ライフサイエンスコーパス: liver tumor

1 nagement of hepatoblastoma, a rare pediatric liver tumor.

2 gy at 1 wk after treatment in the VX2 rabbit liver tumor.

3 thelial-mesenchymal transition and growth of liver tumor.

4 cally occurs in HCC but is uncommon in other liver tumors.

5 cranial indications such as lung, spine, and liver tumors.

6 emnants (FLR) to allow curative resection of liver tumors.

7 e types of agents might be effective against liver tumors.

8 been extensively used to manage unresectable liver tumors.

9 of Tgfbr2 alone (Tgfbr2(KO) ) did not induce liver tumors.

10 sporter in accounting for drug resistance in liver tumors.

11 rrest, and apoptosis in telomerase-deficient liver tumors.

12 antly decreased the multiplicity and size of liver tumors.

13 at high levels in proliferating liver and in liver tumors.

14 signaling; both are aberrantly expressed in liver tumors.

15 actually resulted in earlier development of liver tumors.

16 novel transarterial radiation treatment for liver tumors.

17 protein that display increased incidence of liver tumors.

18 has limited application for use in advanced liver tumors.

19 mental liver transplantation or resection of liver tumors.

20 hepatic inflammation and develop spontaneous liver tumors.

21 ted from hepatic tissues of all F1 mice with liver tumors.

22 complexes are involved in the development of liver tumors.

23 after partial hepatectomy (PH) and in human liver tumors.

24 herapeutic liver resection for patients with liver tumors.

25 y resistant to developing carcinogen-induced liver tumors.

26 P, exhibited lung tumors; some mice also had liver tumors.

27 iagnostic and therapeutic approach to common liver tumors.

28 luding chronic hepatitis C, fatty liver, and liver tumors.

29 hat Rassf1a homozygous knockout mice develop liver tumors.

30 n at stage 1 enabling resection of extensive liver tumors.

31 events OIS and cooperates with RAS to induce liver tumors.

32 bled ablative doses to be delivered to large liver tumors.

33 at high exposure levels and on female mouse liver tumors.

34 carbon tetrachloride and DEN/TCPOBOP induced liver tumors.

35 s are not the origin for hepatotoxin-induced liver tumors.

36 % of Tlr4-/- NS5A Tg mice fed HCFD developed liver tumors.

37 ntra-arterial transcatheter drug delivery to liver tumors.

38 with regard to the (99m)Tc-MAA uptake of the liver tumors.

39 ffects correlate with increased frequency of liver tumors.

40 ture that was not associated previously with liver tumors.

41 hepatocellular carcinomas and 21 metastatic liver tumors (13 colon, five other, and three unknown pr

42 mall cell lung tumors, 61 ovarian tumors, 70 liver tumors, 156 glioblastoma multiform samples, 27 eso

43 higher proportion of NS5A Tg mice developed liver tumors (39%) than mice that did not express HCV NS

44 aging-guided percutaneous cryoablation of 65 liver tumors (62 metastases, three hepatocellular carcin

45 exhibited a higher incidence of macroscopic liver tumors (71%) and cysts (86%) compared to a 21.4% a

46 GS: Atrial fibrillation ablation procedures, liver tumor ablations, and extracorporeal shock wave lit

47 methylation caused development of multifocal liver tumors accompanied by Apc LOH.

48 hepatocellular carcinoma (FL-HCC) is a rare liver tumor affecting adolescents and young adults with

49 two independent clones seeded the metastatic liver tumor after having diverged at different time poin

50 of shRNAs against Anln mRNA developed fewer liver tumors after administration of diethylnitrosamine

51 orrelate with greater necrosis in rabbit VX2 liver tumors after DEB TACE.

52 atients with extensive primary and secondary liver tumors after failure of first radioembolization.

53 bitor rapamycin diminishes FBP enrichment in liver tumors after hydrodynamic gene delivery of AKT pla

54 s a large-scale WGS dataset consisting of 88 liver tumors along with adjacent normal tissues.

55 ta-catenin stabilization in human and murine liver tumors also implicates this pathway in hepatocyte

56 Following percutaneous cryoablation of liver tumors, alterations in liver enzymes, myoglobin, a

57 active nucleoside triphosphates (NTP) in the liver tumor and high conversion in other tissues.

58 r carcinoma (HCC) is the most common primary liver tumor and the third greatest cause of cancer-relat

59 e, 40-88 years) underwent RF ablation for 26 liver tumors and 17 renal tumors.

60 cholangiocarcinoma (CCC) are the most common liver tumors and a leading cause for cancer-related deat

61 n perfusion values before and after TACE for liver tumors and adjacent liver tissue were compared by

62 for the early detection of urinary tract and liver tumors and aid in the classification and prognosti

63 therapeutic strategy for MYC-overexpressing liver tumors and highlight the relevance of transcriptio

64 Id1 is strongly expressed in human and mouse liver tumors and in hepatocellular carcinoma (HCC) cell

65 ted whether MAN2A1-FER is expressed by human liver tumors and its role in liver carcinogenesis.

66 stry for the ductular reaction and malignant liver tumors and several systemic disorders are among re

67 f high (124)I-IAZGP uptake in orthotopic rat liver tumors are consistent with independent measures of

68 logic consensus classification for pediatric liver tumors as a whole, with particular focus on the hi

69 lpha and G6PC, was up-regulated in the mouse liver tumors as well as in primary human HCC.

70 ted in HBV-mediated HCCs, is demethylated in liver tumors at CpG dinucleotides flanking the NF-kappaB

71 odel, with male experimental mice developing liver tumors at reduced latency and higher tumor penetra

72 atocellular carcinoma, which resembled human liver tumors, based on genomic and histologic analyses.

73 ean age, 61.0 y) with nonresectable advanced liver tumors (breast cancer liver metastases, n = 7; col

74 plantation for the treatment of benign solid liver tumors (BSLT) is not well defined.

75 In male mice, liver tumor burden was recently found to correlate with

76 endogenous albumin production while reducing liver tumor burden.

77 ation at the KMT2B locus is present in three liver tumors, but absent in their matched adjacent norma

78 ase of phosphorylated ERK1/2 in all types of liver tumors, but nuclear localization of beta-catenin,

79 To address this issue, we generated murine liver tumors by constitutively active AKT-1 (AKT) and be

80 uggest that viruses and hepatoxins may cause liver tumors by simply driving hepatocyte turnover witho

81 show that viable tumor regions in malignant liver tumors can be differentiated from fibrous and necr

82 In four rabbits implanted with eight VX2 liver tumors, catheters were positioned in the hepatic a

83 herapeutic developments for the treatment of liver tumors caused by distinct genetic mutations.

84 dendritic cells (DCs) pulsed ex vivo with a liver tumor cell line lysate (HepG2) in patients with ad

85 selected microRNAs that are up-regulated in liver tumor cells can promote malignant features, contri

86 t autocrine stimulation of TGF-beta in human liver tumor cells correlates with a mesenchymal-like phe

87 However, liver tumor cells develop mechanisms to overcome its sup

88 Once liver tumor cells have developed, STAT3 likely acts as a

89 sion, microRNAs with decreased expression in liver tumor cells may normally aid in limiting neoplasti

90 Treatment of primary mouse hepatocytes and liver tumor cells with Wnt5a led to a notable decrease i

91 In liver tumor cells, we recently showed that MYC inactivat

92 Liver tumors, characterized by hepatic steatosis, develo

93 nuclear receptor Shp(-/-) liver tissues and liver tumors compared with wild-type mice.

94 -expression of Igf2 accelerated formation of liver tumors, compared to mice with livers expressing on

95 ects were documented in a set of HBV-related liver tumors consistent with the likelihood that downreg

96 of Toll-like receptor 4 (TLR4), and develop liver tumors containing tumor-initiating stem-like cells

97 Molecules secreted by liver tumors contributing to HSC activation and peritumo

98 ibly targeting the microenvironment in which liver tumors develop.

99 c-Met were coinjected into CCND1-null mice, liver tumors developed despite the absence of CCND1.

100 derived from PBP(DeltaLiv) hepatocytes; all liver tumors developing in Pbp(DeltaLiv) mice maintained

101 -expression of AKT and c-Met triggered rapid liver tumor development and mice required to be euthaniz

102 f1, c-Myc, and their combination may promote liver tumor development by distinct mechanisms.

103 enitor cells transduced with TLR4 results in liver tumor development in mice following repetitive LPS

104 itor cells, underlying the increased risk of liver tumor development in obese individuals.

105 correlated with a significant retardation of liver tumor development in this strain versus the Mdr2-K

106 t that CCND1 expression is not essential for liver tumor development induced by c-Met and beta-cateni

107 of a pro-death Bcl-2 family protein, Bid, in liver tumor development using a neonatal diethylnitrosam

108 N-Ras resulted in a dramatic acceleration of liver tumor development when compared with mice overexpr

109 etween the AKT and Ras pathways in promoting liver tumor development, and the pivotal role of mTORC1-

110 hol-induced deregulation of Pol III genes in liver tumor development.

111 cascades in mediating AKT and N-Ras-induced liver tumor development.

112 jb1-Prkaca fusion and monitored the mice for liver tumor development.

113 NA levels, pluripotency gene expression, and liver tumor differentiation.

114 rrx1a stimulates metastatic outgrowth in the liver, tumor differentiation, and MET.

115 profiled miRNA expression changes in de novo liver tumors driven by MYC and/or RAS, two canonical onc

116 s the conspicuity of malignant hypervascular liver tumors during the late hepatic arterial phase whil

117 ular carcinoma cell line HUH7, as well as in liver tumors, esophageal adenocarcinoma, glioblastoma mu

118 HepG2 liver tumors exhibited high peak uptake (836.6 +/- 86.6

119 Consistent with this possibility, mouse liver tumors exhibited reduced Tet1 protein levels.

120 n be safely applied to patients with primary liver tumors far advanced or/and pretreated.

121 hepatitis, fatty degeneration, cirrhosis and liver tumors, FGF21 levels in hepatocytes or phenotypica

122 nodular hyperplasia (FNH) is a common benign liver tumor for which conservative management is indicat

123 ingle i.p. injection of DEN, AHR antagonized liver tumor formation and growth by regulating cell prol

124 Increased hepatocyte proliferation and liver tumor formation have also been observed in FGF19 t

125 that RIPK1 deficiency decreases DEN-induced liver tumor formation in a TNFR1-dependent manner.

126 -UV-MS correlated well with TD 50 values for liver tumor formation in rats.

127 xamined the role of Se and selenoproteins in liver tumor formation in TGFalpha/c-Myc transgenic mice,

128 through which TGF-beta signaling may promote liver tumor formation in the setting of p53 loss reveale

129 nflammation, and fibrosis but rarely induced liver tumor formation in wild-type mice.

130 of VD deprivation (VDD) in in vivo models of liver tumor formation revealed striking three-fold incre

131 anti-miR-494 treatment of primary MYC-driven liver tumor formation significantly diminishes tumor siz

132 of p53, independent of TGF-beta, may affect liver tumor formation through effects on a common liver

133 n A2-deficient hepatocytes, where a delay in liver tumor formation was observed.

134 kinase activity did not inhibit DEN-induced liver tumor formation, showing that kinase-independent f

135 on and Pol III gene transcription to promote liver tumor formation.

136 lian liver growth and a potent suppressor of liver tumor formation.

137 effect of hypomethylation on intestinal and liver tumor formation.

138 In liver tumors from animals modeling HBx- and HBV-mediated

139 Significantly, liver tumors from HBx/c-myc bitransgenic mice and chroni

140 ceptor (Egfr) gene were common in SB-induced liver tumors from male mice (10/10, 100%) but infrequent

141 of PTEN leads to spontaneous development of liver tumors from progenitor cells.

142 elationship between Plk1 and Suz12/Znf198 in liver tumors from X/c-myc bitransgenic mice and woodchuc

143 Notably, liver tumors from X/c-myc bitransgenic mice exhibited do

144 endothelial NO synthase (eNOS)-derived NO on liver tumor growth and metastasis in relation to adjacen

145 o rats, but was without effect in inhibiting liver tumor growth in rats with more advanced tumors.

146 icacy of lapatinib to significantly suppress liver tumor growth was tested in an orthotopic, syngenei

147 After liver tumors had formed, hypoxia was induced by vascular

148 Local transcatheter delivery of sorafenib to liver tumors has the potential to reduce systemic toxici

149 Benign and malignant liver tumors have been more frequently reported with the

150 The study included 25 patients with primary liver tumors (hepatocellular carcinoma: n = 3, intrahepa

151 e oncogenic function of STAT3 in DEN-induced liver tumor, hepatocyte-specific STAT3 knockout mice wer

152 female FXR(-/-) mice spontaneously developed liver tumors; however, no other tumors were developed af

153 sential for initiation of carcinogen-induced liver tumors; however, whether FoxM1 constitutes a thera

154 Exome sequencing analysis of 243 liver tumors identified mutational signatures associated

155 Although they did not spontaneously develop liver tumors, IL-22TG mice were more susceptible to diet

156 Hepatoblastoma is the most common malignant liver tumor in childhood.

157 For a solitary malignant liver tumor in the left lateral segment, should laparosc

158 phy (CT)-guided percutaneous RF ablations of liver tumors in 26 patients (13 men, 13 women; mean age,

159 (99m)Tc-MAA) uptake of primary and secondary liver tumors in a large patient cohort before (90)Y radi

160 tion of Trp53 alone (Trp53(KO) ) resulted in liver tumors in approximately 41% of mice by 10 months o

161 fficient to hypothesize a mode of action for liver tumors in female mice.

162 has been shown to increase the incidence in liver tumors in mice in a 2-year bioassay conducted by t

163 eric cDNA leads to the formation of indolent liver tumors in mice that closely resemble human FL-HCC.

164 ahepatic injection of HB cell lines leads to liver tumors in mice with growth patterns and biologic,

165 rexpression of IGF2 accelerates formation of liver tumors in mice with hepatic expression of MYC and

166 mas (HCCs) and in diethylnitrosamine-induced liver tumors in mice, which is primarily due to transcri

167 ynergistic effects during the development of liver tumors in mice.

168 human HCC samples and promotes formation of liver tumors in mice.

169 ocks cytokinesis and inhibits development of liver tumors in mice.

170 n (TRADD)-dependent hepatocyte apoptosis and liver tumors in NEMO(LPC-KO) mice, revealing distinct ki

171 atoma cells and reduces growth of orthotopic liver tumors in rats.

172 activated receptor alpha (PPARalpha), induce liver tumors in rodents and may produce cholestasis in h

173 diet resulted in advanced ACF formation and liver tumors in wild type mice.

174 systems: two different human cell lines, in liver tumors in wild-type mice, and in mice that carried

175 mportant role in unregulated liver growth in liver tumors, in regulated growth during liver regenerat

176 ets with high sugar content had the greatest liver tumor incidence while dietary fat intake was not a

177 ients with surgically unresectable malignant liver tumors, including 34 patients with primary uveal m

178 th GRP94 and PTEN accelerated development of liver tumors, including both hepatocellular carcinoma (H

179 RNA in a cirrhotic rat model with multifocal liver tumors increased circulating serum albumin by over

180 ditional mutant livers have multiple foci of liver tumors, indicating that the combined activities of

181 cellular carcinoma (HCC) is the main type of liver tumor induced by kras(V12) expression.

182 At the molecular level, liver tumors induced by AKT/c-Met display activation of

183 effect of the TGF-beta signaling pathway on liver tumors induced by phosphatase and tensin homolog (

184 ress, consequently suppressing injury-driven liver tumor initiation.

185 A highly invasive surgical resection of the liver tumor is the main approach used to eliminate the t

186 Because development of liver tumors is associated with increasing age, we inves

187 est that loss of promoter-associated 5hmC in liver tumors licenses reprograming of DNA methylation at

188 nt stromal myofibroblasts and matrix because liver tumors maintain a rich, vascular stromal network e

189 ete response, including regressions of bulky liver tumor masses, ongoing beyond 7 y following adoptiv

190 35-77 years) with 60 malignant hypervascular liver tumors (mean diameter, 20.1 mm +/- 16.4 [standard

191 study, the diethylnitrosamine (DEN)-induced liver tumor model and the chronic carbon tetrachloride (

192 he detection of hypoxia in an orthotopic rat liver tumor model by comparing regions of high (124)I-IA

193 rterial embolization (TAE) in the VX2 rabbit liver tumor model by using multimodality imaging, includ

194 with that of ablation alone (n = 6) for VX2 liver tumor model in rabbits.

195 In an advanced murine metastatic liver tumor model, IL-2 inhibited tumor growth in a dose

196 s feeding arteries after TAE in a rabbit VX2 liver tumor model.

197 liver inflammation was compared between two liver tumor models using a combination of AKT-CAT or AKT

198 mor size are apparent in mouse xenograft and liver tumor models.

199 Mice with an eNOS deficiency developed liver tumors more frequently in response to carcinogens

200 stratification by all of the major pediatric liver tumor multicenter trial groups.

201 -type mice, ArKO mice, and ArKO mice bearing liver tumors (n = 3-5/group), and in nude mice bearing h

202 ted serum alanine aminotransferase (ALT) and liver tumor necrosis factor alpha (Tnf-alpha) levels.

203 histopathological characteristics, increased liver tumor necrosis factor alpha and IL-6, decreased gl

204 Liver tumor necrosis factor alpha levels were higher in

205 sferase and tumor necrosis factor-alpha, and liver tumor necrosis factor-alpha and interleukin 1beta

206 We sequenced insertions in 63 liver tumor nodules and identified at least 16 genes/loc

207 administration reduced serum IL-6 levels and liver tumor numbers to levels similar to those observed

208 he presence of CD133/Nanog-positive cells in liver tumors of alcohol-fed NS5A Tg mice.

209 These results were confirmed in liver tumors of HBV X gene transgenic mice.

210 genomes found integrated in genomic DNA from liver tumors of patients with hepatocellular carcinoma (

211 o detect HSV1-tk transgene expression in the liver tumors of patients.

212 tients presenting with primary or metastatic liver tumors often face the dilemma that the remaining l

213 Liver tumors often require extended liver resection, ove

214 Patients with single liver tumors or as many as 3 nodules </=3 cm are classif

215 curative resection of marginally resectable liver tumors or metastases in patients that might otherw

216 resection secondary to primary or metastatic liver tumors, or in living donor liver transplantation,

217 nsgenic mice and followed the development of liver tumors over time, characterizing cellular and mole

218 P MR imaging can depict serial reductions in liver tumor perfusion during TAE.

219 aging can depict serial reductions in rabbit liver tumor perfusion during transcatheter arterial embo

220 ion in a line phantom and reduced noise in a liver tumor phantom when PICCS was compared with FBP.

221 Our study suggests that liver tumor phenotype is defined by a combination of dri

222 factor (GM-CSF; sargramostim) for malignant liver tumors, predominantly hepatic metastases from pati

223 re positive, 2 equivocal and 14 negative for liver tumors) previously studied by the US National Toxi

224 transgenic zebrafish resulted in accelerated liver tumor progression in males.

225 However, potential contributions of VD to liver tumor progression in the context of TGF-beta signa

226 the significance of Galpha12 upregulation in liver tumor progression, implicating Galpha12 as an attr

227 ine model, supporting a HCC-HSC crosstalk in liver tumor progression.

228 EMT is associated with a high rate of liver tumor proliferation, invasion, and metastasis in v

229 ary or genetic obesity is a potent bona fide liver tumor promoter in mice.

230 tive androstane receptor (CAR), a well-known liver tumor promoter that mediates toxic bile acid signa

231 lar carcinoma (HCC) development, acting as a liver tumor promoter.

232 Together, our findings suggest that liver tumor promotion is enhanced by an impaired metabol

233 effective strategy for targeted ablation of liver tumors, prompting its further evaluation for HCC t

234 They also formed a broad spectrum of liver tumors, ranging from cholangiocarcinoma to hepatoc

235 sts among the TGF-beta and CXCR4 pathways in liver tumors, reflecting a novel molecular mechanism tha

236 In advanced liver tumors, repeated whole-liver treatments with (90)Y

237 angiography in localizing and/or visualizing liver tumors ("seeing" the tumor) and targeting tumors t

238 llular carcinoma is a rare primary malignant liver tumor, significantly different from generic hepato

239 d increased risk of death versus the largest liver tumor size less than 3 cm (P = .05).

240 Only the largest liver tumor size more than 5 cm was found to be a signif

241 tion of the naked mAbs reduced splenomegaly, liver tumor spots, and tumor burden in BLCL-engrafted im

242 ive studies from the International Childhood Liver Tumor Strategy Group (SIOPEL 2 [S2] and SIOPEL [S3

243 t of the multicenter international childhood liver tumors strategy group, SIOPEL-1, study in 1990.

244 The INT-0098 Intergroup Liver Tumor Study demonstrated no statistically signific

245 INT-0098 Intergroup Liver Tumor Study demonstrated that patients with HB tre

246 ansplantation to patients with nonresectable liver tumors such as hepatocellular carcinoma and colore

247 and in both an in vitro and in vivo model of liver tumors, suggesting a new target for liver cancer c

248 ng correlated with FGF21 expression in human liver tumors, suggesting that treatment of glutamine-add

249 Autophagy-mediated miR-224 degradation and liver tumor suppression were further confirmed by the au

250 t, thus indicating this factor as a possible liver tumor suppressor gene.

251 Furthermore, we find that TRIB2 relieves the liver tumor suppressor protein C/EBPalpha-mediated inhib

252 These findings identify TGR5 as a novel liver tumor suppressor that may serve as an attractive t

253 lfatase, sulfatase 1 (SULF1), functions as a liver tumor suppressor, but the role of the related sulf

254 ling paradoxically promotes the formation of liver tumors that arise in the setting of p53 inactivati

255 Liver tumors that arose exhibited markedly elevated leve

256 S: Hepatocellular adenomas (HCAs) are benign liver tumors that can be assigned to molecular subtypes

257 Hepatocellular adenomas (HCAs) are benign liver tumors that can be assigned to molecular subtypes

258 Spontaneous liver tumors that developed in AlfpCre(+)Trp53(Delta2-10

259 point genes compared with chemically induced liver tumors that developed mice with wild-type Trp53.

260 nd Tsc1fl/fl;Ptenfl/fl;AlbCre mice developed liver tumors that differed in size, number, and histolog

261 ines into the livers of mice would result in liver tumors that resemble their clinical counterparts.

262 amma in tumor-bearing mice and regression of liver tumors that was abolished in IFN-gamma((-/-)) mice

263 al biliary tract disorders, and pathology of liver tumors, the emerging data have important diagnosti

264 The size and number of liver tumors, the ratio between liver and body weight, a

265 tion, CPS1 was silenced or down-regulated in liver tumor tissues compared with the matched noncancero

266 2(KO) ) decreased the frequency of mice with liver tumors to around 17% and delayed the age of tumor

267 netic lesions commonly associated with human liver tumors to reconstruct genetic progression to hepat

268 Tumor-to-liver, tumor-to-blood, tumor-to-muscle, and tumor-to-bon

269 The average tumor-to-red marrow, tumor-to-liver, tumor-to-lungs, and tumor-to-kidneys ratios were

270 significantly higher tumor-to-lung, tumor-to-liver, tumor-to-spleen, and tumor-to-muscle ratios.

271 hat the major contributor to creation of the liver tumor transcriptome was changes in gene copy numbe

272 Between 2003 and 2011, 260 patients with liver tumors treated by RE were studied (standard protoc

273 For other liver tumors, tumor size (P = .001) and tumor burden (P

274 rs) known or suspected to have hypervascular liver tumors underwent dual-energy 64-section multidetec

275 Sixteen rats with liver tumors underwent TAE with 1 mg (group 1) or 3 mg (

276 aracterization and quantification of the VX2 liver tumor viability after drug-eluting beads transarte

277 the DW MR criteria for benign and malignant liver tumors were applied, 44 of 90 (49%) lesions would

278 We found that liver tumors were generally induced from multiple foci d

279 In seven rabbits in which nine VX2 liver tumors were implanted, T2*-weighted gradient-echo

280 In contrast, no liver tumors were observed in wild-type mice of the same

281 approved study, New Zealand white rabbit VX2 liver tumors were treated transarterially with DOX-loade

282 ng primary, disseminated lung, or metastatic liver tumors were uniformly cured after administration o

283 out (ArKO) mice that spontaneously developed liver tumors were used as an additional in vivo model to

284 ast, in intrahepatic xenografts in cirrhotic livers, tumors were dominated by epithelial traits repro

285 rcinoma or metastatic liver disease or other liver tumors, were identified.

286 opic responses, including the development of liver tumors, when it is chronically activated by struct

287 with tumor suppressor activity in breast and liver tumors where it is mutated; however, the critical

288 high dose of chemotherapy or radiation into liver tumors while minimizing the impact on liver parenc

289 arterial catheter-directed administration to liver tumors while permitting MRI/CT visualization for p

290 with primary (n = 92) or secondary (n = 274) liver tumors who had received (90)Y radioembolization we

291 mary (n = 8) or secondary (n = 35) malignant liver tumors who underwent computed tomography (CT)-guid

292 ), which is also a hotspot mutation in human liver tumors whose incidence correlates with AFB1 exposu

293 proton beam radiotherapy was directed to the liver tumor with an additional 1-2 cm margin.

294 patic cholangiocarcinomas (ICCs) are primary liver tumors with a poor prognosis.

295 1 year, 5 of 9 Axin1fl/fl/Cre mice developed liver tumors with histologic features of HCC.

296 Rb family triple knockout mice develop liver tumors with histopathological features and gene ex

297 1 or codeletion of Rassf1a and Sav1 produced liver tumors with much higher efficiency than single del

298 tage hepatectomy for patients with extensive liver tumors with predicted small liver remnants, which

299 tained 2-7 days apart in seven patients with liver tumors with two scanning phases (phase 1: 30-secon

300 express Myc and Akt1 in liver, which develop liver tumors, with or without hepatic expression of Igf2