer, significantly accelerates hepatocarcinogenesis.
102 ew molecular mechanisms at play in Mongolian hepatocarcinogenesis.
103 (EGFR) pathway during liver regeneration and hepatocarcinogenesis.
104 and HBV X protein (HBx) acts as cofactor in hepatocarcinogenesis.
105 ar ATP and P2Y(2) receptors (P2Y(2)R) during hepatocarcinogenesis.
106 ontribute to epigenetic dysregulation during hepatocarcinogenesis.
107 CD8(+) T lymphocytes, leading to accelerated hepatocarcinogenesis.
108 bile acid signaling, inhibits NAFLD-induced hepatocarcinogenesis.
109 quired for liver regeneration, survival, and hepatocarcinogenesis.
110 abolism, as well as promotes cell growth and hepatocarcinogenesis.
111 EBP1, significantly delayed, AKT/Ras-induced hepatocarcinogenesis.
112 wo oncogenes and other molecules involved in hepatocarcinogenesis.
113 g as a highly oncogenic driver mechanism for hepatocarcinogenesis.
114 ) and diethylnitrosamine (DEN)-induced mouse hepatocarcinogenesis.
115 odel enables the dissection of all stages of hepatocarcinogenesis.
116 ak is required for c-Met/beta-catenin-driven hepatocarcinogenesis.
117 cin and 4EBP1A4 completely inhibited AKT/Ras hepatocarcinogenesis.
118 exhibits important yet opposing functions in hepatocarcinogenesis.
119 iliary compartment and hepatocytes in murine hepatocarcinogenesis.
120 an, Meg-3, and Mirg, which are implicated in hepatocarcinogenesis.
122 ce our understanding of the role of AEG-1 in hepatocarcinogenesis, a transgenic mouse with hepatocyte
124 miRNAs have recently been implicated in hepatocarcinogenesis, although the actions and mechanism
125 ted protein (YAP) plays an important role in hepatocarcinogenesis, although the potential role of YAP
127 e role of c-MYC as a master regulator during hepatocarcinogenesis and establish a new gatekeeper role
128 the notion that Dlc-1 protein is involved in hepatocarcinogenesis and has oncosuppressive activity in
129 cle, a mechanistic link between HBx-mediated hepatocarcinogenesis and host cell DNA replication remai
130 r the TAL-mediated branch of the PPP against hepatocarcinogenesis and identify NAC as a promising tre
132 ) is one of the major factors in HBV-induced hepatocarcinogenesis and is essential for the establishm
133 n performed to evaluate the role of SALL4 in hepatocarcinogenesis and its potential as a molecular ta
134 the incidence of diethylnitrosamine-induced hepatocarcinogenesis and malignant progression are suppr
135 contradiction underscores the complexity of hepatocarcinogenesis and predicts uncertainty in targeti
136 ral and molecular mechanisms responsible for hepatocarcinogenesis and should have substantial value f
137 targets implicate their role in NASH-induced hepatocarcinogenesis and suggest their use in the diagno
138 V1 on human outcomes and experimental murine hepatocarcinogenesis and to elucidate its mechanism of a
139 del to scrutinize the molecular mechanism of hepatocarcinogenesis and to evaluate the efficacy of nov
140 al cross talks among multiple pathways along hepatocarcinogenesis and to test the therapeutic potenti
143 can provide insight into the role of HCV in hepatocarcinogenesis and, conversely, the effect of HCC
145 1q, 8p, 8q, and 17p occur as early events in hepatocarcinogenesis, and 12q, 17q25 and 20q occur as la
146 are resistant to diethylnitrosamine-induced hepatocarcinogenesis, and Akt2(-/-) mice display a high
148 el insights on the function of lncRNA-driven hepatocarcinogenesis, and paves the way for further inve
149 removal of senescent hepatocytes to prevent hepatocarcinogenesis, and that this process required CXC
150 -1 is essential for NF-kappaB activation and hepatocarcinogenesis, and they reveal new roles for AEG-
151 ain insight into the molecular mechanisms of hepatocarcinogenesis, and to identify potential HCC mark
153 (miRNA) dysregulation in the early stages of hepatocarcinogenesis are hampered by the difficulty of d
157 ults established the iAST model of inducible hepatocarcinogenesis as a robust and versatile preclinic
158 nisms involved in obesity- and NAFLD-induced hepatocarcinogenesis as well as potential early markers
159 sed diethylnitrosamine-induced (DEN-induced) hepatocarcinogenesis, as an increased number of large tu
160 tools for models of cellular plasticity and hepatocarcinogenesis, as well as lines for use in cellul
161 f GCIP in mouse liver suppressed DEN-induced hepatocarcinogenesis at an early stage of tumor developm
162 ports the hypothesis that HBx contributes to hepatocarcinogenesis, at least in part, by promoting cha
163 with beta-catenin mutations contributing to hepatocarcinogenesis, AXIN1 and AXIN2 mutations appear t
164 tations were highly related to the step-wise hepatocarcinogenesis because mutations were identified i
165 the rates of chromosomal aberrations during hepatocarcinogenesis, but only telomerase-proficient mic
168 cooperation of AEG-1 and c-Myc in promoting hepatocarcinogenesis by analyzing hepatocyte-specific tr
169 a potential new marker for HCC and regulates hepatocarcinogenesis by directly targeting CDKN1A/p21 ex
170 Down-regulation of hSulf1 contributes to hepatocarcinogenesis by enhancing heparin-binding growth
172 fibrosis in the liver, but also to suppress hepatocarcinogenesis by inhibiting EGFR-dependent hepato
173 ively, these results show that NEMO prevents hepatocarcinogenesis by inhibiting RIPK1 kinase activity
174 1 (PITX1) functions as a tumor suppressor in hepatocarcinogenesis by regulating the expression level
176 able to reduce HCC incidence; nevertheless, hepatocarcinogenesis can occur in the absence of active
177 ltahep) mice) exhibited a marked increase in hepatocarcinogenesis caused by diethylnitrosamine (DEN).
178 displayed severely enhanced chemical-induced hepatocarcinogenesis compared with wild-type controls.
179 it results in the development of HCC tumors (hepatocarcinogenesis) concomitantly with liver cirrhosis
180 malignant transformation and progression in hepatocarcinogenesis, consequences of c-MYC activation f
181 ts considered immune tolerant indicated that hepatocarcinogenesis could be underway-even in patients
184 chemical (DEN treatment) and genetic-induced hepatocarcinogenesis (disruptions in LKB1, p53, MST1/2,
185 from animals modeling HBx- and HBV-mediated hepatocarcinogenesis, downregulation of chromatin regula
187 chanistic studies suggested that accelerated hepatocarcinogenesis driven by AKT and N-Ras resulted fr
188 arly and sensitive biomarker for TAA-induced hepatocarcinogenesis due to its consistent elevation dur
189 ges in hepatic gene expression that underlie hepatocarcinogenesis following hepatitis C virus (HCV) i
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
195 at in a rat model of inflammation-associated hepatocarcinogenesis, heterozygous deficiency of p53 res
196 We focus on the role of these pathways in hepatocarcinogenesis, how they are altered, and the cons
201 so suppressed spontaneous liver fibrosis and hepatocarcinogenesis in animals with hepatocyte-specific
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
215 androgen receptor (AR) was increased during hepatocarcinogenesis in normal female or male mice, resp
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 events involved in the multistep process of hepatocarcinogenesis in the resistant-hepatocyte rat mod
221 xamined the relationship of gamma-OHPdG with hepatocarcinogenesis in two animal models and its potent
226 atitis B virus X protein (pX), implicated in hepatocarcinogenesis, induces DNA damage because of re-r
232 Furthermore, the role of Bid in promoting hepatocarcinogenesis is in contrast to its reported role
234 chanisms of hepatitis B virus (HBV)-mediated hepatocarcinogenesis is needed to gain insights into the
240 NA binding protein that enhances MYC-induced hepatocarcinogenesis, is predictive of NELFE/MYC-driven
243 genetic variants associated with HBV-related hepatocarcinogenesis may already play an important role
244 The foci of the Solt-Farber experimental hepatocarcinogenesis model have identical morphological
245 approach has been applied to an experimental hepatocarcinogenesis model to discover early individual
247 of liver damage; in the case of HBsAg-driven hepatocarcinogenesis, NF-kappaB in hepatocytes acts as a
248 virus (HBV) X protein (pX) is implicated in hepatocarcinogenesis of chronically infected HBV patient
250 ive stimulation and/or a growth advantage in hepatocarcinogenesis of woodchucks with chronic WHV infe
252 were linked to early genomic alterations in hepatocarcinogenesis, particularly gains of 1q and 8q.
253 esults demonstrate a direct role of HBV in a hepatocarcinogenesis pathway that involves the interacti
254 ignaling and Smad adaptor ELF suppress human hepatocarcinogenesis, potentially through cyclin D1 dere
255 rlying molecular mechanisms leading to human hepatocarcinogenesis, providing the scientific rationale
256 t sterilization restricted to late stages of hepatocarcinogenesis reduced HCC, suggesting that the in
257 ptible to spontaneous and chemically induced hepatocarcinogenesis relative to females of other inbred
265 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 ion links partial hepatectomy to accelerated hepatocarcinogenesis; this suggests a new therapeutic ap
272 n of SPD protects against liver fibrosis and hepatocarcinogenesis through activation of microtubule a
273 1/PUMA-dependent apoptosis promotes chemical hepatocarcinogenesis through compensatory proliferation,
274 eta over-expression, thereby contributing to hepatocarcinogenesis through global transcriptional repr
275 reduced the N-nitrosodiethylamine-initiated hepatocarcinogenesis to the levels of Cre-Ctrl mice.
277 quirement of lipogenesis in AKT/c-Met driven hepatocarcinogenesis using conditional Fatty Acid Syntha
278 e we examine androgen receptor (AR) roles in hepatocarcinogenesis using mice lacking AR in hepatocyte
279 ivation of the c-Met protooncogene to induce hepatocarcinogenesis via in vitro and in vivo approaches
280 stic dissection suggests that AR may promote hepatocarcinogenesis via increased cellular oxidative st
283 nexpectedly, however, liver regeneration and hepatocarcinogenesis was impaired in p21-deficient mice
287 n the diethylnitrosamine (DEN)-induced mouse hepatocarcinogenesis, we demonstrated that overexpressio
288 ution of additional Wnt pathway molecules to hepatocarcinogenesis, we examined beta-catenin, AXIN1 an
289 ole in hepatocyte growth, proliferation, and hepatocarcinogenesis, we generated transgenic mice with
290 urther understand the molecular mechanism of hepatocarcinogenesis, we have investigated the promoter
292 mediator of c-Met- and beta-catenin-induced hepatocarcinogenesis, we investigated the genetic intera
293 uppressor gene candidates relevant for human hepatocarcinogenesis, we performed genome-wide methylati
294 RNAs (miRNAs) that may have a causal role in hepatocarcinogenesis, we used an animal model in which C
296 act telomeres, p53 mutation had no effect on hepatocarcinogenesis, whereas in the setting of telomere
297 tanding on the molecular mechanisms inducing hepatocarcinogenesis, which almost never occurs in healt
299 e proliferation and define a murine model of hepatocarcinogenesis with direct relevance to human HCC.
300 es 63 and 73 impedes inflammation-associated hepatocarcinogenesis, yet deleting c-Jun only in hepatoc