ライフサイエンスコーパス: HCC

1 HCCs detected by surveillance programs at an early stage

2 Between 2002 and 2013, 186 HCC patients underwent SLK-HCC and 3599 patients underwe

3 ng 60 clinical samples' RNA-seq data from 20 HCC patients, we have identified and characterized 8,603

4 ochemical analyses, in a training set of 228 HCC samples.

5 A total of 233 HCC cases were reported after 26,163 person-years of fol

6 Thirty-two HCC patients with 39 HCC lesions underwent mpMRI including diffusion-weighted

7 independent predictors of worse RFS, grade 4 HCC's (P < 0.0001, HR: 5.6), vascular invasion (P = 0.01

8 Of the 48 (61.5%) HCCs identified by surveillance, 43.8% were detected by

9 lly distinct sorafenib-resistant human Huh-7 HCC cell lines in order to identify new mechanisms to ab

10 present study, in vitro cell models using a HCC cell line, HepG2, and human endothelial cells, HUVEC

11 em factors associated with receipt of active HCC therapy and overall survival.

12 candidate therapeutic lead to treat advanced HCC.

13 iportal-type subclass represented 29% of all HCCs; expressed a hepatocyte nuclear factor 4A-driven ge

14 common among non-HCC malignancies than among HCCs for both readers (R1: 24 of 36 [66.7%] vs 13 of 124

15 We analyzed HCC samples from patients to determine if these inhibito

16 and Group BDLT, respectively; P = 0.407) and HCC recurrence rates (10.9% and 11.2% for Group LDLT and

17 correlated with elevated mTORC2 activity and HCC in human patients.

18 HCV infection is implicated in cirrhosis and HCC, but the molecular players and signaling pathways co

19 X/LPA in the causative link of cirrhosis and HCC.

20 ndidates with advanced renal dysfunction and HCC may be considered for SLK.

21 FIB-4 score is a better predictor of HD and HCC in HCV-positive persons.

22 mparison with control, uninfected livers and HCC, allowing us to identify pre-neoplastic epigenetic a

23 d the risk of decompensation, mortality, and HCC in a dose-dependent manner (P for trend <0.0001, <0.

24 e on rates of decompensation, mortality, and HCC in HBV-, HCV-, and alcohol-related cirrhosis.

25 e and risk of decompensation, mortality, and HCC were estimated.

26 esigned to systemically investigate the anti-HCC efficacy of WA.

27 d of patients with radiographically apparent HCC have non-AFP-producing tumors that have more favorab

28 HBV-associated cirrhosis and HBV-associated HCC groups.

29 d cirrhosis and ultimately to HBV-associated HCC.

30 cases show that patients with HCV-associated HCC can attain excellent responses to sorafenib treatmen

31 1.6; P = 0.043) and AFP greater than 400 at HCC diagnosis (HR, 3.0; P < 0.001) predicted HCC recurre

32 epatocyte precursor cells (which then become HCC cells that express progenitor cell markers), or to t

33 We characterized the association between HCC surveillance receipt and patient knowledge, attitude

34 not support a strong biological link between HCC and any of the investigated psychological variables.

35 LF from NASH), and hepatocellular carcinoma (HCC) (decreases in percentages of patients with HCC from

36 ic recurrent small hepatocellular carcinoma (HCC) against the diaphragmatic dome.

37 e of cirrhosis and hepatocellular carcinoma (HCC) and increasingly an indicator for liver transplanta

38 early detection of hepatocellular carcinoma (HCC) and prolongs survival.

39 arcinoma (ICC) and hepatocellular carcinoma (HCC) are clinically disparate primary liver cancers with

40 Patients with hepatocellular carcinoma (HCC) can receive Model for End-Stage Liver Disease (MELD

41 shown to attenuate hepatocellular carcinoma (HCC) development, thus implicating ATX/LPA in the causat

42 veloping recurrent hepatocellular carcinoma (HCC) following liver transplantation (LT).

43 ltrasonography for hepatocellular carcinoma (HCC) for individuals with cirrhosis is recommended.

44 b in patients with hepatocellular carcinoma (HCC) has been undervalued due to the absence of complete

45 n events and human hepatocellular carcinoma (HCC) has generated controversy about the causal or incid

46 e and mortality of hepatocellular carcinoma (HCC) have been reported to be plateauing in the United S

47 FAM83H and MYC in hepatocellular carcinoma (HCC) have been reported.

48 ansposase leads to hepatocellular carcinoma (HCC) in mice that corresponds to around 10% of human HCC

49 reases the risk of hepatocellular carcinoma (HCC) in patients with chronic HBV and HCV infection.

50 asive diagnosis of hepatocellular carcinoma (HCC) in patients with cirrhosis.

51 ere is a change of hepatocellular carcinoma (HCC) incidence in chronic hepatitis B patients under lon

52 Hepatocellular carcinoma (HCC) is a common cancer that frequently overexpresses th

53 Hepatocellular carcinoma (HCC) is more prevalent in men than women, but the reason

54 Hepatocellular carcinoma (HCC) is one of the most commonly diagnosed cancers in th

55 Hepatocellular carcinoma (HCC) is the second leading cause of cancer related-death

56 Hepatocellular carcinoma (HCC) is the second-leading cause of cancer-related death

57 Hepatocellular carcinoma (HCC) is the third leading form of cancer worldwide, and

58 Hepatocellular carcinoma (HCC) is the third most deadly cancer in the US, with a m

59 Hepatocellular carcinoma (HCC) occurs more frequently and aggressively in men than

60 from patients with hepatocellular carcinoma (HCC) on tumors samples and their corresponding non-tumor

61 ansplantable (R&T) hepatocellular carcinoma (HCC) patients, to try to obviate upfront liver transplan

62 common feature of hepatocellular carcinoma (HCC) progression.

63 ted with increased hepatocellular carcinoma (HCC) recurrence after liver transplantation (LT), but no

64 l therapy (LRT) on hepatocellular carcinoma (HCC) recurrence and survival after liver transplantation

65 Hepatocellular carcinoma (HCC) represents the fifth-most common form of cancer wor

66 242 patients with hepatocellular carcinoma (HCC) to search for gene signatures associated with chrom

67 operable localized hepatocellular carcinoma (HCC) who are eligible for both SBRT and RFA.

68 ts with inoperable hepatocellular carcinoma (HCC) who are ineligible for thermal ablative techniques.

69 e in patients with hepatocellular carcinoma (HCC) who meet Milan criteria by imaging and underwent LT

70 ith advanced-stage hepatocellular carcinoma (HCC) with portal vein thrombosis (PVT) treated with (90)

71 R4 by FGF19 drives hepatocellular carcinoma (HCC), a disease with few, if any, effective treatment op

72 ce that cells from hepatocellular carcinoma (HCC), a highly metastatic cancer, undergo epithelial to

73 Hepatocellular carcinoma (HCC), a primary malignancy of the liver, is the second l

74 risk of cirrhosis, hepatocellular carcinoma (HCC), and CHB-associated mortality.

75 in poor prognosis hepatocellular carcinoma (HCC), often associated with chronic hepatitis B virus (H

76 ents with advanced hepatocellular carcinoma (HCC), the multikinase inhibitor sorafenib is the only sy

77 cancer, including hepatocellular carcinoma (HCC).

78 at WL was >/=15 or hepatocellular carcinoma (HCC).

79 factors for human hepatocellular carcinoma (HCC).

80 size and suppress hepatocellular carcinoma (HCC).

81 s) predisposing to hepatocellular carcinoma (HCC).

82 atment of advanced hepatocellular carcinoma (HCC).

83 and progression of hepatocellular carcinoma (HCC).

84 undergoing LT for hepatocellular carcinoma (HCC).

85 e of cirrhosis and hepatocellular carcinoma (HCC).

86 s of patients with hepatocellular carcinoma (HCC).

87 cancers, including hepatocellular carcinoma (HCC).

88 sis progressing to hepatocellular carcinoma (HCC).

89 as an oncogene in hepatocellular carcinoma (HCC).

90 More than 80% of hepatocellular carcinomas (HCCs) develop in fibrotic or cirrhotic livers, suggestin

91 Hepatocellular carcinomas (HCCs) exhibit a diversity of molecular phenotypes, raisi

92 l distribution of hepatocellular carcinomas (HCCs) is dominated by its incidence in developing countr

93 Human hepatocellular carcinomas (HCCs), which arise on a background of chronic liver dama

94 We collected HCC samples from 59 patients who underwent surgical rese

95 huge protein), the histone cleavage complex (HCC), and a subset of polyadenylation factors including

96 Males are 8 times more likely to develop HCC than females, an effect largely driven by sex hormon

97 thout HBV or HCV infection, only 6 developed HCC or died from liver-related disease.

98 25 patients developed HCC with total follow-up of 1,363 person-years.

99 lignant liver disease at risk for developing HCC (P < 0.0001).

100 IL-6/STAT3 axis in potentiating FGF19-driven HCC in mice, a finding which may have translational rele

101 evaluated, their application to FGF19-driven HCC may be limited by dose-limiting toxicities mediated

102 ed patients had a higher proportion of early HCC (70.2% vs. 40.0%; P = 0.009), with no difference in

103 gin were corroborated by lower than expected HCC recurrence, suggesting that tumor sizes at the margi

104 evaluated the ratio of observed to expected HCC recurrence by tumor size.

105 hanges similar to those detected in human FL-HCC, which included genes that affect cell cycle and mit

106 umors in mice that closely resemble human FL-HCC.

107 activity of DNAJB1-PRKACA, implying that FL-HCC does not simply result from enhanced PRKACA expressi

108 en repeatedly identified in patients with FL-HCC.

109 ltivariate predictors of mortality following HCC recurrence were identified to develop a risk score m

110 956 for CCA stage I-II versus PSC, 0.904 for HCC versus control, and 0.894 for intrahepatic CCA versu

111 3B-6527 as a candidate therapeutic agent for HCC cases that exhibit increased expression of FGF19.

112 inhibitor provides a promising candidate for HCC targeted therapy because Pin1 is overexpressed in mo

113 that STAT3 in hepatocytes is dispensable for HCC formation when mammalian sterile 20-like kinase 1 an

114 icles might be a promising targeted drug for HCC therapy as PLLA is biocompatible, biodegradable and

115 ive cohort study of adults undergoing LT for HCC between January 2001 and December 2012.

116 eating a healthy diet precluded the need for HCC surveillance, and 34.0% believed that HCC surveillan

117 th those listed with 22 exception points for HCC (HCC22) to determine the LABMELD for which statistic

118 her molecules increased predictive power for HCC incidence.

119 months) wait times and an increased risk for HCC recurrence post-LT.

120 blished to determine the individual risk for HCC recurrence.

121 offering a potential therapeutic target for HCC.

122 2 might be a powerful therapeutic target for HCC.

123 and offer promising therapeutic targets for HCC and other cancers.

124 pecificity and positive predictive value for HCC (R1, two fewer false-positive findings).

125 ower vascular transit time were observed for HCCs (P < 0.05).

126 independently associated with more frequent HCC development beyond year 5 in multivariable analysis.

127 r needed to screen to prevent one death from HCC of 77.

128 Primary and rare high-grade HCC developed in a genetic mouse model.

129 Inclusion criteria were patients who had HCC with tumor PVT.

130 transplantation after stratification by HALT-HCC score with a cutoff of 17; conversely, among the 963

131 ort, prognosis worsened with increasing HALT-HCC score (5-year overall survival of 78.7% [95% CI 76.9

132 models closely recapitulated advanced human HCC and displayed a striking acquisition of CC-related p

133 LXRalpha pathway was also observed in human HCC cell lines and datasets.

134 However, the role of this cascade in human HCC remains unclear.

135 fficacy and cytotoxicity to a range of human HCC cells as well as healthy human hepatocytes.

136 mice that corresponds to around 10% of human HCC.

137 e expression and role of FAM83H in 163 human HCCs and further investigated the relationship between F

138 e identified a critical role of SNHG6-003 in HCC.

139 ns as an endogenous sponge for miR-141-3p in HCC.

140 sorafenib with the MEK inhibitor AZD6244 in HCC.

141 eatment shown to provide survival benefit in HCC patients progressing on sorafenib treatment.

142 Dendritic cells, monocytes, and B cells in HCC tumors expressed ligands for these receptors.

143 m all 50 states to better analyze changes in HCC incidence in the entire United States.

144 y understood mechanism of chemoresistance in HCC.

145 on to overcome sorafenib treatment escape in HCC.

146 rtantly, NOX4 gene deletions are frequent in HCC patients, correlating with higher tumour grade.

147 ne of the most frequently amplified genes in HCC patients.

148 m EV concentration was found to be higher in HCC than in all the other groups.

149 HCC from HCV or ALD and a small increase in HCC among persons with NASH).

150 of embolotherapy and autophagy inhibition in HCC.

151 ycolytic metabolism influences metastasis in HCC remains unclear.

152 ng which may have translational relevance in HCC pathogenesis.

153 nism underlying the involvement of RPS15A in HCC pathogenesis and the clinical significance of RPS15A

154 s a novel mechanism for the GOF of p53-RS in HCC.

155 le cancer-driving pathways simultaneously in HCC cells.

156 e identified a mechanism for acquiring SR in HCC that is through the aberrant expression of the TYRO3

157 ), which is associated with poor survival in HCC and interleukin-6 (IL6) expression.

158 well as new potential therapeutic targets in HCC.

159 activation occurs after sorafenib therapy in HCC, and if so, if it impacts the therapeutic efficacy.

160 PRS did not explain variance in HCC.

161 ty, called CIN25 and CIN70, were detected in HCCs from patients with shorter survival time or early c

162 ibitory pathways prevent T-cell responses in HCCs and to find ways to restore their antitumor functio

163 Each individual HCC line had a significantly higher percentage of exogen

164 cts against diethylnitrosamine (DEN)-induced HCCs, whereas liver-specific c-Fos expression leads to r

165 HDAC2 restored FBP1 expression and inhibited HCC cell growth.

166 It also effectively inhibited HCC development in the diethylnitrosamine-injected mice.

167 r initial treatment of localized, inoperable HCC is not cost-effective.

168 ave been proposed to transform directly into HCC cells (via a sequence of genetic alterations), to de

169 ognostic importance of treating intrahepatic HCC even in patients with metastatic disease.

170 mpMRI features is promising for non-invasive HCC characterization on the imaging, histologic and geno

171 r 5 represent the main risk factors for late HCC development.

172 ermine possible factors associated with late HCC occurrence.

173 oped for patients with inoperable, localized HCC who were eligible for both RFA and SBRT to evaluate

174 diversity results obtained from Alb-R26(Met) HCC versus control livers to design an "educated guess"

175 o 18 months should be the target to minimize HCC recurrence.

176 herapy because Pin1 is overexpressed in most HCC and activates numerous cancer-driving pathways.

177 signaling components were expressed in most HCC cells, and activation of TGF-beta signaling promoted

178 ospective studies aimed at stratifying NAFLD-HCC risk.

179 rs641738 T allele was associated with NAFLD-HCC (OR 1.65, 1.08-2.55; n = 765), particularly in those

180 t, the rim pattern was more common among non-HCC malignancies than among HCCs for both readers (R1: 2

181 We show that nonproliferative HCCs preserve the zonation program that distributes meta

182 suppressed ROS production and the ability of HCC metastasis.

183 lusion IRE offers safe, complete ablation of HCC tumors in patients with contraindications to other c

184 ed between SLK-HCC and SLK in the absence of HCC (SLK-A) groups to reduce confounding.

185 In silico analyses of HCC, utilizing published profiling studies showed an inv

186 In an analysis of HCC samples from 956 patients, we found almost 25% to ex

187 thways in stem cells as the primary cause of HCC initiation.

188 , 0.79; 95% CI, 0.71-0.89) within 30 days of HCC diagnosis, and review by a multidisciplinary tumor b

189 was to examine the risk and determinants of HCC in patients cured with DAA.

190 uld be used to study the gender disparity of HCC, we compared the difference of liver tumorigenesis b

191 irrhosis had the highest annual incidence of HCC after SVR (1.82 vs 0.34/100 person-years in patients

192 D feeding induced a much higher incidence of HCC in male mice with substantially increased intrahepat

193 inhibited growth, migration and invasion of HCC cells.

194 Patients demonstrated high levels of HCC-related knowledge (summary score, 77.7%); however, 4

195 uggesting that tumor sizes at the margins of HCC transplant criteria may be subject to inaccurate rep

196 erleukin-6 (IL-6), is a critical mediator of HCC development.

197 ger tumor regression in a xenograft model of HCC.

198 rachloro-1,4-bis(pyridyloxy)benzene model of HCC.

199 o 5 or higher that were highly predictive of HCC recurrence (C statistic, 0.77).

200 regression model to identify the presence of HCC-derived CTCs in nine of 16 (56%) untreated patients

201 which can be utilized for prioritization of HCC LT candidates.

202 Cumulative probabilities of HCC recurrence at 1 and 5 years were 5.7% and 12.8%, res

203 Gab2 mediates the pathologic progression of HCC by integrating multiple signaling pathways and sugge

204 elevant biomarker for predicting the risk of HCC and its recurrence.

205 Patients with SVR may still have a risk of HCC and need to be regularly monitored.

206 The associated risk of HCC in patients with SVR was 0.37 (0.22-0.63) for those

207 with a considerable reduction in the risk of HCC.

208 etabolic risk factors with increased risk of HCC; smoking has a significant effect on this associatio

209 We reviewed a sample of HCC patients for tumor size and stage at diagnosis.

210 R26(Met) tumors, characterizes a subgroup of HCC patients with poor prognosis.

211 sion of FAM83H predicted shorter survival of HCC patients.

212 Treatment of HCC cells with HDAC inhibitors or knockdown of HDAC1 and

213 otential for the prevention and treatment of HCC.

214 tor ATRA in the development and treatment of HCC.

215 s at 11q13 and 6p21 (in approximately 15% of HCCs).

216 As many as 40% of HCCs are clonal, with alteration of key tumor-suppressor

217 sequencing have led to the classification of HCCs based on molecular features and assigned them to ca

218 y enhanced the inhibitory potency of ATRA on HCC cell growth, improving IC50 by over 3-fold.

219 ck-down abolished ATRA inhibitory effects on HCC cells and ATRA-PLLA did not inhibit normal liver cel

220 nsights into the inhibitory effect of SFN on HCC tumor angiogenesis as well as tumor growth, and indi

221 Patients were followed until death or HCC diagnosis.

222 ptions, of which 245 (6%) had false-positive HCC.

223 inicopathologic predictors of posttransplant HCC recurrence, data on prognosis following recurrence a

224 HCC diagnosis (HR, 3.0; P < 0.001) predicted HCC recurrence in multivariable analysis.

225 or to Milan criteria (explant) in predicting HCC recurrence by the net reclassification index (P < .0

226 and that loss of KLF4 expression in primary HCC may contribute to activation of oncogenic TGF-beta s

227 ar features, which was absent in the primary HCC tumors.

228 nd any evidence to suggest that DAAs promote HCC.

229 ion of RAF dimers and ERK signaling promotes HCC cell survival, prevents apoptosis via downregulation

230 and Data System category 5 or biopsy-proven HCC and who were undergoing TAE were enrolled from Octob

231 TAZ to promote severe hepatomegaly and rapid HCC initiation and progression.

232 o groups with a total of 151 local recurrent HCC lesions abutting the diaphragm.

233 group A knockout mice and remarkably reduced HCC incidence in these mice to 14% from 100% in the cont

234 In multivariable Cox regression, HCC was not associated with post-LT survival among all p

235 PCR of genomic DNA isolated from HBV-related HCCs and HBV replicating cells, and examined DNA methyla

236 HBV-related HCCs expressing increased SALL4 exhibited demethylation

237 ALL4 expression in hepatitis C virus-related HCCs correlated with demethylation of these CpG sites.

238 rnational, multicenter cohort of R0 resected HCC patients were categorized by MC status at presentati

239 eutic to treat refractory and drug-resistant HCC.

240 viously established inducible and reversible HCC model - the kras(V12) transgenic zebrafish.

241 ity score matching was performed between SLK-HCC and SLK in the absence of HCC (SLK-A) groups to redu

242 002 and 2013, 186 HCC patients underwent SLK-HCC and 3599 patients underwent SLK-A.

243 y and economic technique for recurrent small HCC abutting the diaphragm, and both CT-RFA and L-RFA ar

244 esence of Globo H, SSEA-3 and SSEA-4 in some HCC tissues and their absence in normal liver was establ

245 These findings indicate that some HCCs might be susceptible to therapeutic agents designed

246 exist, including safety and risk-stratified HCC surveillance among patients who received long-term N

247 blocked PI3K/Akt/Mdm2 pathway and suppressed HCC cell survival.

248 In surgical HCC specimens from a cohort of 136 patients, PDGFRalpha

249 the SLT strategy's potential for cure in R&T HCC patients, and to identify predictors for its success

250 of dropout from all causes at 6 months in T1 HCC patients who underwent LRT was 5.3%, while in the ot

251 RT was 5.3%, while in the other series of T1 HCC patients who did not receive LRT, the dropout rate a

252 of 2.4 years and the progression rate to T2 HCC were 30% and 88%, respectively.

253 For adults with T2 HCC awaiting LT, transplant with any bridging therapy sh

254 or HCC surveillance, and 34.0% believed that HCC surveillance was not necessary if they had a normal

255 The HCC risk decreases beyond year 5 of ETV/TDF therapy in C

256 We therefore assessed the HCC incidence beyond year 5 of entecavir/tenofovir (ETV/

257 al of this study was to identify barriers to HCC surveillance, using data from the Veterans Health Ad

258 sed dramatically from normal to cirrhotic to HCC tissues from human patients.

259 as frequently been reported to contribute to HCC.

260 This ability of Erasin also extends to HCC-827 cells with acquired resistance against Erlotinib

261 uced MBOAT7 expression and may predispose to HCC in patients without cirrhosis, suggesting it should

262 thylnitrosamine-injected mice, both prone to HCC development.

263 ere observed for metastases in comparison to HCCs (P < 0.05).

264 natively, progenitor cells also give rise to HCCs and iCCAs with markers of progenitor cells.

265 Thirty-two HCC patients with 39 HCC lesions underwent mpMRI includi

266 s and harms in cirrhosis patients undergoing HCC surveillance.

267 Using HCC cell lines, we found that short hairpin RNA-mediated

268 ntrol, and 0.894 for intrahepatic CCA versus HCC.

269 ne at 152 sites in 21 countries, adults with HCC who tolerated sorafenib (>/=400 mg/day for >/=20 of

270 versity transplant center of 665 adults with HCC who underwent an LT during the period from 1989 to 2

271 ort, baseline sICAM-1 MFI is associated with HCC incidence.

272 on recurrence, and it may be associated with HCC recurrence after liver transplantation.

273 erformed to identify factors associated with HCC surveillance receipt during the 12-month period prec

274 ional lncRNAs and biomarkers associated with HCC tumorigenesis and metastasis.

275 ing RNAs (lncRNAs) have been associated with HCC, but a comprehensive analysis of their specific asso

276 analysis of their specific association with HCC metastasis has not been conducted.

277 nt increase and consistently correlated with HCC development in all three animal models.

278 ipients data to compare patients listed with HCC who received exception points versus patients listed

279 We compared advanced stage patients with HCC (American Joint Committee on Cancer stage III/IV) wh

280 serum cytokine profiles of 411 patients with HCC (n = 102: 32% HBV, 54% HCV, 14% non-viral) and witho

281 fered as first-line therapy to patients with HCC and well-compensated cirrhosis instead of primary LT

282 Records from 861 cirrhotic patients with HCC consecutively listed for either LDLT (n = 79) or BDL

283 ) (decreases in percentages of patients with HCC from HCV or ALD and a small increase in HCC among pe

284 of antiviral treatment for HCV patients with HCC or DCC relative to LT is an important area of clinic

285 ategy for the treatment of HCV patients with HCC or DCC waitlisted for LT.

286 tal of 417 and 235 consecutive patients with HCC underwent RS and TACE MWA, respectively.

287 in nine of 16 (56%) untreated patients with HCC versus one of 31 (3%) patients with nonmalignant liv

288 y and safety of regorafenib in patients with HCC who have progressed during sorafenib treatment.

289 e untreated) to advanced stage patients with HCC who received no therapy (control).

290 database was used to identify patients with HCC who underwent liver transplantation between 2002 and

291 as to compare outcomes between patients with HCC who underwent SLK and those who received SLK for oth

292 ss of LRT in the management of patients with HCC who were on the LT waitlist.

293 d well-tolerated treatment for patients with HCC; it is highly effective and may be more effective th

294 8 patients listed for liver transplants with HCC exception points from 2006 to 2013, 9,168 of whom we

295 Data on the outcomes for patients with HCCs that do not produce AFP are limited.

296 uish cirrhotic HBV patients with and without HCC (AUC 0.503) or HCV patients with and without HCC (AU

297 (AUC 0.503) or HCV patients with and without HCC (AUC 0.63).

298 32% HBV, 54% HCV, 14% non-viral) and without HCC (n = 309: 39% HBV, 39% HCV, 22% non-viral).

299 s with HBV or HCV infection, with or without HCC, have distinctly different cytokine profiles, sugges

300 ucasian chronic hepatitis B patients without HCC at baseline who received ETV/TDF for >/=1 year.

301 h beta-catenin mutants (S33Y, S45Y) to yield HCC in mice.