ライフサイエンスコーパス: liver cancer

1 se consequences (development of cirrhosis or liver cancer).

2 CUGBP1 is reduced in patients with pediatric liver cancer.

3 he steatosis had a potential to develop into liver cancer.

4 pathway might be developed as treatments for liver cancer.

5 the converged pathways in NMJ formation and liver cancer.

6 ly associated with good clinical outcomes in liver cancer.

7 has been shown to accelerate progression of liver cancer.

8 t of NKG2D in a model of inflammation-driven liver cancer.

9 surgery, still the main curative option for liver cancer.

10 n treating advanced renal-cell carcinoma and liver cancer.

11 ifications and resembled hypermethylation in liver cancer.

12 showing the highest positive correlation for liver cancer.

13 scence program limiting tumor cell growth in liver cancer.

14 present a unique model of immune response in liver cancer.

15 orrect defective repair during cirrhosis and liver cancer.

16 eatment for aggressive subtypes of pediatric liver cancer.

17 has been associated with the development of liver cancer.

18 ility as an adjunct therapy in management of liver cancer.

19 -specific roles for CCR2(+) myeloid cells in liver cancer.

20 an important link between HCV infection and liver cancer.

21 , and type II diabetes mellitus with risk of liver cancer.

22 se-of-death ensemble model for cirrhosis and liver cancer.

23 infection and poor prognosis HBV-associated liver cancer.

24 for the treatment of primary and metastatic liver cancer.

25 (ESLD), such as decompensated cirrhosis and liver cancer.

26 represent a relevant therapeutic strategy in liver cancer.

27 various clinical formats in the treatment of liver cancer.

28 nsidered to be a metabolic predisposition to liver cancer.

29 it can also result in cirrhosis and primary liver cancer.

30 rogressive scarring, cirrhosis, and possibly liver cancer.

31 disease, heart disease, type 2 diabetes and liver cancer.

32 K as a putative new prognostic biomarker for liver cancer.

33 nfection is a leading cause of cirrhosis and liver cancer.

34 ts, both in the NAFLD group, died of primary liver cancer.

35 tly biological modules, which related to the liver cancer.

36 CT during transarterial chemoembolization of liver cancer.

37 tion is a common cause of the development of liver cancer.

38 ple at high risk of death from cirrhosis and liver cancer.

39 ace glycoprotein that associates with Wnt in liver cancer.

40 insights into the etiology and treatment of liver cancer.

41 with non-Hodgkin lymphoma, lung cancer, and liver cancer.

42 been purportedly related to a lower risk of liver cancer.

43 cation and the development of HBV-associated liver cancer.

44 ar hepatocellular carcinoma (FL-HCC), a rare liver cancer.

45 ntrol to disease progression, cirrhosis, and liver cancer.

46 liver and that their abundance is altered in liver cancer.

47 geal cancer and hepatitis B and C viruses in liver cancer.

48 with men having the highest US incidence of liver cancer.

49 ver diseases from hepatitis to cirrhosis and liver cancer.

50 ne is a potential agent for the treatment of liver cancer.

51 bute to the development of cancer, including liver cancer.

52 r Sorafenib (SFB) usually fails to eradicate liver cancer.

53 insights for immunotherapeutic strategies in liver cancer.

54 cture, is also a potential driver of primary liver cancer.

55 novel therapeutic option in the treatment of liver cancer.

56 HCV) is one of the major etiologic agents of liver cancer.

57 flammation and impair immune surveillance in liver cancer.

58 h pancreatic adenocarcinoma and another with liver cancer.

59 million people who are at risk of developing liver cancer.

60 as a potential therapeutic agent for primary liver cancer.

61 ent in human malignancies, including primary liver cancer.

62 might be developed for treatment of primary liver cancer.

63 0.82% with liver disease, including primary liver cancer.

64 ammation and metabolic pathways important in liver cancer.

65 on) and cause hepatitis, liver cirrhosis and liver cancer.

66 e developed as therapeutics for this form of liver cancer.

67 CUGBP1 is a key event in the development of liver cancer.

68 ay, were found to be tightly associated with liver cancer.

69 g technology to deliver therapeutic genes to liver cancer.

70 linical murine model of steatosis-associated liver cancer.

71 can result in progressive liver disease and liver cancer.

72 a common risk factor for the development of liver cancer.

73 ts millions worldwide, causing cirrhosis and liver cancer.

74 of patients with liver metastases or primary liver cancer.

75 er time and constituted <10% of all reported liver cancers.

76 early-onset portal hypertension and primary liver cancers.

77 contain mutations most commonly detected in liver cancers.

78 angiocarcinoma (n = 36), the two most common liver cancers.

79 -defining cancers (NADCs: lung cancer, 2.3%; liver cancer, 0.9%).

80 Deleted in Liver Cancer 1 (DLC1) is a RHO GTPase-activating protein

81 and 0.05%; colorectal cancer, 1.0% and 1.5%; liver cancer, 1.1% and 0.4%; Hodgkin lymphoma, 0.9% and

82 ; 421628 due to kidney cancer; 487518 due to liver cancer; 13927 due to testicular cancer; and 829396

83 with decompensated cirrhosis (DCC), 2% with liver cancer, 2% with a history of transplant, and 8% wh

84 The Barcelona Clinic Liver Cancer algorithm is the most widely used staging s

85 d were more likely to die from their primary liver cancer (all P < 0.0001).

86 Patients who have liver cirrhosis and liver cancer also have reduced farnesoid X receptor (FXR

87 187 600 (24.5%) of 766 000 cases of liver cancer and 121 700 (38.4%) of 317 000 cases of end

88 kinase substrate, were further confirmed in liver cancer and adjacent normal tissue collected from i

89 Liver cancer and cirrhotic complications are rare.

90 One patient discontinued treatment due to liver cancer and died 22 days after treatment discontinu

91 we have combined preclinical mouse models of liver cancer and genetic studies of a human liver biopsy

92 cers, mortality from combined hepatocellular liver cancer and intrahepatic cholangiocarcinoma (ICC) h

93 deacetylase 4 (HDAC4) is highly expressed in liver cancer and known to regulate oncogenesis through c

94 heir effects were studied in mouse models of liver cancer and regeneration.

95 rited and acquired liver diseases as well as liver cancer and regeneration.

96 mellitus are associated with higher risks of liver cancer and that the association may differ by stat

97 g high potency to reverse gene expression in liver cancer and validate that all four compounds are ef

98 leukemia, prostate, pancreatic, ovarian, and liver cancers and has shown promise in cancer glycobioma

99 l aberrations not previously associated with liver cancer, and almost 80% contain the DNAJB1-PRKACA f

100 the global incidence and mortality rates of liver cancer, and evaluated the association between inci

101 s were found significantly enriched for the "liver cancer" annotation.

102 er 5 cm, was associated with higher risks of liver cancer, approximately equally by sex (overall, HR

103 pite intensive investigations, mechanisms of liver cancer are not known.

104 Liver cancers are typically inflammation-associated canc

105 ve early detection of primary and metastatic liver cancers as well as for monitoring treatment and gu

106 mutations in genes commonly associated with liver cancers, as observed in human FL-HCC.

107 ss") asymmetry dominating UV-, smoking-, and liver-cancer-associated mutations and replicative ("R-cl

108 Stratified analyses assessed whether the BMI-liver cancer associations differed by hepatitis sera-pos

109 , as well as the proportion of cirrhosis and liver cancer attributable to each cause.

110 ver tumorigenesis and clarify the classes of liver cancer based on molecular features and how they af

111 gression and maintenance in a mouse model of liver cancer, based on oncogenic transformation and adop

112 g patients according to the Barcelona Clinic Liver Cancer (BCLC) classification.

113 The nomogram of the Barcelona Clinic Liver Cancer (BCLC) has accurate outcome prediction.

114 and were stratified by the Barcelona Clinic Liver Cancer (BCLC) stage and the duration of sorafenib

115 ed patients with HCC of all Barcelona Clinic Liver Cancer (BCLC) stages for eligibility.

116 Several variables including Barcelona Clinic Liver Cancer (BCLC) staging system, tumor size, and seru

117 The optimal management for Barcelona Clinic Liver Cancer (BCLC) very early-stage HCC is undetermined

118 id models in furthering the understanding of liver cancer biology and in developing personalized-medi

119 rden of HBV and HCV (including cirrhosis and liver cancer burden) and HIV at the country, regional, a

120 of AKT may contribute to the development of liver cancer by facilitating persistent HBV replication,

121 may make a major contribution to HCV-induced liver cancer by shifting Ras signaling away from prosene

122 understanding of the cell types originating liver cancer can aid in exploring molecular mechanisms o

123 were early-stage tumors by Barcelona Clinic Liver Cancer, Cancer of the Liver Italian Program, and t

124 acute viral hepatitis, and for cirrhosis and liver cancer caused by viral hepatitis, by age, sex, and

125 nsports citrate across cell membranes, halts liver cancer cell growth by altering both energy product

126 of CaMKK2 function is sufficient to inhibit liver cancer cell growth, and the growth defect resultin

127 pendent protein kinase 4 (CaMKIV) to control liver cancer cell growth.

128 ter overexpressed in hepatocarcinoma and the liver cancer cell line HepG2.

129 alian target of rapamycin signaling in human liver cancer cell lines and in both an in vitro and in v

130 BACKGROUND & AIMS: Human tumors and liver cancer cell lines express the product of a fusion

131 Treatment of human liver cancer cell lines with FFAs exacerbated the EMT ph

132 lentiviral shRNA knockdown in several human liver cancer cell lines, we demonstrated that TTK boosts

133 ivator GRIP1 in MCF-7 human breast and HepG2 liver cancer cell lines.

134 hat all four compounds are effective in five liver cancer cell lines.

135 s indicate a prominent novel role for Id1 in liver cancer cell metabolic adaptation.

136 EMT in hepatic stellate cell (HSC) and human liver cancer cells (HepG2) and the potential role of EVE

137 thereby enabling the efficient detection of liver cancer cells (HepG2).

138 ingly, CCDC3, as a secreted protein, targets liver cancer cells and increases long chain polyunsatura

139 ver stem cells (LSCs) into highly metastatic liver cancer cells in premalignant liver tissue.

140 aMKK2 with STO-609 impairs tumorigenicity of liver cancer cells in vivo.

141 Blocking lipogenesis in cultured liver cancer cells is sufficient to decrease cell viabil

142 ibit Wnt/beta-catenin signaling in colon and liver cancer cells regardless of whether this pathway is

143 quired in human hepatoma cell line 7 (Huh-7) liver cancer cells to maintain BOK at low levels, and BO

144 The expression of FAM83H is elevated in liver cancer cells, and nuclear expression of FAM83H pre

145 omoter was hypermethylated in both colon and liver cancer cells, leading to the production of high le

146 critical determinants of the growth of human liver cancer cells, providing a strong rationale to eluc

147 ctrochemical biosensors for the detection of liver cancer cells.

148 f SCP1 increased the c-Myc protein levels in liver cancer cells.

149 n the enrichment of nuclear FBP1 and FBP2 in liver cancer cells.

150 bearing liver, limits intrahepatic spread of liver cancer cells.

151 er CD133, which is located on the surface of liver cancer cells.

152 p in the regulation of invasive potential in liver cancer cells.

153 ination with Bcl-XL inhibition on a panel of liver cancer cells.

154 he monodisperse CDs in MCF-7 cells and Huh-7 liver cancer cells.

155 tiforme) cell lines and knocked out in HUH7 (liver cancer) cells.

156 gged form of MAN2A1-FER in NIH3T3 and HEP3B (liver cancer) cells; Golgi were isolated for analysis.

157 Patients from 5 liver cancer centers in the United States who had liver

158 of liver tumors, suggesting a new target for liver cancer chemoprevention and/or chemotherapy.

159 been numerous advances in the management of liver cancer, cirrhosis, and diabetes mellitus.

160 llular carcinoma (HCC) with Barcelona Clinic Liver Cancer classification because of its exclusive art

161 Primary liver cancer comprises hepatocellular carcinoma (HCC), i

162 Downregulation of AMOTL2 is found in human liver cancers, correlating with the concomitant activati

163 clinical data in a TCGA cohort and published liver cancer data.

164 For liver cancer datasets, significantly differentially expr

165 Unspecified liver cancer decreased over time and constituted <10% of

166 oteins in plasma may be a promising tool for liver cancer detection.

167 he ITA.LI.CA staging system for prognoses of liver cancer developed by Alessandro Vitale and colleagu

168 y TRbeta1, is an early and relevant event in liver cancer development and is species and etiology ind

169 ction is considered the main risk factor for liver cancer development, the molecular mechanisms deter

170 ting beta-defensin 1 plays a crucial role in liver cancer development.

171 SD1-mediated H3K4me2 histone modification in liver cancer development.

172 rtant role in protecting HCV progression and liver cancer development.

173 ase genome replication and are implicated in liver cancer development.

174 g of the pathways involved in HCV-associated liver cancer development.

175 in late stages when liver decompensation or liver cancer develops.

176 After enrollment, 2,162 incident liver cancer diagnoses were identified.

177 current evidence linking obesity, NAFLD and liver cancer, discusses its clinical impact and describe

178 e asymmetrically localized RhoGAP Deleted in liver cancer (DLC1) in the cytoplasm at the cell front.

179 r jagged1 (Jag1) in a mouse model of primary liver cancer driven by v-akt murine thymoma viral oncoge

180 However, the possibility of recurrent liver cancer due to incomplete ablation of the tumor mak

181 Primary liver cancer encompasses both hepatocellular carcinoma (

182 ntries with potentially increasing trends of liver cancer for preventive actions.

183 ndent mechanism of FBP protein enrichment in liver cancer; further studies will have to show whether

184 is and is frequently associated with primary liver cancer globally.

185 ted patients with HCC managed by the Italian Liver Cancer Group.

186 Liver cancer has been most frequent among Asian/Pacific

187 Although liver cancer has long had some of the most rapidly incre

188 Incidence rates for liver cancer have increased 3-fold since the mid-1970s i

189 ar pathway hubs, and their overexpression in liver cancer (hepatocellular carcinoma [HCC]) stimulates

190 etween coffee intake and the primary form of liver cancer-hepatocellular carcinoma (HCC).

191 kidney (HEK293), cervical cancer (HeLa), and liver cancer (HepG2).

192 nished the growth and tumor weight of murine liver cancer homografts.

193 mellitus was associated with higher risk of liver cancer (HR = 2.61; 95% CI, 2.34-2.91).

194 nfection that will progress to cirrhosis and liver cancer in 2-10% of patients.

195 Despite being the most common liver cancer in children, hepatoblastoma (HB) is a rare

196 patoblastoma (HB) is the most common primary liver cancer in children.

197 Examination of liver cancer in diethylnitrosamine (DEN)-treated CUGBP1-

198 Overnutrition can promote liver cancer in mice and humans that have liver damage c

199 MAN2A1-FER resulted in rapid development of liver cancer in mice with hepatic disruption of Pten.

200 activation alone is not sufficient to induce liver cancer in mice.

201 estigated beta-defensin family expression in liver cancer in publicly available datasets and found th

202 s an early detection metric for AFB1-induced liver cancer in this mouse model that will be a useful t

203 peutic potential in an experimental model of liver cancer in vivo.

204 Primary liver cancers in BALB/c.Mdr2(-/-) developed earlier, wit

205 The CR may underestimate the liver cancer incidence by 37%-45%, primarily due to miss

206 Hepatitis C-associated liver cancer increased and constituted 20% in 2010.

207 The estimated annual number of liver cancers increased over time, but the standardized

208 For anal, colorectal, and liver cancer, increasing cumulative incidence, but not h

209 on of the Rb gene family in a mouse model of liver cancer, initially activates a robust gene expressi

210 cent hepatocyte-secreted chemokines suppress liver cancer initiation, they may accelerate the growth

211 anism through which these alterations induce liver cancer is by deregulating signaling pathways.

212 atoblastoma (HBL), the most common childhood liver cancer is cured with surgical resection after chem

213 A unique feature of liver cancer is its close association with liver fibrosi

214 f systemic chemotherapy for the treatment of liver cancer is only marginal.

215 Liver cancer is the second leading cause of cancer morta

216 ocellular carcinoma (HCC) is increasing, and liver cancer is the second leading cause of cancer-relat

217 Primary liver cancer is the second leading cause of cancer-relat

218 lar carcinoma (HCC), the most common form of liver cancer, is steadily growing because obesity, type

219 Using the Italian Liver Cancer (ITA.LI.CA) database as a training set, we

220 to high transfection efficacy to all of the liver cancer lines, but not to hepatocytes.

221 on both simulated data and real data from a liver cancer metabolomics study indicates that our kerne

222 In an orthotopic liver cancer model, increasing SAMe levels by overexpres

223 Results were confirmed in an orthotopic liver cancer model.

224 We used several liver cancer models to address the mechanisms underlying

225 kg/m(2), was associated with higher risks of liver cancer, more so for men (HR = 1.38; 95% CI, 1.30-1

226 e reported statistics combine ICC with other liver cancers, mortality rates of cholangiocarcinoma (CC

227 Here we developed a tamoxifen-inducible liver cancer mouse model with a defined oncogenic driver

228 was attributed to liver disease in 48 (47%; liver cancer: n = 18; miscellaneous, n = 30) and extrahe

229 Liver cancer occurrence in infancy, 1.5 for million chil

230 In human liver cancers, ontology analysis of gene set enrichment

231 d into those proximal to genes implicated in liver cancer or to genes involved in stem cell developme

232 Finally, liver cancer organoid-generated high-grade tumors exhibi

233 metastasis by orthotopic transplantation of liver cancer organoids propagated from primary tumors in

234 g occurred in phenotypically more aggressive liver cancers overexpressing MAT2B variants and GIT1.

235 edented preclinical platform of 24 pediatric liver cancer patient-derived xenografts (PLC-PDXs) from

236 vated in neoplastic tissues from a cohort of liver cancer patients, when compared with adjacent hepat

237 lation is associated with poor prognosis for liver cancer patients.

238 ormal tissue collected from in-house Chinese liver cancer patients.

239 n has reported that the incidence of primary liver cancer (PLC) has slowly declined over the last dec

240 Primary liver cancer (PLC) is the sixth most common cancer world

241 culture system to the propagation of primary liver cancer (PLC) organoids from three of the most comm

242 The Liver Cancer Pooling Project maintains harmonized data f

243 ession to estimate total cirrhosis and total liver cancer prevalence, as well as the proportion of ci

244 VD could therefore be a strong candidate for liver cancer prevention in the context of aberrant Smad3

245 Fibrolamellar carcinoma (FLC) is a unique liver cancer primarily affecting young adults and charac

246 Liver cancer, primarily encompassing hepatocellular carc

247 This article reviews the Barcelona-Clinic Liver Cancer protocol for the diagnosis, staging, and tr

248 In human liver cancer, RASSF1A frequently undergoes methylation a

249 sial reports suggest a potential increase in liver cancer recurrence upon use of DAAs.

250 The heterogeneity of liver cancer represents a clinical challenge.

251 Human liver cancer research currently lacks in vitro models th

252 Cirrhosis and liver cancer result when these pathways become dysregula

253 , hepatitis infection, and other established liver cancer risk factors.

254 there was a null association between BMI and liver cancer risk for participants who were sera-positiv

255 Increased risk was mainly found for liver cancer (risk = 3.5%; SIR = 1805), pancreatic cance

256 offee were RR = 0.73, 95% CI = 0.67-0.79 for liver cancer, RR = 0.97, 95% CI = 0.96-0.98 for prostate

257 ls of TERT and tRNA correlated in breast and liver cancer samples.

258 tial use of these two orthogonal markers for liver cancer screening in patients with high-risk cirrho

259 These biodegradable and liver cancer-selective NPs are a promising technology to

260 , a model of chronic inflammation-associated liver cancer, significantly accelerates hepatocarcinogen

261 67 years; 77% male; and 22% Barcelona Clinic Liver Cancer stage A and 78% stage B or C.

262 +/- 8 [standard deviation]; Barcelona Clinic Liver Cancer stage A, n = 4; Barcelona Clinic Liver Canc

263 iver Cancer stage A, n = 4; Barcelona Clinic Liver Cancer stage B, n = 28; predominant cause, alcohol

264 ormance status 0 91.7%, and Barcelona Clinic Liver Cancer stage C 83.3%).

265 patocellular carcinoma with Barcelona Clinic Liver Cancer stage C disease or stage B disease that was

266 sorafenib patients had more Barcelona Clinic Liver Cancer stage D ( P < .001), higher Model for End-S

267 hers the mCXCL1-mTORC1 pathway as crucial in liver cancer stem cell maintenance and highlights it as

268 Liver cancer stem cells (CSCs) have been identified and

269 /5 might be a good candidate for therapy for liver cancer stem cells together with liver cirrhosis.

270 n species (ROS) and ATP content in rat LCSC (Liver Cancer Stem Cells) -2 cells exposed to the drug.

271 For patients with liver cancer, surgical resection is a principal treatmen

272 ncer (TNBC) and in ovarian, endometrial, and liver cancers, TDP tumors conjointly exhibit tumor prote

273 ged chronic infection and increased risk for liver cancer than genotype B.

274 , females are less susceptible to developing liver cancer than males, and it remains unclear how nutr

275 e showed these mice develop much more severe liver cancer that is associated with elimination of the

276 patocellular carcinoma (FL-HCC) is a primary liver cancer that predominantly affects children and you

277 llular carcinoma (FL-HCC), a rare but lethal liver cancer that primarily affects adolescents and youn

278 In liver cancer, the ERK-mediated XPO5 suppression reduces

279 Despite improvements in the management of liver cancer, the survival rate for patients with hepato

280 Therapies for primary liver cancer, the third leading cause of cancer-related

281 ace glypican 3 (GPC3), a possible marker for liver cancer theranostics, on the surface of a liver cel

282 a promising candidate for immunotoxin-based liver cancer therapy.

283 hat SCP1 is a potential tumor suppressor for liver cancers through dephosphorylating c-Myc Ser62.

284 ssion was decreased in the majority of human liver cancer tissues, and its reduced expression was sig

285 distinguish FLC from 25 other liver and non-liver cancer types.

286 The global incidence of liver cancer varied widely by nine-fold, and was negativ

287 reveal a novel link between NR2E3, AHR, and liver cancer via LSD1-mediated H3K4me2 histone modificat

288 belt and along the Mississippi River, while liver cancer was high along the Texas-Mexico border, and

289 n, 65 years +/- 5) with primary or secondary liver cancer were retrospectively included in this insti

290 n, we present an oncogenic role of FAM83H in liver cancer, which is closely associated with the oncog

291 Here, we identified an important step of liver cancer, which is the neutralization of tumor suppr

292 Liver cancer, which typically develops on a background o

293 patients underwent intraarterial therapy for liver cancer with either conventional TACE or TACE with

294 (HCC) is the most commonly diagnosed form of liver cancer with high morbidity and mortality.

295 nvasiveness in cholangiocarcinoma, a primary liver cancer with scarce treatment opportunities and dis

296 inoma (HCC) are clinically disparate primary liver cancers with etiological and biological heterogene

297 irus is a leading cause of liver disease and liver cancer, with approximately 3% of the world's popul

298 rikingly better outcomes compared to typical liver cancers, with 5-year survival rates of 57% to 100%

299 apeutic response in patients with metastatic liver cancer, without increasing systemic side effects.

300 global human pathogen and the main cause of liver cancer worldwide.