ライフサイエンスコーパス: hepatocellular

1 of the present study was to investigate the hepatocellular activation of c-Jun and STAT3 by Schistos

2 Hepatocellular activation of c-Jun was demonstrated by n

3 t can lead to steatohepatitis and a risk for hepatocellular adenoma or carcinoma.

4 Background Hepatocellular adenomas (HCAs) are rare benign liver tum

5 lular adenomas, new lesions occurred only in hepatocellular adenomas at risk of progression.

6 th hepatic nuclear factor 1alpha-inactivated hepatocellular adenomas being the most common subtype sh

7 n Long-term MRI follow-up showed that 78% of hepatocellular adenomas had long-term stability or regre

8 Patients with multiple hepatocellular adenomas were more likely to show progres

9 After resection of solitary hepatocellular adenomas, new lesions occurred only in he

10 included a cholangiocarcinoma and a combined hepatocellular and cholangiocarcinoma.

11 rimary contributors to fibrosis in models of hepatocellular and cholestatic injury.

12 rvical, brain, breast, prostate, pancreatic, hepatocellular, and other tumors.

13 ar improved steatosis, lobular inflammation, hepatocellular ballooning and fibrosis stage.

14 ral agents (DAAs) holds promise for reducing hepatocellular cancer (HCC).

15 This strategy is particularly relevant to hepatocellular cancer, which is treated clinically with

16 tage liver diseases, including cirrhosis and hepatocellular cancer.

17 pathways and/or intermediate stages, such as hepatocellular cancer.

18 up-regulation of glucose metabolism to favor hepatocellular carcinogenesis (HCC), but the upstream si

19 ed evidence that schistosomiasis can promote hepatocellular carcinogenesis.

20 included colorectal liver metastases (69%), hepatocellular carcinoma (18%), non-colorectal liver met

21 ard ratio [HR], 0.40 [95% CI, 0.28-0.56) and hepatocellular carcinoma (20 studies, n = 84 491; pooled

22 t (J-C), becomes the driver of fibrolamellar hepatocellular carcinoma (FL-HCC).

23 ts undergoing liver transplantation (LT) for hepatocellular carcinoma (HCC) (exploratory analysis of

24 becular-massive" (MTM) histologic subtype of hepatocellular carcinoma (HCC) (MTM-HCC) represents an a

25 iver complication -hepatic decompensation or hepatocellular carcinoma (HCC) - or requiring liver tran

26 e principal histologic type of liver cancer, hepatocellular carcinoma (HCC) accounts for the great ma

27 e are conflicting data regarding the risk of hepatocellular carcinoma (HCC) after direct-acting antiv

28 e algorithm (TRA) is used to assess presumed hepatocellular carcinoma (HCC) after local-regional ther

29 Early recurrence of hepatocellular carcinoma (HCC) after surgical resection

30 HCV) and advanced fibrosis remain at risk of hepatocellular carcinoma (HCC) after sustained viral res

31 etabolic traits on the risk of cirrhosis and hepatocellular carcinoma (HCC) among patients with NAFLD

32 re 87.1%, 71.8%, and 62.8% for patients with hepatocellular carcinoma (HCC) and 87.5%, 70.0% and 70.0

33 Hepatobiliary cancers which include hepatocellular carcinoma (HCC) and biliary tract cancers

34 management of primary liver cancers such as hepatocellular carcinoma (HCC) and cholangiocarcinoma (C

35 e examined incidence rates for cirrhosis and hepatocellular carcinoma (HCC) and conducted cause-speci

36 ate that MTR4 is frequently overexpressed in hepatocellular carcinoma (HCC) and is an independent dia

37 l vein thrombosis (PVT) occurs frequently in hepatocellular carcinoma (HCC) and is often diagnosed in

38 patients based on the level of suspicion for hepatocellular carcinoma (HCC) and overall malignancy.

39 Median survival in patients with hepatocellular carcinoma (HCC) and portal vein tumor thr

40 al characteristics of ESLD from cirrhosis or hepatocellular carcinoma (HCC) and the performance of as

41 rly 80% of cirrhotic patients diagnosed with hepatocellular carcinoma (HCC) are not eligible for surg

42 Prevention and treatment options for hepatocellular carcinoma (HCC) are presently limited, un

43 isk-stratification systems for patients with hepatocellular carcinoma (HCC) are required to improve t

44 ioembolization (yttrium-90 [Y90]) is used in hepatocellular carcinoma (HCC) as a bridging as well as

45 w the applicability of our approach, we used hepatocellular carcinoma (HCC) as a model system.

46 th chronic liver disease have lower rates of hepatocellular carcinoma (HCC) as compared to men; it is

47 er transarterial chemoembolization (TACE) in hepatocellular carcinoma (HCC) because of the potential

48 cation is extremely complex in patients with hepatocellular carcinoma (HCC) because this neoplasm ari

49 splant (LT) prioritization for patients with hepatocellular carcinoma (HCC) beyond Milan Criteria (MC

50 rates according to screening guidelines for hepatocellular carcinoma (HCC) by OcC and OvC status.

51 from healthy and HBV-infected donors toward hepatocellular carcinoma (HCC) cells containing integrat

52 Here we show that activated AKT in human hepatocellular carcinoma (HCC) cells phosphorylates cyto

53 We examined hepatocellular carcinoma (HCC) development in alcohol We

54 s with normal liver function and facilitates hepatocellular carcinoma (HCC) development, representing

55 ase SULF2 has been associated with increased hepatocellular carcinoma (HCC) growth and poor patient s

56 There are limited data on hepatocellular carcinoma (HCC) growth patterns, particul

57 eached epidemic proportions and in parallel, hepatocellular carcinoma (HCC) has become one of the fas

58 Among them, an increased risk of hepatocellular carcinoma (HCC) has been registered.

59 Hepatocellular carcinoma (HCC) has high relapse and low

60 To date, genomic analyses of hepatocellular carcinoma (HCC) have been limited to earl

61 t of HIV infection on the risk of developing hepatocellular carcinoma (HCC) in HCV-infected patients

62 association between diabetes and the risk of hepatocellular carcinoma (HCC) in NASH patients with cir

63 Genetic factors and steatosis predispose to hepatocellular carcinoma (HCC) in patients with chronic

64 C virus (HCV) infection is the main cause of hepatocellular carcinoma (HCC) in the United States (US)

65 viral infections are major risk factors for hepatocellular carcinoma (HCC) in the United States and

66 Mongolia has the highest incidence of hepatocellular carcinoma (HCC) in the world, but its cau

67 critical role in liver tissue damage and in hepatocellular carcinoma (HCC) initiation and progressio

68 CSCs) are considered as main players for the hepatocellular carcinoma (HCC) initiation, metastasis, d

69 Hepatocellular carcinoma (HCC) is a liver tumor that usu

70 Hepatocellular carcinoma (HCC) is a most deadly malignan

71 Hepatocellular carcinoma (HCC) is an aggressive malignan

72 Hepatocellular carcinoma (HCC) is an increasingly common

73 Hepatocellular carcinoma (HCC) is clearly age-related an

74 Hepatocellular carcinoma (HCC) is difficult to detect, c

75 ions in cancer driver genes in patients with hepatocellular carcinoma (HCC) is highly diverse, which

76 The molecular background of hepatocellular carcinoma (HCC) is highly heterogeneous,

77 The risk for hepatocellular carcinoma (HCC) is increased in acute hep

78 Hepatocellular carcinoma (HCC) is one of most common can

79 The pathogenesis of hepatocellular carcinoma (HCC) is poorly understood, but

80 Hepatocellular carcinoma (HCC) is the fourth leading cau

81 Hepatocellular carcinoma (HCC) is the most common cause

82 Hepatocellular carcinoma (HCC) is the most common form o

83 Hepatocellular carcinoma (HCC) is the most common primar

84 Hepatocellular carcinoma (HCC) is the second most common

85 Hepatocellular carcinoma (HCC) is the sixth most common

86 Hepatocellular carcinoma (HCC) is the third most frequen

87 in patients with hepatitis C virus (HCV) and hepatocellular carcinoma (HCC) listed for liver transpla

88 associated with the overall survival (OS) of hepatocellular carcinoma (HCC) patients treated with tra

89 rapy (LRT) in a large, multicenter cohort of hepatocellular carcinoma (HCC) patients undergoing liver

90 on between mouse liver development and human hepatocellular carcinoma (HCC) proteomic profiles reveal

91 ce after transarterial embolization (TAE) of hepatocellular carcinoma (HCC) provides a compelling cli

92 Currently, no surveillance guidelines for hepatocellular carcinoma (HCC) recurrence after liver tr

93 Sorafenib (SOR) is currently used for hepatocellular carcinoma (HCC) recurring after liver tra

94 ht and sex on liver transplantation (LT) for hepatocellular carcinoma (HCC) remains unclear.

95 Hepatocellular carcinoma (HCC) represents the sixth most

96 Hepatocellular carcinoma (HCC) surveillance is associate

97 Hepatocellular carcinoma (HCC) surveillance is associate

98 PRMT6) regulates aerobic glycolysis in human hepatocellular carcinoma (HCC) through nuclear relocaliz

99 itional expression of MYC and Twist1 enables hepatocellular carcinoma (HCC) to metastasize in >90% of

100 LT) in patients who achieved down-staging of hepatocellular carcinoma (HCC) to Milan criteria.

101 ath and the resulting cell debris stimulates hepatocellular carcinoma (HCC) tumor growth via an "eico

102 atitis B virus (HBV) is the leading cause of hepatocellular carcinoma (HCC) worldwide.

103 sion and negatively with Keap1 expression in hepatocellular carcinoma (HCC) xenografts and specimens.

104 ression plays key roles in tumors, including hepatocellular carcinoma (HCC), a malignancy with no eff

105 arkers in human alcoholic hepatitis (AH) and hepatocellular carcinoma (HCC), and mouse liver tumor in

106 n about the mutational landscape of advanced hepatocellular carcinoma (HCC), and predictive biomarker

107 Owing to the marked sexual dimorphism of hepatocellular carcinoma (HCC), sex hormone receptor sig

108 Hepatocellular carcinoma (HCC), the most common type of

109 pite significant progression in the study of hepatocellular carcinoma (HCC), the role of the proteaso

110 , this difference is predominantly driven by hepatocellular carcinoma (HCC), which accounts for 75% o

111 r recurrence after liver transplantation for hepatocellular carcinoma (HCC), with and without hypothe

112 liver complication-hepatic decompensation or hepatocellular carcinoma (HCC)-or requiring liver transp

113 We report a covalent chemistry-based hepatocellular carcinoma (HCC)-specific extracellular ve

114 ral major factors limit our understanding of hepatocellular carcinoma (HCC).

115 proposed to contribute to the progression of hepatocellular carcinoma (HCC).

116 r disease which often leads to cirrhosis and hepatocellular carcinoma (HCC).

117 h a greater risk of liver cirrhosis (LC) and hepatocellular carcinoma (HCC).

118 are deregulated in disease states, including hepatocellular carcinoma (HCC).

119 ha (ERalpha) might impact the progression of hepatocellular carcinoma (HCC).

120 RT) over sorafenib in patients with advanced hepatocellular carcinoma (HCC).

121 ncreased fibrosis staging and development of hepatocellular carcinoma (HCC).

122 rate during compensatory regeneration and in hepatocellular carcinoma (HCC).

123 o rescue (FTR) following liver resection for hepatocellular carcinoma (HCC).

124 n relation to the morbidity in patients with hepatocellular carcinoma (HCC).

125 granted to liver transplant candidates with hepatocellular carcinoma (HCC).

126 disease influences the risk of cirrhosis and hepatocellular carcinoma (HCC).

127 (HBV)-the major cause of liver cirrhosis and hepatocellular carcinoma (HCC).

128 ction is one of the major causal factors for hepatocellular carcinoma (HCC).

129 rease the risk of various cancers, including hepatocellular carcinoma (HCC).

130 adioembolization (TARE) in participants with hepatocellular carcinoma (HCC).

131 down-regulated in human sorafenib-resistant hepatocellular carcinoma (HCC).

132 for developing alcohol-related cirrhosis and hepatocellular carcinoma (HCC).

133 liver cirrhosis, hepatic decompensation, and hepatocellular carcinoma (HCC).

134 H), potentially progressing to cirrhosis and hepatocellular carcinoma (HCC).

135 on a separate data set of 2369 patients with hepatocellular carcinoma (HCC).

136 inflammation to cirrhosis, liver failure or hepatocellular carcinoma (HCC).

137 utcomes after liver transplantation (LT) for hepatocellular carcinoma (HCC).

138 umerous malignancies including viral-derived hepatocellular carcinoma (HCC).

139 (lncRNAs) are often aberrantly expressed in Hepatocellular Carcinoma (HCC).

140 PRMT1 regulates the tumor immune response in hepatocellular carcinoma (HCC).

141 of liver transplants (LT) are performed for hepatocellular carcinoma (HCC).

142 is strongly overexpressed in mouse and human hepatocellular carcinoma (HCC).

143 plays a critical role in the progression of hepatocellular carcinoma (HCC).

144 nonalcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC).

145 ike phenotypes in diverse cancers, including hepatocellular carcinoma (HCC).

146 es and is associated with the development of hepatocellular carcinoma (HCC).

147 ciency virus (HIV) are at risk of developing hepatocellular carcinoma (HCC).

148 er injury is a risk factor for cirrhosis and hepatocellular carcinoma (HCC).

149 of liver function and a tumor suppressor in hepatocellular carcinoma (HCC).

150 ivating mutations of beta-catenin itself [in hepatocellular carcinoma (HCC)].

151 Here, we devise a strategy for targeting hepatocellular carcinoma (HCC, one of the deadliest mali

152 P < 0.001) and rather weak in patients with hepatocellular carcinoma (HR, 1.003; P = 0.038).

153 sed risks of cholangiocarcinoma (HR, 28.46), hepatocellular carcinoma (HR, 21.00), pancreatic cancer

154 ed to activate FXR both in mice and in human hepatocellular carcinoma (Huh-7) cells.

155 We analyzed primary hepatocellular carcinoma (n = 10) and metastatic gastroi

156 nt incidentally detected second tumours were hepatocellular carcinoma (nine patients, 20% of 45 incid

157 lication of process measures (i.e., rates of hepatocellular carcinoma [HCC] screening, endoscopic var

158 for end-stage liver disease (ESLD; including hepatocellular carcinoma [HCC]), non-acquired immunodefi

159 g-term risks for liver-related events (i.e., hepatocellular carcinoma [HCC], hepatic decompensation,

160 m can be used to predict viable or nonviable hepatocellular carcinoma after ablation.

161 rumab compared with placebo in patients with hepatocellular carcinoma and alpha-fetoprotein concentra

162 To test this hypothesis, HUH-7 hepatocellular carcinoma and AML12 normal hepatocytes we

163 We present an unusual case of a patient with hepatocellular carcinoma and biliary invasion, who had h

164 e initial findings to pre-clinical models of hepatocellular carcinoma and breast cancer, we discovere

165 nificantly associated with increased risk of hepatocellular carcinoma and death (P < 0.01) but not de

166 ty attributed to decompensated cirrhosis and hepatocellular carcinoma and examined the population-lev

167 nts, partial grafts, malignancies other than hepatocellular carcinoma and fulminant hepatitis.

168 ual tests on laboratory mice with inoculated hepatocellular carcinoma and in clinical conditions on p

169 een benign and malignant lesions, especially hepatocellular carcinoma and liver metastasis, and the s

170 egression modeling, we estimated the risk of hepatocellular carcinoma and liver-related mortality, ac

171 ssociated with a significantly lower risk of hepatocellular carcinoma and lower liver-related mortali

172 Moreover, CNApp reproduces recurrent CNAs in hepatocellular carcinoma and predicts colon cancer molec

173 broader background information on pediatric hepatocellular carcinoma and rationale for recommendatio

174 sis (1.77 [1.00-3.14], P = 0.05), history of hepatocellular carcinoma and/or liver transplantation (7

175 Hepatocellular carcinoma as a complication is linked to

176 Adults with cirrhosis awaiting LT without hepatocellular carcinoma at nine LT centers in the Unite

177 ce the risk of progressive liver disease and hepatocellular carcinoma but is often administered for a

178 The study included five cohorts, and the two hepatocellular carcinoma cohorts, groups A and F, are de

179 have a higher mortality risk and more severe hepatocellular carcinoma compared to HCV monoinfected pa

180 minations for both the test data set and the hepatocellular carcinoma data set.

181 re on mortality, hepatic decompensation, and hepatocellular carcinoma development in a large national

182 d-line setting for patients with an advanced hepatocellular carcinoma from the German statutory healt

183 e (56)Fe ion irradiation on the formation of hepatocellular carcinoma in mice.

184 Microwave ablation in patients with hepatocellular carcinoma is a safety treatment modality

185 egressed tumor growth in the xenograft human hepatocellular carcinoma mouse model.

186 Microwave ablation was applied to 42 hepatocellular carcinoma nodules in 31 patients.

187 olizumab alone in patients with unresectable hepatocellular carcinoma not previously treated with sys

188 control stage (benign) to the early stage of hepatocellular carcinoma on an eight-stage disease datas

189 patients underwent liver transplantation for hepatocellular carcinoma or adenoma.

190 are in the second-line treatment of advanced hepatocellular carcinoma over a lifetime horizon.

191 Twenty-three hepatocellular carcinoma patients undergoing RE treatmen

192 ve androgen receptor splice variants promote hepatocellular carcinoma progression by regulating the e

193 Hepatocellular carcinoma screening in NAFLD patients wit

194 lder recipients and especially patients with hepatocellular carcinoma seem to be less affected by an

195 osis helped identify macrotrabecular-massive hepatocellular carcinoma subtype with high specificity.

196 er Diseases criteria) confirmed unresectable hepatocellular carcinoma that was not amenable to curati

197 trospective review included 53 patients with hepatocellular carcinoma treated with radioembolization

198 umor response in locally advanced inoperable hepatocellular carcinoma treated with TARE.

199 tter overall survival and disease control in hepatocellular carcinoma treated with transarterial radi

200 population and appears to result in improved hepatocellular carcinoma treatment response.

201 rafenib versus Radioembolization in Advanced Hepatocellular Carcinoma trial.

202 ies, we demonstrate the use of ClonArch on a hepatocellular carcinoma tumor with ~280 sequencing biop

203 patients with NAFLD, the annual incidence of hepatocellular carcinoma was 1.8 cases per 1000 person-y

204 ow-up, the estimated cumulative incidence of hepatocellular carcinoma was 4.0% among aspirin users an

205 or each TA-allele, the risk of cirrhosis and hepatocellular carcinoma was reduced by 15% and 28%, res

206 y analysis was performed where patients with hepatocellular carcinoma were included.

207 codes of cirrhosis and without a history of hepatocellular carcinoma were included.

208 Adults without hepatocellular carcinoma who were on the liver transplan

209 Hepatocellular carcinoma with biliary ductal invasion is

210 Conclusion Hepatocellular carcinoma with nuclear factor E2-related

211 atients was not different from patients with hepatocellular carcinoma within Milan receiving exceptio

212 s study describes trends in the incidence of hepatocellular carcinoma within the Veterans Health Admi

213 chronic infection remains the major cause of hepatocellular carcinoma worldwide, with more than half

214 growth of Clostridium difficile(1), promote hepatocellular carcinoma(2) and modulate host metabolism

215 (steatosis, steatohepatitis, cirrhosis, and hepatocellular carcinoma) recognized in human NAFLD when

216 tality rates from liver disease (cirrhosis + hepatocellular carcinoma), but data are lacking at the l

217 a: 17 had colorectal liver metastases, 1 had hepatocellular carcinoma, 1 had mass-forming cholangioca

218 y included 6 patients (melanoma, 1; lung, 4; hepatocellular carcinoma, 1).

219 c applications in hepatocyte growth biology, hepatocellular carcinoma, and HCV pathogenesis.

220 inhibition protects against prostate cancer, hepatocellular carcinoma, and metabolic derangements ind

221 s including ascites, hepatic encephalopathy, hepatocellular carcinoma, esophageal variceal bleed, and

222 account for any differences by diagnosis of hepatocellular carcinoma, hepatitis C virus, nonalcoholi

223 besity and inflammation are risk factors for hepatocellular carcinoma, however, the role of Nod2 in o

224 including bridging fibrosis, cirrhosis, and hepatocellular carcinoma, in this population.

225 s an option for sorafenib-resistant advanced hepatocellular carcinoma, increasing overall survival an

226 of aberrant MHC II in malignancy, including hepatocellular carcinoma, is also reviewed.

227 s of low-dose aspirin (<=160 mg) on incident hepatocellular carcinoma, liver-related mortality, and g

228 ning on clinical outcomes such as mortality, hepatocellular carcinoma, or cirrhosis.

229 excluding those listed for multiple organs, hepatocellular carcinoma, or living donor LT.

230 t its complications, including cirrhosis and hepatocellular carcinoma, pharmacological interventions

231 mia, prostate cancer and hepatitis B-induced hepatocellular carcinoma, repeated infusions of these po

232 cant morbidity and mortality from cirrhosis, hepatocellular carcinoma, solid organ malignancies, diab

233 In human hepatocellular carcinoma, the presence of a migration-as

234 Adjusted 10-year cumulative probabilities of hepatocellular carcinoma, vascular events, and nonhepati

235 ifferent gastrointestinal cancers, including hepatocellular carcinoma, which is currently undruggable

236 The permanent activation of hepatocellular carcinoma-associated proto-oncogenes such

237 -forming cholangiocarcinoma, and 1 had mixed hepatocellular carcinoma-mass-forming cholangiocarcinoma

238 n, including 497 with cirrhosis and 113 with hepatocellular carcinoma.

239 ier to current immuno-oncologic therapies in hepatocellular carcinoma.

240 trahepatic hyperdensities, as well as a 3 cm hepatocellular carcinoma.

241 sease: cirrhosis, hepatic decompensation, or hepatocellular carcinoma.

242 n attractive approach for chemoprevention of hepatocellular carcinoma.

243 HBV) is a leading cause of liver failure and hepatocellular carcinoma.

244 ab (anti-VEGF) in patients with unresectable hepatocellular carcinoma.

245 ct against IRI and IRI-induced metastasis of hepatocellular carcinoma.

246 sue which was histologically consistent with hepatocellular carcinoma.

247 se to the development of liver cirrhosis and hepatocellular carcinoma.

248 clinical spectrum ranging from steatosis to hepatocellular carcinoma.

249 development of cirrhosis, liver failure, and hepatocellular carcinoma.

250 fficacious in the treatment of patients with hepatocellular carcinoma.

251 se and as a potential therapeutic target for hepatocellular carcinoma.

252 hepatic malignancy such as hepatoblastoma or hepatocellular carcinoma.

253 an progress to cirrhosis, liver failure, and hepatocellular carcinoma.

254 ocol while pSTAT3 expression was detected in hepatocellular carcinoma.

255 erum sodium score was 18 (14-22); and 37 had hepatocellular carcinoma.

256 a biomarker-selected patient population with hepatocellular carcinoma.

257 ted HSCs in fibrotic tissues associated with hepatocellular carcinoma.

258 of pyruvate into the mitochondria, promoting hepatocellular carcinoma.

259 non-coding RNA (lncRNA) which is induced in hepatocellular carcinoma.

260 antiviral therapy vs no therapy with risk of hepatocellular carcinoma.

261 gallstone cholangitis and a newly diagnosed hepatocellular carcinoma.

262 n promotes hepatocyte growth and progress to hepatocellular carcinoma.

263 er Disease score 6-29) were enrolled, 26 had hepatocellular carcinoma.

264 hronic viral hepatitis, liver cirrhosis, and hepatocellular carcinoma.

265 and pembrolizumab for treatment of advanced hepatocellular carcinoma.

266 Interestingly, in hepatocellular-carcinoma (HCC) patients, a significant S

267 Hepatocellular carcinomas (HCC) exhibit distinct promote

268 Background Intermediate stage hepatocellular carcinomas (HCCs) are treated by inducing

269 Most hepatocellular carcinomas (HCCs) develop in patients wit

270 itors are effective in the treatment of some hepatocellular carcinomas (HCCs), but these tumors do no

271 Hepatocellular carcinomas (OR 0.319, 95% CI 0.107-0.949,

272 re, LRPPRC suppresses genome instability and hepatocellular carcinomas and promotes survivals in mice

273 LRPPRC knockout mice develop more and larger hepatocellular carcinomas and survive a shorter lifespan

274 signature was enriched in a subset of human hepatocellular carcinomas characterized by comparatively

275 safety of microwave ablation (MWA) in small hepatocellular carcinomas sized <= 3 cm, determine long-

276 Treatment of hepatocellular carcinomas using our glypican-3 (GPC3)-ta

277 driver of growth and survival in a subset of hepatocellular carcinomas, making selective FGFR4 inhibi

278 ersible damage to the liver and, ultimately, hepatocellular carcinomas.

279 water and assesses the cytotoxicity in liver hepatocellular cells.

280 The liver injury can present with a hepatocellular, cholestatic or mixed pattern of disease.

281 The average SUV(max) of hepatocellular, colorectal, head-neck, ovarian, pancreat

282 ith LV-Co, and correlated with biomarkers of hepatocellular damage.

283 erized by liver steatosis, inflammation, and hepatocellular damage.

284 an infiltration of T-lymphocytes in areas of hepatocellular damage.

285 mits the transition from simple steatosis to hepatocellular death; thus, activation might ameliorate

286 Erythropoietin-producing human hepatocellular (Eph) receptors are targeted by ephrin pr

287 Moreover, DNA damage as determined by hepatocellular expression of gammaH2A.X and of genes rel

288 it the growth of RTK-addicted cell lines and hepatocellular (HCC) cells in vitro and in vivo.

289 ists reduce lipid accumulation in the liver, hepatocellular inflammation, hepatic injury, and fibrosi

290 is (FIB-4, APRI, and Forns index scores) and hepatocellular injury (levels of aminotransferases).

291 similarly sensitized to cathepsin-dependent hepatocellular injury and death from IL-1beta/TNF in com

292 There was continued alleviation of hepatocellular injury in knockout mice despite ongoing c

293 s correlated with effluent concentrations of hepatocellular injury markers, including alkaline phosph

294 te kidney injury, gastrointestinal symptoms, hepatocellular injury, hyperglycemia and ketosis, neurol

295 On severe hepatocellular injury, invasive DR has been proposed to

296 calyx damage correlates with the severity of hepatocellular injury.

297 surround the bile duct after cholestatic and hepatocellular injury.

298 Mice homozygous for either mutation had hepatocellular iron loading and decreased liver hepcidin

299 ab GTPase that may play an important role in hepatocellular metabolism.

300 ne the relationship between coagulopathy and hepatocellular tropism, we compared infection and diseas