ライフサイエンスコーパス: liver tumor

1 thelial-mesenchymal transition and growth of liver tumor.

2 nagement of hepatoblastoma, a rare pediatric liver tumor.

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

4 a (HCC) is the most common primary malignant liver tumor.

5 patocellular adenomas (HCAs) are rare benign liver tumors.

6 hat Rassf1a homozygous knockout mice develop liver tumors.

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

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

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

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

11 carbon tetrachloride and DEN/TCPOBOP induced liver tumors.

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

13 % of Tlr4-/- NS5A Tg mice fed HCFD developed liver tumors.

14 ntra-arterial transcatheter drug delivery to liver tumors.

15 which predisposes mice to the development of liver tumors.

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

17 ffects correlate with increased frequency of liver tumors.

18 ture that was not associated previously with liver tumors.

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

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

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

22 ficantly upregulated genes in obese/diabetic liver tumors.

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

24 sporter in accounting for drug resistance in liver tumors.

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

26 antly decreased the multiplicity and size of liver tumors.

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

28 signaling; both are aberrantly expressed in liver tumors.

29 actually resulted in earlier development of liver tumors.

30 novel transarterial radiation treatment for liver tumors.

31 protein that display increased incidence of liver tumors.

32 r carcinoma (HCC) is the most common form of liver tumors.

33 ntitative noninvasive imaging biomarkers for liver tumors.

34 ral aggressive cancers, including breast and liver tumors.

35 pattern and development of fewer and smaller liver tumors.

36 aque bead (VERB) chemoembolization of rabbit liver tumors.

37 k genomic and transcriptomic profiles of 765 liver tumors.

38 PPS in patients with initially nonresectable liver tumors.

39 stiffness and fluidity to the malignancy of liver tumors.

40 ent in CT-guided microwave ablation (MWA) of liver tumors.

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

42 been extensively used to manage unresectable liver tumors.

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

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

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

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

49 gic levels and developed significantly fewer liver tumors after administration of diethylnitrosamine

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 athy (HE), pulmonary hypertension (PaHT), or liver tumors, among other complications.

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

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

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

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

60 ereotactic radiofrequency ablation (SRFA) of liver tumors and identify variables associated with decr

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

62 g in microwave ablation to accurately target liver tumors and increases accuracy for out-of-plane tar

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

64 hepatocytes triggered regression of primary liver tumors and melanoma-derived liver metastases.

65 ergone clinically indicated CT-guided MWA of liver tumors and were able to receive a CT contrast agen

66 tations in 3 histologically distinct primary liver tumors (angiosarcoma of the liver (ASL), cholangio

67 and in clinical conditions on patients with liver tumors are presented and discussed.

68 Obesity/diabetes-associated liver tumors are specifically vulnerable to cyclin D1 de

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

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

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

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

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

74 Materials and Methods A total of 21 VX2 liver tumor-bearing New Zealand white rabbits were used

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

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

77 The 2 patients with the highest liver tumor burden died within 6 mo of treatment, with t

78 ible safety concerns in patients with a high liver tumor burden should inform patient selection for f

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

80 endogenous albumin production while reducing liver tumor burden.

81 n pathway in both the expanding HPCs and the liver tumors but spared its orthodox pathway in pericent

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

106 red in response to TBT exposure and preceded liver tumor development.

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

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

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

110 We found that normal hepatocytes surrounding liver tumors displayed activation of YAP and TAZ and tha

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

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

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

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

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

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

117 ncreased polyploid hepatocytes develop fewer liver tumors following chronic liver damage.

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

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

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

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

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

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

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

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

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

127 in mice significantly attenuates DEN-induced liver tumor formation.

128 members, including APOBEC3B, fail to promote liver tumor formation.

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

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

131 tively, the overall 1-year, recurrence-free, liver-tumor-free, and extrahepatic disease-free survival

132 often necessary to segment and visualize the liver tumor from abdominal computed tomography images.

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

134 Thus, one urgent issue is how to convert the liver tumors from cold to hot and responsive, which may

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

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

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

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

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

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

141 e released Mn(2+) , and inhibited orthotopic liver tumor growth via synergistic SDT/CDT.

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

143 ECM remodeling, macrophage polarization, and liver tumor growth.

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

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

146 e, aiming at removing primarily unresectable liver tumors, has been criticized for safety issues with

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

148 ery has been proposed for patients with deep liver tumors having complex relationships.

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

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

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

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

153 tionale for applying this approach to survey liver tumor immunity and to stratify patients for immune

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

155 Trp53(KO)/C-Myc(OE) mice developed liver tumors in 3-5 weeks; injections of anti-PD1 did no

156 2011 to 2017 577 patients underwent SRFA for liver tumors in 892 ablation sessions.

157 (99m)Tc-MAA) uptake of primary and secondary liver tumors in a large patient cohort before (90)Y radi

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

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

160 Liver tumors in male mice were enriched in pathways and

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

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

163 We investigated mechanisms of resistance of liver tumors in mice to infiltrating T cells.

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 ocks cytokinesis and inhibits development of liver tumors in mice.

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

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

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

170 tial selective therapeutic vulnerability for liver tumors in obese/diabetic patients.

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

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

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

174 Liver tumor incidence and tumor numbers were strongly re

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

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

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

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

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

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

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

182 Further, this signature was enriched in liver tumors initiated by hydrodynamic injections of act

183 nd hepatocellular carcinoma (HCC), and mouse liver tumor initiating stem cell-like cells (TICs).

184 cogene yes-associated protein (YAP) controls liver tumor initiation and progression via cell extrinsi

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

186 Malignant liver tumor is one of the main causes of human death.

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

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

189 izes with KRAS(G12D) to induce an aggressive liver tumor leading to metastasis formation and reduced

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

191 issue interactions and their contribution to liver tumor malignancy remains elusive.

192 erapeutic targeting of Yap/Taz in aggressive liver tumors marked by elevated Myc/beta-catenin activit

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

194 35-77 years) with 60 malignant hypervascular liver tumors (mean diameter, 20.1 mm +/- 16.4 [standard

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

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

197 Conclusion MRI in a rabbit liver tumor model was used to visualize resistance mecha

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

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

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

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

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

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

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

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

206 NEMO, which develop inflammation-associated liver tumors (Nemo(LPC-KO) and Nemo(LPC-KO)Cxcr6(eGfp/eG

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

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

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

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

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

212 Liver tumors often require extended liver resection, ove

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

233 We perform the proposed algorithm to the Liver Tumor Segmentation Challenge dataset and evaluate

234 vary from one patient to another, automatic liver tumor segmentation is still a difficult task.

235 ieve more accurate and robustness results on liver tumor segmentation task.

236 lar pH-specific MR spectroscopy of untreated liver tumors showed acidosis (mean extracellular pH, 6.7

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

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

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

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

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

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

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

244 thway is a crucial component of p53-mediated liver tumor suppression and outline the mechanism by whi

245 ons for BRUCE in ATR activation in vitro and liver tumor suppression in vivo.

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

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

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

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

250 n significantly more weight and develop more liver tumors than similarly treated WT mice.

251 Hepatocellular carcinoma (HCC) is a liver tumor that usually arises in patients with cirrhos

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

253 Liver tumors that arose exhibited markedly elevated leve

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

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

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

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

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

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

260 We collected 50 liver tumors that were split into two experimental condi

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

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

263 2(KO) ) decreased the frequency of mice with liver tumors to around 17% and delayed the age of tumor

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

265 mal-tissue ratios as represented by tumor-to-liver, tumor-to-kidney, and tumor-to-muscle ratios incre

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

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

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

269 , which was effective in treating orthotopic liver tumors under obese/diabetic conditions.

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

271 (hazard ratio [HR], 1.22; 95%CI, 0.98-1.53], liver tumor volume (HR, 1.002; 95%CI, 1.0004-1.003), sub

272 In studies of mice with liver tumors, we found that CXCR6 mediated NKT-cell and

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

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

275 Liver tumors were induced in wild-type and P2y(2)r (-/-)

276 2016, 60 New Zealand white rabbits with VX2 liver tumors were randomly treated with VERBs at differe

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

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

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

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

281 abled targeted, noninvasive drug delivery to liver tumors while monitored with B-mode guidance and wi

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

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

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

285 Methods: Consecutive patients with liver tumors who underwent HBS before and after (90)Y ra

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

287 nts had a total of 41 primary and metastatic liver tumors with a median size of 9.0 cm (8.0-18.0 cm)

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

289 r very large (>=8 cm) primary and metastatic liver tumors with curative treatment intent.

290 degree of molecular heterogeneity among 580 liver tumors with diverse ethnicities and etiologies by

291 1 year, 5 of 9 Axin1fl/fl/Cre mice developed liver tumors with histologic features of HCC.

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

293 1 or codeletion of Rassf1a and Sav1 produced liver tumors with much higher efficiency than single del

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

295 sequence and the similar pixel intensity of liver tumors with their surrounding tissues, besides, th

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

297 r patients having >=1 deep centrally located liver tumor, with or without middle hepatic vein (MHV) i

298 f portal vein thromboses in patients without liver tumors, with and without cirrhosis.

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

300 activity of doxorubicin released locally in liver tumor xenografts without inducing any adverse effe