ライフサイエンスコーパス: HCC

1 HCC as a cause of morbidity and mortality in the HBV/HIV

2 HCC guidelines worldwide have provided surveillance reco

3 HCC is an important complication in the HIV/HBV infected

4 HCC pathology involves epithelial to mesenchymal transit

5 HCC recurred in 28 of 57 (49%) patients with previous hi

6 HCC risk remained above the accepted thresholds for surv

7 HCC risk was also higher in patients with alcohol use, o

8 HCC surveillance remains underused in clinical practice,

9 HCC was confirmed based on characteristic CT scan findin

10 HCCs with NRF2 pathway mutation had a shorter time to lo

11 firmation was available for 143 nodules (122 HCCs, 18 non-HCC malignancies, and three benign nodules)

12 A total of 216 HCC patients who underwent DEB-TACE from October 2008 to

13 This retrospective study included 282 HCC liver transplant recipients.

14 thods: A tissue microarray was built from 36 HCC samples and from matching surrounding cirrhotic tiss

15 respectively, comparable to survival in 382 HCC patients without PVTT undergoing upfront LDLT (5-y O

16 Among the overall 801 HCC, the most frequently mutated genes were telomerase r

17 etwork for Organ Sharing (UNOS) data, 14 844 HCC patients listed for LT from 2005 to 2015 were identi

18 limited guidance/recommendations addressing HCC surveillance in patients with NAFLD outside the cont

19 present an evidence-based review addressing HCC risk in patients with NAFLD and provide Best Practic

20 (2007-2020) on systemic therapy for advanced HCC and provide recommended care options for this patien

21 rldwide, however, the treatment for advanced HCC remains unsatisfactory.

22 escribe the mutational landscape of advanced HCC and to identify predictors of primary resistance to

23 Twenty-two percent of advanced HCC harbored potentially druggable genetic alterations,

24 most frequent mutations in ctDNA of advanced HCC were TERT promoter (51%), TP53 (32%), CTNNB1 (17%),

25 of AR antagonists in patients with advanced HCC by evaluating potential resistance mechanisms to AR-

26 ete tumor response in patients with advanced HCC treated by a specific MET inhibitor.

27 rst-line treatment of patients with advanced HCC, Child-Pugh class A liver disease, and ECOG PS 0-1.

28 clinical efficacy for patients with advanced HCC.

29 e safety profiles for patients with advanced HCC.

30 Although HCC is associated with chronic viral infections, alcohol

31 n-related adjunctive therapies to ameliorate HCC pathophysiology.

32 We develop an HCC EV purification system (i.e., EV Click Chips) by syn

33 95% CI, 1.54-1.88; P = 1.52 x 10(-26) ) and HCC (OR, 1.77; 95% CI, 1.58-1.98; P = 2.31 x 10(-23) ).

34 val [CI], 0.72-0.88; P = 8.13 x 10(-6) ) and HCC (OR, 0.77; 95% CI, 0.68-0.89; P = 2.27 x 10(-4) ), w

35 te and functions of PROM1(+) cells in AH and HCC are unknown.

36 in the cross-talk between stellate cells and HCC cells.

37 kers of liver disease and with cirrhosis and HCC in 110,761 individuals from Copenhagen, Denmark, and

38 ic trait increased the risk of cirrhosis and HCC in patients with NAFLD.

39 for developing alcohol-related cirrhosis and HCC were determined using logistic regression analysis.

40 development of alcohol-related cirrhosis and HCC.

41 , benefited most with regard to OS, DFS, and HCC-recurrence (HR: 0.49-0.59, P = 0.0079-0.0245).

42 ly associated with the stage of fibrosis and HCC.

43 riptomic analysis of cultured hepatocyte and HCC cells found that cyclin D1 knockdown induced the exp

44 enetically activated cell proliferation, and HCC.

45 al (OS), recurrence-free survival (RFS), and HCC recurrence (HCC-R) were compared between patients wi

46 g a tumor from a patient with HCV-associated HCC and evaluating this model's therapeutic potential.

47 long-term outcomes of large NAFLD-associated HCC cohorts are lacking.

48 Despite evidence that NAFLD-associated HCC may arise in the absence of cirrhosis, is often diag

49 s compared to patients with viral-associated HCC.

50 Hepatitis B and C virus-associated HCC became less common, and more patients were diagnosed

51 ivator of PP2A (SMAP) efficiently attenuates HCC tumorigenesis in xenograft mouse models.

52 combined administration of a Listeria-based HCC vaccine, Lmdd-MPFG, and the anti-PD-1 immune checkpo

53 The TE-based HCC risk model predicted 0% of HCC occurrence at 3 years

54 Because HCC risk is not homogenous and may decrease with fibrosi

55 Over time, mortality has improved for both HCC and non-HCC recipients and across the full range of

56 PVRL1, which is up-regulated by HCC cells, stabilizes cell surface PVR, which interacts

57 lism to favor hepatocellular carcinogenesis (HCC), but the upstream signaling events remain poorly de

58 tologic subtype of hepatocellular carcinoma (HCC) (MTM-HCC) represents an aggressive form of HCC and

59 e of liver cancer, hepatocellular carcinoma (HCC) accounts for the great majority of liver cancer dia

60 for patients with hepatocellular carcinoma (HCC) and 87.5%, 70.0% and 70.0% for patients with intrah

61 y overexpressed in hepatocellular carcinoma (HCC) and is an independent diagnostic marker predicting

62 l in patients with hepatocellular carcinoma (HCC) and portal vein tumor thrombosis (PVTT) is 2-6 mont

63 ave lower rates of hepatocellular carcinoma (HCC) as compared to men; it is unknown if there are sex-

64 lization (TACE) in hepatocellular carcinoma (HCC) because of the potential for profound adverse event

65 vated AKT in human hepatocellular carcinoma (HCC) cells phosphorylates cytosolic phosphoenolpyruvate

66 on and facilitates hepatocellular carcinoma (HCC) development, representing a major threat to human h

67 re limited data on hepatocellular carcinoma (HCC) growth patterns, particularly in Western cohorts, d

68 risk of developing hepatocellular carcinoma (HCC) in HCV-infected patients who achieve sustained viro

69 Hepatocellular carcinoma (HCC) is an increasingly common indication for liver tran

70 Hepatocellular carcinoma (HCC) is clearly age-related and represents one of the de

71 Hepatocellular carcinoma (HCC) is one of most common cancers worldwide, however, t

72 Hepatocellular carcinoma (HCC) is the most common primary malignant liver tumor.

73 Hepatocellular carcinoma (HCC) is the third most frequent cause of cancer-related

74 C virus (HCV) and hepatocellular carcinoma (HCC) listed for liver transplantation (LT).

75 olization (TAE) of hepatocellular carcinoma (HCC) provides a compelling clinical correlate of this ph

76 currently used for hepatocellular carcinoma (HCC) recurring after liver transplantation (LT) when HCC

77 Hepatocellular carcinoma (HCC) represents the sixth most commonly diagnosed cancer

78 Hepatocellular carcinoma (HCC) surveillance is associated with early tumor detecti

79 lycolysis in human hepatocellular carcinoma (HCC) through nuclear relocalization of pyruvate kinase M

80 debris stimulates hepatocellular carcinoma (HCC) tumor growth via an "eicosanoid and cytokine storm.

81 tumors, including hepatocellular carcinoma (HCC), a malignancy with no effective treatment.

82 dscape of advanced hepatocellular carcinoma (HCC), and predictive biomarkers of response to systemic

83 xual dimorphism of hepatocellular carcinoma (HCC), sex hormone receptor signaling has been implicated

84 on in the study of hepatocellular carcinoma (HCC), the role of the proteasome in regulating cross tal

85 minantly driven by hepatocellular carcinoma (HCC), which accounts for 75% of LC cases.

86 ransplantation for hepatocellular carcinoma (HCC), with and without hypothermic oxygenated liver perf

87 ding viral-derived hepatocellular carcinoma (HCC).

88 antly expressed in Hepatocellular Carcinoma (HCC).

89 immune response in hepatocellular carcinoma (HCC).

90 are performed for hepatocellular carcinoma (HCC).

91 in mouse and human hepatocellular carcinoma (HCC).

92 the progression of hepatocellular carcinoma (HCC).

93 isease (NAFLD) and hepatocellular carcinoma (HCC).

94 cancers, including hepatocellular carcinoma (HCC).

95 the development of hepatocellular carcinoma (HCC).

96 risk of developing hepatocellular carcinoma (HCC).

97 causal factors for hepatocellular carcinoma (HCC).

98 tegy for targeting hepatocellular carcinoma (HCC, one of the deadliest malignancies).

99 ated events (i.e., hepatocellular carcinoma [HCC], hepatic decompensation, or liver-related death/tra

100 ntermediate stage hepatocellular carcinomas (HCCs) are treated by inducing ischemic cell death with t

101 Most hepatocellular carcinomas (HCCs) develop in patients with chronic hepatitis, which

102 memory B cells were higher in CHC-N and CHC-HCC groups than LC with a good predictive accuracy of LC

103 CHC-with LC (CHC-LC), and CHC-with HCC (CHC-HCC).

104 frail patients, respectively, beyond the CMS-HCC model alone.

105 The frailty index addition to the CMS-HCC model predicted on average an additional $2712, $791

106 By co-culturing HCC-cells with stellate cells, we found that HCC-cells a

107 enrollment but median APRI >= 2.0 developed HCC.

108 2,794 developed cirrhosis, and 253 developed HCC during a mean of 9 years follow-up.

109 % female; median age 62 years), 35 developed HCC (3.9%), and the median follow-up was 45 months (rang

110 ltrasound for patients at risk in developing HCC.

111 ted with a lower adjusted risk of developing HCC [sHR=0.27, 95% IC (0.08-0.90); p=0.034].

112 ociated with an increased risk of developing HCC in univariate (HR = 1.4; 95% CI = 1.1-1.8; P < 0.01)

113 A total of 3349 newly diagnosed HCC patients were enrolled and retrospectively analyzed.

114 and downstream glycolytic alterations during HCC development, highlighting the REGgamma-proteasome as

115 For patients with early HCC who are not candidates for surgical resection, ablat

116 iviral therapy fails to completely eliminate HCC risk.

117 vein injection of proto-oncogenes, enhanced HCC development.

118 The established HCC mouse models were characterized at histopathological

119 Nine of them (90%) experienced HCC recurrence within 1 year, supporting vh-DNA as an in

120 Thirty-three patients (69%) died, 94% for HCC progression.

121 n to be a potential therapeutic approach for HCC.

122 AR-SVs may be therapeutically beneficial for HCC.

123 ntial of CD147-CAR-modified immune cells for HCC patients.

124 sts BCCIP dysregulation as a risk factor for HCC and offers a novel mouse model for future investigat

125 These data have important implications for HCC surveillance in cured HCV patients.

126 omparing era, post-LT mortality improved for HCC (adjusted HR, 0.55; 95% CI, 0.40-0.74) and non-HCC r

127 Patients receiving LT) for HCC are at a high risk for tumor recurrence.

128 nd better treatment are certainly needed for HCC, primary prevention efforts aimed at decreasing the

129 sease, providing potential opportunities for HCC early detection.

130 tients without cirrhosis who are at risk for HCC.

131 ns include recommendations for screening for HCC in persons at risk, treatment with antivirals, and a

132 ess impact of PS on mortality separately for HCC and non-HCC recipients.

133 These associations were stronger for HCC.

134 liver recipients (n = 70), transplanted for HCC at an external center (Center B).

135 Y90 is an effective treatment for HCC in the setting of bridging/downstaging to LT.

136 isk patients who had long-term follow-up for HCC development.

137 indicative of a unique intrinsic biology for HCCs in the United States.

138 icate a 42% decrease in unfiltered MeHg from HCC inflow to outflow.

139 -free survival rates compared to HBV and HCV-HCC cases.

140 tion of HCC mouse models that captured human HCC diversity.

141 onfirm this altered lipid signature in human HCC and show a positive correlation of monounsaturated P

142 s confirmed the in vitro data, and the human HCC clinical sample survey and tissue staining also conf

143 l and clinical studies in efforts to improve HCC immunotherapy.

144 NA nanoparticle predominantly accumulated in HCC tumor sites and efficiently inhibited the tumor grow

145 tingly, mTORC1 enhances REGgamma activity in HCC, forming a positive feedback regulatory loop.

146 3 and FOXO3 levels are tightly correlated in HCC patients.

147 inhibitor, could enhance the cytotoxicity in HCC cells with a lower BRCA1 expression, and suppressing

148 nknown if there are sex-based differences in HCC recurrence post-liver transplant.

149 DDR1 is supported by its marked elevation in HCC which is inversely associated with patient survival.

150 gene and is important for MTR4 expression in HCC cells, indicating that MTR4 is a mediator of the fun

151 We analyzed GLS2 expression in HCC, GBM and neuroblastoma cells, as well as in monkey C

152 s, and an emerging role for immunotherapy in HCC.

153 n be overcome by means of NRF2 inhibition in HCC cell lines.

154 models for preoperative detection of MVI in HCC.Supplemental material is available for this article.

155 tenin expression and downstream signaling in HCC cells in a dose-dependent manner.

156 RNA expression of TYMS, TK-1, and SLC29A1 in HCC.

157 rative nucleoside transporter 1 (SLC29A1) in HCC compared with liver tissue, we conducted a proof-of-

158 Because previous PET studies in HCC have been hampered by high background liver signal,

159 OS was significantly better than in HCC-PVTT patients receiving no intervention or palliativ

160 a clinical diagnosis, which may be useful in HCC surveillance.

161 that we interrogated, 9 were able to induce HCC.

162 survival was 82 days among the HIV-infected HCC patients compared to 181 days among those without HI

163 sion, we aimed to identify patients with low HCC risk based on the prediction of noninvasive markers

164 the impact of LRT in patients with beyond-MC HCC from the U.S. Multicenter HCC Transplant Consortium

165 We hypothesize that lncRNAs modulate HCC prognoses through differential deregulation of key l

166 btype of hepatocellular carcinoma (HCC) (MTM-HCC) represents an aggressive form of HCC and is associa

167 P = .03) were independent predictors of MTM-HCC subtype.

168 ether preoperative MRI can help identify MTM-HCCs in patients with HCC.

169 tify 65% (17 of 26; 95% CI: 44%, 83%) of MTM-HCCs (sensitivity) with a specificity of 93% (117 of 126

170 with beyond-MC HCC from the U.S. Multicenter HCC Transplant Consortium (20 centers, 2002-2013).

171 2637) cPR from the United States Multicenter HCC Transplant Consortium (UMHTC), and multivariable pre

172 endent tumor-suppressing pathway in multiple HCC cell lines.

173 Murine HCC cell lines were generated from each tumor model, cha

174 This novel collection of murine HCC models and corresponding cell lines establishes the

175 is present in individuals with NRF2-mutated HCC and if this resistance can be overcome by means of N

176 The NAFLD-HCC patients had a trend for higher recurrence-free surv

177 available for 143 nodules (122 HCCs, 18 non-HCC malignancies, and three benign nodules).

178 djusted HR, 0.55; 95% CI, 0.40-0.74) and non-HCC recipients (0.48; 95% CI, 0.42-0.55), but this did n

179 mortality has improved for both HCC and non-HCC recipients and across the full range of PS.

180 f PS on mortality separately for HCC and non-HCC recipients.

181 t, 36 of 452 (8%) patients developed de novo HCC, 4-year cumulative probability being 9% (95% confide

182 0.04) were independent predictors of de novo HCC.

183 The TE-based HCC risk model predicted 0% of HCC occurrence at 3 years in patients with score 0 (base

184 HBV was found in 69.5% of HCC and 47.2% of cirrhosis cases, and HCV in 6.4% and 3.

185 otic persons were Child-Pugh C, and 67.9% of HCC patients had advanced or terminal disease at present

186 ations of nonviral or nonalcoholic causes of HCC development.

187 aimed at establishing a novel collection of HCC mouse models that captured human HCC diversity.

188 potential for noninvasive early detection of HCC from at-risk cirrhotic patients with an area under r

189 Timely detection of HCC recurrence and its clonality is required to implemen

190 stage of fibrosis, or by the development of HCC.

191 f SREBPs, lipogenesis and the development of HCC.

192 s conducted; 18 patients with a diagnosis of HCC by the criteria of the American Association for the

193 5 of 75), respectively, for the diagnosis of HCC.

194 ) (MTM-HCC) represents an aggressive form of HCC and is associated with poor survival.

195 ulated gene expression and reduced growth of HCC cells in culture and xenografts of HCC tumors, sugge

196 carcinoma worldwide, with more than half of HCC patients being chronic HBV carriers, even if underly

197 Cumulative incidence of HCC at 5 years was 7.6% in UMHS and 1.8% in PUHSC cohort

198 epressive function of REX1 in maintenance of HCC cells by regulating MKK6 binding and p38 MAPK signal

199 Management of HCC should not be different from that indicated for non

200 ment strategy for the clinical management of HCC, particularly in the West.

201 as been established in preclinical models of HCC with the clinical failure of AR antagonists in patie

202 The main endpoint was the occurrence of HCC.

203 Predictors of HCC emergence were: HCV genotype 3 [sHR=7.9 (2.5-24.9);

204 city were the only independent predictors of HCC recurrence.

205 stic marker predicting the poor prognosis of HCC patients.

206 cells are key players in the progression of HCC, as they create a fibrotic micro-environment and pro

207 The quarterly incidence rate of HCC remained stable between 1.00 and 1.23/100 person-yea

208 MRI can be used to evaluate the response of HCC to radioembolization.

209 to identify patients with a very low risk of HCC development after SVR.

210 N or NUCs, substantially reduces the risk of HCC development, even if antiviral therapy fails to comp

211 uccessfully treated with DAAs and at risk of HCC did not regress after 3.6 years of follow-up.

212 s/normal ALT; they also had a higher risk of HCC, although it did not reach statistical significance

213 SVR reduced the risk of HCC.

214 The cumulative 1, 2, and 3-year risks of HCC were 1.1%, 1.9% and 2.8%, respectively.

215 e recently proposed for precise selection of HCC patients for transplantation.

216 nt noncancerous liver tissues of a subset of HCC patients with a relatively poor prognosis.

217 tosis of debris, resulting in suppression of HCC tumor growth.

218 AFP can still be used in the surveillance of HCC in Indonesia for its high sensitivity value.

219 ction on age at presentation and survival of HCC.

220 otential therapeutic target for treatment of HCC.

221 anti-PD1 might be developed for treatment of HCC.

222 vo mouse model with orthotopic xenografts of HCC cells confirmed the in vitro data, and the human HCC

223 th of HCC cells in culture and xenografts of HCC tumors, suggesting that inhibition of PJA1 may be be

224 eriportal area and subsequent development of HCCs.

225 ransferase to platelet ratio index (APRI) on HCC risk.

226 s an emerging issue, the number of papers on HCC in beta-thalassemia patients is limited and based on

227 group was subdivided into CHC-without LC or HCC (N-CHC), CHC-with LC (CHC-LC), and CHC-with HCC (CHC

228 d ischemia resistance in NRF2-overexpressing HCC cell lines.

229 asome as a potential target for personalized HCC therapy.

230 ents with HCC, but also associated with poor HCC prognosis.

231 cells induced cytolysis of antigen-positive HCC cells and cells infected with HBV in vitro, causing

232 ot single antigen (GPC3(-)CD147(+)) positive HCC cells and does not cause severe on-target/off-tumor

233 a viral exposure signature that can predict HCC among at-risk patients prior to a clinical diagnosis

234 rnative model with FIB-4 similarly predicted HCC risk.

235 who underwent ablation therapy for presumed HCC followed by liver transplantation between January 20

236 be beneficial in treating HCC or preventing HCC development in at-risk patients.Significance: These

237 d by NCOA5 deficiency and metformin prevents HCC development via alleviating p21(WAF1/CIP1) overexpre

238 difications using publicly available primary HCC datasets (1,019 samples).

239 lassical exhausted state observed in primary HCC.

240 Hepatocyte-derived NPY promoted HCC progression by Y5R activation.

241 We calculated the overall and quarterly HCC incidence rates.

242 iR-30e-3p was downregulated in human and rat HCCs, and its downregulation associated with TP53 mutati

243 nce-free survival (RFS), and HCC recurrence (HCC-R) were compared between patients within MC (n = 3,5

244 Patients with recurrent HCC after LT from 2002 to 2016 were reviewed from 3 tran

245 F1/CIP1) expression and subsequently reduced HCC incidence in Ncoa5(+/-) male mice.

246 lation and mTOR activity and thereby reduces HCC cell survival.

247 HBV-related HCC can be prevented by reducing the exposure to HBV by

248 integration in 50 patients with HBV-related HCC was determined by the Hybridization capture-based ne

249 After treatments, NAFLD-related HCC patients had longer overall but not recurrence-free

250 All patients had a single HCC lesion on liver imaging that was 1.8-6.5 centimeters

251 odels functionalize early and advanced stage HCCs and revealed unique biological features of liver ca

252 r findings suggest that ERalpha can suppress HCC cell invasion via altering the ERalpha/circRNA-SMG1.

253 sus 32.1%), particularly in patients with T1 HCC (OR, 3.41; 95% CI, 1.08-10.80).

254 Recent data confirm that HCC represents the fifth most common cancer and is the s

255 HCC-cells with stellate cells, we found that HCC-cells activate IREalpha in stellate cells, thereby c

256 The HCC EV-derived molecular signatures exhibit great potent

257 The HCC policy change was associated with decreased waitlist

258 evidence of seasonal export of MeHg from the HCC, annual loads indicate a 42% decrease in unfiltered

259 f hepatitis B virus (HBV) integration in the HCC chromosome, as a circulating biomarker for this clin

260 Our comprehensive picture of the HCC ecosystem provides deeper insights into immune evasi

261 us olaparib led to better suppression of the HCC progression.

262 (greatest from September to December) of the HCC.

263 olaparib sensitivity to better suppress the HCC cell growth via a synergistic mechanism that may inv

264 nt of a novel therapy to better suppress the HCC progression.

265 nt of novel therapies to better suppress the HCC progression.

266 We observed (1) that the HCC is a net sink for both IHg and MeHg, (2) interannual

267 e of ERalpha/miR-141-3p/GSN signaling to the HCC progression.

268 ease, genetic factors that contribute to the HCC risk remain unknown.

269 nd safety but limited therapeutic benefit to HCC patients, suggesting low response rate.

270 lly deliver microRNA-loaded nanoparticles to HCC.

271 studies performed >= 30 days apart prior to HCC treatment.

272 conferred the highest risk of progression to HCC.

273 e penultimate step in the progression toward HCC.

274 th a 25% lower risk of post-liver transplant HCC recurrence (95CI 0.57-0.99).

275 egression analysis for post-liver transplant HCC recurrence highlighted that even after accounting fo

276 icantly lower rates of post-liver transplant HCC recurrence than men (4.0 v.

277 bition of PJA1 may be beneficial in treating HCC or preventing HCC development in at-risk patients.Si

278 emoresistance thus, synergistically treating HCC.

279 urring after liver transplantation (LT) when HCC is unsuitable for surgical/locoregional treatments.

280 Cirrhosis was strongly associated with HCC risk (adjusted hazard ratio = 4.13, 95% confidence i

281 sure signature significantly associated with HCC status among at-risk individuals in the validation c

282 (N-CHC), CHC-with LC (CHC-LC), and CHC-with HCC (CHC-HCC).

283 dy of patients with cirrhosis diagnosed with HCC from 2008 to 2017 at six US and European health syst

284 d August 2015, patients newly diagnosed with HCC were recruited and provided demographic and clinical

285 n in liver of male immunocompetent mice with HCC, induced by hydrodynamic tail vein injection of prot

286 this pilot clinical trial, participants with HCC scheduled for sublobar TARE were randomized to under

287 mitigate waitlist dropout for patients with HCC awaiting LT.

288 er transplantation to selected patients with HCC outside of traditional criteria.

289 els for predicting survival of patients with HCC treated by surgical resection.

290 In a preliminary cohort of patients with HCC treated with sorafenib, increased miR-30e-3p circula

291 s retrospective study included patients with HCC treated with surgical resection between January 2008

292 1953 patients with HCC underwent various anatomical hepatectomies with the

293 and posttransplant outcomes in patients with HCC, before and after implementation of the 6-month wait

294 tion of SREBP1 in samples from patients with HCC, but also associated with poor HCC prognosis.

295 All patients with HCC-recurrence after LT treated with SOR in 2 centers we

296 can help identify MTM-HCCs in patients with HCC.

297 ve Risk: 1.299, p < 0.0001) in patients with HCC.

298 s an uncommon presentation for patients with HCC.

299 HIV-positive patients presented with HCC at a younger age than HIV-negative patients, this ef

300 ective review for patients transplanted with HCC between April 2008 and June 2017.