ライフサイエンスコーパス: TACE

1 TACE activation is central to the pathogenesis of NASH a

2 TACE and AREG, but not TGF-alpha, were overexpressed in

3 TACE deficiency in oligodendrocyte progenitor cells foll

4 TACE genetic depletion in OPs abrogates EGFR activation

5 TACE is a major shedding protease, responsible for the l

6 TACE is a potential target to treat TNF-alpha-dependent

7 TACE plus RT was more therapeutically beneficial than TA

8 TACE was discontinued for toxicity in four of 44 (9%) pa

9 TACE with drug-eluting beads (DEB-TACE), a novel drug de

10 There were 41 (RS, 11; TACE MWA, 30) instances of progression occurring after a

11 , median age 63 (34-84) years] underwent 111 TACE sessions.

12 42 (38.2%) TACE procedures resulted in complications [PEF 28 (25.2%

13 ly undergone local-regional therapy (RS, 41; TACE MWA, 80; mean age, 65.4 years; 84 men [69.4%]) and

14 c mice, albuminuria, increased Src pTyr-416, TACE activation, ERK and EGFR phosphorylation, glomerula

15 83 of 370 patients (22.4%) after 107 of 513 TACE procedures (20.8%) met the predefined criteria.

16 rospective study, 370 patients underwent 513 TACE procedures between October 2014 and September 2016.

17 Our simulations reveal that directly after a TACE- treatment an unstable tumour state can be observed

18 ligand transforming growth factor alpha in a TACE-dependent manner.

19 Patients that undergo a TACE-treatment are categorised in partial and complete r

20 tegrin receptors by magnetic beads activated TACE and shed HB-EGF and TGF-alpha.

21 decreased TACE promoter luciferase activity, TACE expression, and TACE enzymatic activity in wtDCs or

22 increased TACE promoter luciferase activity, TACE expression, and TACE enzymatic activity in wtDCs.

23 vents premature Neogenin shedding by ADAM17 (TACE).

24 substrate ectodomain sheddase enzyme ADAM17 (TACE) in macrophages.

25 o paralleled the reduced activity of ADAM17 (TACE).

26 id not alter the levels of ADAM10 and ADAM17/TACE.

27 nd TGF-alpha is mediated via integrin-ADAM17/TACE interactions.

28 ferentiation via alpha6beta1 integrin-ADAM17/TACE signaling pathway.

29 way, triggered by the metalloprotease ADAM17/TACE, and a lipid droplet (LD)-mediated mechanism of pro

30 After TACE with 70-150-mum SEBs, ITSC was 40.4 mug/g on day 1

31 e radiotracer delivery parameter K (1) after TACE was observed.

32 n of VEGFR2 was inhibited until day 14 after TACE with both sizes of SEBs.

33 to compare images obtained before and after TACE showed a significant reduction in tumor enhancement

34 cone-beam CT was performed before and after TACE.

35 d as pain and/or nausea beyond 6 hours after TACE that required intravenous medication for symptom co

36 e cone-beam CT can be used immediately after TACE with doxorubicin-eluting beads to predict HCC tumor

37 The ADC ratio 1 month after TACE was an independent predictor of PFS, which showed s

38 Responses 1 month after TACE were assessed with the ADC change relative to basel

39 cluding DW imaging, before and 1 month after TACE.

40 was performed at baseline and 1 month after TACE.

41 nts underwent transplantation 4 months after TACE, allowing the association between response and hist

42 mean (18)F-FLT PET uptake was observed after TACE, correlating with an observed PET response of 60% (

43 7.42 dB median decrease in tumor power after TACE compared to only a 0.06 dB median decrease with con

44 Results Maximum PSC after TACE with 100-300-mum SEBs was 0.002 mug/mL on day 1.

45 Lesion response after TACE by modified RECIST was 58% (14 patients with 24 les

46 ponse rate (ORR), safety, and survival after TACE by using idarubicin-loaded beads for unresectable H

47 cipants underwent a curative treatment after TACE.

48 Imaging was repeated 6-8 wk after TACE.

49 Although TACE achieves substantial necrosis of the tumor, complet

50 and TNFko DCs, indicating that AP-2alpha and TACE are inversely dependent on sTNF and are functionall

51 hHSC time dependently expressed AR and TACE.

52 er luciferase activity, TACE expression, and TACE enzymatic activity in wtDCs or TNFko DCs.

53 er luciferase activity, TACE expression, and TACE enzymatic activity in wtDCs.

54 ng that MUC1 is required for CSE-induced and TACE-mediated TNF-alpha secretion.

55 lphaTACE), that colocalizes with MT1-MMP and TACE on the cell surface.

56 IMP-1 with superb affinities for MT1-MMP and TACE, to the glycosyl-phosphatidyl inositol anchor of pr

57 llate cells by a NOX2-dependent pathway, and TACE was induced after exposure to AGEs.

58 ma-secretase cleavage complex (PS1, PS2) and TACE (ADAM17), which releases the Trop2 intracellular do

59 nsecutive patients with HCC underwent RS and TACE MWA, respectively.

60 production of reactive oxidative species and TACE activity significantly increased with an increase i

61 to DCA resulted in colocalization of Src and TACE to the cell membrane, resulting in AREG-dependent a

62 Median overall survival in TEA and TACE was 24.3 months (95% confidence interval [CI]: 12.8

63 The role of NOX2, Sirt1, Timp3, and TACE was evaluated in choline-deficient L-amino acid def

64 nd metalloprotease 17 (ADAM17; also known as TACE) was found to be critical for hBD-3 induction, whil

65 ity over other zinc metalloproteases such as TACE, MMP2, MMP3, MMP13, and MMP14.

66 TPD significantly attenuated TACE-mediated disease models of sepsis, rheumatoid arthr

67 ncerns about potential side effects, because TACE also protects the skin and intestinal barrier by ac

68 ion type, presence of PVTT, and time between TACE and RT.

69 e (ERK) activity, which can be eliminated by TACE knockout, suggesting that these waves of oscillator

70 d dynamic (18)F-FLT PET with KSF followed by TACE.

71 Thus, modulation of Nrg1TIII by TACE/ADAM17 inhibition may represent a general treatment

72 d on autocrine/paracrine signals produced by TACE.

73 atic HCC, treatment of intrahepatic tumor by TACE may be associated with improved survival.

74 and metalloprotease 17 (ADAM17, also called TACE), which is responsible for the cleavage of membrane

75 Transarterial chemoembolisation (TACE) is the standard of care for patients with intermed

76 to describe transarterial chemoembolisation (TACE) therapies.

77 ractory to trans-arterial chemoembolization (TACE) and stereotactic body radiotherapy (SBRT), with an

78 to transcatheter arterial chemoembolization (TACE) based on immune markers and tumor biology in patie

79 Trans-arterial chemoembolization (TACE) is an important yet variably effective treatment f

80 Transcatheter arterial chemoembolization (TACE) is currently considered a first-line therapy for u

81 Transcatheter arterial chemoembolization (TACE) is the first-line therapy recommended for patients

82 er transcatheter arterial chemoembolization (TACE) with two different sizes of sunitinib-eluting bead

83 ing transarterial hepatic chemoembolization (TACE) for hepatocellular carcinoma.

84 orafenib or transarterial chemoembolization (TACE) by HCC-associated comorbidities.

85 my (RS) and transarterial chemoembolization (TACE) combined with microwave ablation (MWA) in the trea

86 ation (TAE)/transarterial chemoembolization (TACE) in a state of cell cycle arrest-a function that ma

87 ntial after transarterial chemoembolization (TACE) in hepatocellular carcinoma (HCC) because of the p

88 mbined with transarterial chemoembolization (TACE) in treating pediatric hepatoblastoma.

89 Transarterial chemoembolization (TACE) is the main treatment for intermediate stage hepat

90 r the first transarterial chemoembolization (TACE) procedure.

91 Transarterial chemoembolization (TACE) using lipiodol-based regimens, including the admin

92 Transarterial chemoembolization (TACE) was similarly applied to the two groups (60% vs. 6

93 d beads for transarterial chemoembolization (TACE) were previously evaluated for the appropriate dose

94 onventional transarterial chemoembolization (TACE), four underwent conventional TACE with extracellul

95 of SRFA to transarterial chemoembolization (TACE), hepatic resection (HR) and chemotherapy (CTX).

96 neoadjuvant transarterial chemoembolization (TACE).

97 bead (DEB) transarterial chemoembolization (TACE).

98 reated with transarterial chemoembolization (TACE).

99 on (TAE) or transarterial chemoembolization (TACE).

100 All patients received chemotherapy, TACE, and HIFU ablation.

101 Constitutive TACE depletion in OPs in vivo leads to similar alteratio

102 Conventional TACE with doxorubicin, cisplatin, and Ethiodol was perfo

103 py for liver cancer with either conventional TACE or TACE with drug-eluting beads.

104 sponse rates trended higher for conventional TACE (conventional TACE, 65.4%; DEBDOX, 63.8%; hqTACE, 5

105 d higher for conventional TACE (conventional TACE, 65.4%; DEBDOX, 63.8%; hqTACE, 53.8%) (P = .085).

106 own to have similar efficacy to conventional TACE (cTACE); it also exhibits fewer adverse effects res

107 lization (TACE), four underwent conventional TACE with extracellular pH-buffering bicarbonate, and fi

108 esponse rates when treated with conventional TACE, but no significant differences were seen for DEBDO

109 the maturation of the TNF-alpha convertase (TACE), which controls shedding of TNF-alpha and its biol

110 to target the protease TNF-alpha convertase (TACE), which releases TNF-alpha from cells.

111 DEB TACE was followed by 3- and 7-day sacrifice, tumor harve

112 ecrosis in rabbit VX2 liver tumors after DEB TACE.

113 ntinuous sorafenib therapy and on-demand DEB TACE provided excellent local disease control and did no

114 Up to four rounds of DEB TACE therapy were allowed on demand within 6 months.

115 started 1 week before the first round of DEB TACE, which was performed in 6-week cycles.

116 ian weight, 2.8 kg) underwent successful DEB TACE.

117 of sorafenib therapy in combination with DEB TACE may have a survival benefit in patients with advanc

118 DEB-TACE response was based on modified Response Evaluation

119 s associated with overall survival after DEB-TACE, stressing the role of post-TACE events, was perfor

120 s the development of early ascites after DEB-TACE-1 (median OS, 17 months), which was closely related

121 achieved in 50.9% and 57.1% of cTACE and DEB-TACE patients, respectively; at least 50% necrosis was e

122 TACE with drug-eluting beads (DEB-TACE), a novel drug delivery system that produces a slow

123 ined with TACE using drug-eluting beads (DEB-TACE), which was given via the hepatic artery 2-5 weeks

124 emoembolization with drug-eluting beads (DEB-TACE).

125 g beads transarterial chemoembolization (DEB-TACE).

126 Tumors (mRECIST) criteria) to the first DEB-TACE (DEB-TACE-1) was 70.3%; the median OS from DEB-TACE

127 dependent factors for survival following DEB-TACE-1.

128 EB-TACE-1) was 70.3%; the median OS from DEB-TACE-1 was 27 months (95% confidence interval (CI), 24-3

129 n-eluting microspheres (DEB) (hereafter, DEB-TACE) and subsequently underwent transplantation over a

130 urrence to assess independent effects of DEB-TACE response on recurrence.

131 s with HCC who underwent cTACE (n=76) or DEB-TACE (n=35) before OLT at a single center between Januar

132 Early ascites post-DEB-TACE is associated with the survival of patients despite

133 of the development of early ascites post-DEB-TACE.

134 RECIST) criteria) to the first DEB-TACE (DEB-TACE-1) was 70.3%; the median OS from DEB-TACE-1 was 27

135 Poor response to DEB-TACE (SD or DP) was present in 86% of cases and accounte

136 RPRETATION: The addition of sorafenib to DEB-TACE does not improve progression-free survival in Europ

137 Conclusion Response to DEB-TACE is correlated with tumor biology and patients at ri

138 ed in each group that were attributed to DEB-TACE.

139 total of 216 HCC patients who underwent DEB-TACE from October 2008 to October 2015 at a tertiary hos

140 gic response rate to cTACE compared with DEB-TACE in patients undergoing OLT has not been well descri

141 dol was performed for 159 procedures, DEBDOX TACE was performed for 47, and hqTACE was performed for

142 enhanced AP-2alpha expression and decreased TACE promoter luciferase activity in DCs.

143 ly, transfection of AP-2alpha cDNA decreased TACE promoter luciferase activity, TACE expression, and

144 g genetic mouse models to selectively delete TACE expression in oligodendrocyte progenitors cells (OP

145 +/- 0.05; P = .02) using bicarbonate during TACE increased peri- and intratumoral immune cell infilt

146 umor burden (P = .004), drug-eluting embolic TACE (P = .03), doxorubicin dose (P = .003), history of

147 PES, tumor burden, and drug-eluting embolic TACE were identified as the strongest predictors by the

148 Transarterial-chemo-embolization (TACE) is used for palliation of unresectable hepatocellu

149 roteases such as TNFalpha converting enzyme (TACE) (Ki = 4.45 +/- 0.48 muM).

150 factor alpha (TNF-alpha)-converting enzyme (TACE) are prominent membrane-anchored metalloproteinases

151 mor necrosis factor-alpha-converting enzyme (TACE) inhibitor, TAPI-2.

152 nase 17 (ADAM17)/TNFalpha Converting Enzyme (TACE) is associated with inflammatory disorders and canc

153 factor alpha (TNF-alpha)-converting enzyme (TACE) is at the center of inflammatory processes.

154 is generated by TNF-alpha converting enzyme (TACE) proteolytic release of the transmembrane TNF (tmTN

155 factor-alpha (TNF-alpha) converting enzyme (TACE) were also assessed.

156 activity of the TNF-alpha-converting enzyme (TACE), arguing that MUC1 is required for CSE-induced and

157 mor necrosis factor-alpha converting enzyme (TACE), as a novel key modulator of oligodendrocyte (OL)

158 mor necrosis factor-alpha-converting enzyme (TACE), enhanced CXCL12-CXCR4-induced motility and rapid

159 its activator, TNF-alpha converting enzyme (TACE).

160 mor necrosis factor-alpha-converting enzyme (TACE/ADAM17), also ameliorates the neuropathy.

161 mor necrosis factor alpha-converting enzyme (TACE; ADAM17, CD156b), the metalloproteinase shedding CD

162 ere measured at baseline and after the first TACE on contrast material-enhanced magnetic resonance im

163 We investigated the effect of the first TACE on parameters of liver function and tumor response

164 After the first TACE procedure, TACE was repeated twice in 4-week interv

165 ith multifocal, bilobar NELM after the first TACE procedure.

166 nse (CR) rate was 82.9% for RS and 82.5% for TACE MWA (odds ratio, 1.0; 95% confidence interval [CI]:

167 recently described an essential function for TACE/ADAM17 in regulating oligodendrogenesis during post

168 ant trends in which survival was greater for TACE plus RT in patients with PVTT compared with those w

169 followed by 1-mm gelatin-sponge pellets, for TACE.

170 ACE inhibitor IC-3 or in cells isolated from TACE knock-out mice, mechanical strain did not release l

171 al prognosis who may not profit from further TACE sessions.

172 After making a treatment decision (e.g., TACE or surgery), physicians may discover that the alter

173 Our study identifies TACE as an essential player in OL regeneration that may

174 ole for chemotherapy-induced cytotoxicity in TACE effectiveness and supports the use of chemotherapeu

175 jection resulted in a significant decline in TACE activity, procollagen alpha1 (I), alpha smooth musc

176 EGFR overexpression in TACE deficient OLs in vivo restores OL development and p

177 Moreover, EGFR overexpression in TACE-deficient OPs in vivo overcomes the defects in OL d

178 EGFR overexpression in TACE-deficient OPs restores OL survival and development.

179 , we identified an AP-2alpha binding site in TACE promoter and demonstrated, using EMSAs and chromati

180 5:DR3 contributions to PRR outcomes included TACE-induced TNFSF15 cleavage to soluble TNFSF15; solubl

181 ased CD62L may be a consequence of increased TACE-mediated CD62L cleavage and potentially impairs imm

182 of AP-2alpha small interfering RNA increased TACE promoter luciferase activity, TACE expression, and

183 3 (Timp3), we hypothesized that AGEs induce TACE through nicotinamide adenine dinucleotide phosphate

184 h suppression of PPAR-gamma or ERK inhibited TACE activity and TNF-alpha secretion.

185 nerated a stable form of the auto-inhibitory TACE prodomain (TPD), which specifically inhibits in vit

186 predict patient survival early after initial TACE and enabled clear identification of nonresponders.

187 tivity Assay Kit, Fluorimetric, and InnoZyme TACE Activity Kit, respectively.

188 current efficacy and safety data of lipiodol TACE in treatment of HCC.

189 figures of HCC patients undergoing lipiodol TACE appear to be in line with those reported in previou

190 tal of 10,108 patients treated with lipiodol TACE, were selected for the efficacy analysis.

191 of iRhom2 alter its interaction with mature TACE, thereby licensing its proteolytic activity.

192 Mechanistically, TACE regulates oligodendrogenesis by modulating the shed

193 The metalloprotease TACE (tumor necrosis factor alpha converting enzyme) is

194 In contrast, the matrix metalloproteinase/TACE (tumor necrosis factor-alpha-converting enzyme) inh

195 o the cell membrane for simultaneous MT1-MMP/TACE inhibition.

196 Within the extended model TACE is included as a two-step process: First, the purel

197 diagnosed with HCC and treated with multiple TACE cycles between January 1999 and December 2009 at th

198 An absence of TACE was the only other independent risk factor of dropo

199 gher, whereas the expression and activity of TACE were lower, in wild-type DCs (wtDCs) than in TNF kn

200 tifying a significant therapeutic benefit of TACE plus RT for unresectable HCC compared with TACE alo

201 ses of AP-2alpha expression and decreases of TACE expression and activity in wtDCs and TNFko DCs, ind

202 Genetic deletion of TACE in oligodendrocyte progenitor cells (OPs) induces p

203 nd 95% CIs were calculated for the effect of TACE plus RT vs TACE alone on survival, tumor response,

204 s to analyze retrospectively the efficacy of TACE and its impact on OS in patients with metastatic he

205 in mouse models, to enhance the efficacy of TACE.

206 ements as a tool for immediate evaluation of TACE.

207 gest evaluating the technical feasibility of TACE in all metastatic patients.

208 Our study reveals an essential function of TACE in oligodendrogenesis, and demonstrates how this mo

209 Our study reveals an essential function of TACE in supporting OL regeneration and CNS remyelination

210 hieve selective gain- or loss-of-function of TACE or EGFR in OL lineage cells in vivo, we found that

211 Although specific inhibition of TACE is thought to be a viable strategy for inflammatory

212 the ER-to-Golgi transport and maturation of TACE.

213 The mechanisms of TACE and sTNF regulation in DCs remain elusive.

214 r that leverages the endogenous modulator of TACE.

215 Rhbdf2 allows tissue-specific regulation of TACE by selectively preventing its maturation in immune

216 Because the main natural regulator of TACE activity is the tissue inhibitor of metalloproteina

217 ealed that TACE and a combination therapy of TACE and sorafenib were significant prognostic factors i

218 We studied the tolerability of TACE in a cohort of patients with NASH and alcoholic cir

219 uded; 44 participants underwent at least one TACE session.

220 e classified as target progression (RS, one; TACE MWA, nine).

221 NRF2-mutated HCC response to TAE and/or TACE is unknown.

222 Src or TACE inhibition was sufficient to attenuate DCA-induced

223 iver cancer with either conventional TACE or TACE with drug-eluting beads.

224 Finally, we conclude that our TACE model can motivate new therapeutical strategies and

225 , the least regretful strategy is to perform TACE on all patients.

226 m with elevated bilirubin predicted AHD post-TACE.

227 response of the index tumor on pre- and post-TACE magnetic resonance images was assessed retrospectiv

228 They were monitored for post-TACE complications: postembolization fever (PEF), nausea

229 There were no immediate post-TACE deaths.

230 l after DEB-TACE, stressing the role of post-TACE events, was performed.

231 ur size and female gender predicted PEF post-TACE.

232 After the first TACE procedure, TACE was repeated twice in 4-week intervals if indicated

233 a, which rely upon the cell surface protease TACE/ADAM-17.

234 phiregulin, p38 MAPK signalling and protease/TACE activity.

235 eolytic cleavage activation components (PS2, TACE) and restrained expression of the inhibitory compon

236 g TACE plus RT and a control group receiving TACE alone with data for at least 1-year survival or tum

237 ls that included a treatment group receiving TACE plus RT and a control group receiving TACE alone wi

238 se and total bilirubin in patients receiving TACE plus RT compared with those receiving TACE alone.

239 Patients receiving TACE plus RT showed significantly better 1-year survival

240 g TACE plus RT compared with those receiving TACE alone.

241 This study newly defines that sTNF regulates TACE in mouse DCs by engaging the AP-2alpha transcriptio

242 ception of the strategy and no pre-resection TACE are predictors of successful SLT strategy.

243 Conclusion SEB TACE resulted in minimal PSC, high ITSC, and sustained V

244 ze of VX2 tumors treated with 70-150-mum SEB TACE increased less (-2%) than that of tumors treated wi

245 An ART score of >/=2.5 prior the second TACE identifies patients with a dismal prognosis who may

246 and the presence of ascites prior the second TACE.

247 Mechanistically, uPAR sequestered TACE within lipid rafts to prevent Notch1 activation, th

248 High glucose stimulated Src, TACE, epidermal growth factor receptor (EGFR), mitogen-a

249 ndicate a role for Src in a high glucose-Src-TACE-heparin-binding epidermal growth factor-EGFR-MAPK-s

250 ith HCC were treated with 232 superselective TACE procedures using C-arm cone-beam CT at one institut

251 ed, except in hematopoietic cells, supported TACE maturation and shedding of the EGFR ligand TGF-alph

252 cifically inhibits in vitro and cell-surface TACE, but not the related ADAM10, and effectively modula

253 Sustained TACE activity may perpetuate EGFR signaling and reduce a

254 We achieve this by fusing T1(TACE), a designer TIMP-1 with superb affinities for MT1-

255 RT was more therapeutically beneficial than TACE alone for treating HCC, and should be recommended f

256 sional progression were longer with TEA than TACE (TTP, 34.6 months [95% CI: 28.2, 41] vs 26.05 month

257 R in OL lineage cells in vivo, we found that TACE is critical for EGFR activation in OLs following de

258 Furthermore, we found that TACE-dependent activation of Notch1 in basal kerantinocy

259 ocyte progenitors cells (OPs), we found that TACE/ADAM17 is required for supporting OL regeneration f

260 yses and Cox regression models revealed that TACE and a combination therapy of TACE and sorafenib wer

261 These results show that TACE is a target of, and is downregulated by, sTNF-induc

262 e complication rate was 8.9% and 4.9% in the TACE MWA and RS groups, respectively (P = .46).

263 ths (95% CI: 7.7 months, 19.1 months) in the TACE MWA group (P > .99).

264 Jun pathway, lead to the upregulation of the TACE (also known as ADAM17) inhibitor TIMP-3, and lead t

265 In contrast, in samples incubated with the TACE inhibitor IC-3 or in cells isolated from TACE knock

266 Patients underwent a median of three TACE cycles and received 13 infusions of bevacizumab ver

267 ha enhances epithelial wound healing through TACE, ERK, and GEF-H1.

268 itation assays, that AP-2alpha could bind to TACE promoter in a TNF-dependent manner.

269 Overall, iRhom2 binds to TACE throughout its lifecycle, implying that iRhom2 is a

270 servation was the lower complete response to TACE in the PHT group (12% vs. 36%; P = 0.001).

271 midine ((18)F-FLT) PET to assess response to TACE.

272 nal prognostic effect of adding sorafenib to TACE treatment in this patient cohort.

273 for the ongoing clinical program for the TPZ-TACE regimen in HCC treatment.

274 ndomised, placebo-controlled, phase 3 trial (TACE 2) in 20 hospitals in the UK for patients with unre

275 CC (July 2011 - December 2014), 84 underwent TACE.

276 HCC were included in the trial and underwent TACE with idarubicin-eluting beads.

277 h HCC hepatocellular carcinoma who underwent TACE transarterial chemoembolization before surgery.

278 9.6 years; age range, 23-72 years) underwent TACE with doxorubicin-eluting microspheres (DEB) (hereaf

279 Physician preferences on surgery versus TACE were elicited in terms of regret; threshold probabi

280 ib improves progression-free survival versus TACE with placebo.

281 calculated for the effect of TACE plus RT vs TACE alone on survival, tumor response, and adverse even

282 We aimed to determine whether TACE with sorafenib improves progression-free survival v

283 ted with sorafenib, 42 patients (19.5%) with TACE and 23 patients (10.7%) received treatment with TAC

284 e reveal that iRhom2 remains associated with TACE throughout the secretory pathway, and is stabilised

285 pies need to be assessed in combination with TACE to improve patient outcomes.

286 HIFU combined with TACE is a safe and promising method with a low rate of s

287 ice-daily) or matching placebo combined with TACE using drug-eluting beads (DEB-TACE), which was give

288 (OR, 2.73 [95% CI, 1.95-3.81]) compared with TACE alone.

289 E plus RT for unresectable HCC compared with TACE alone.

290 tissue, with PET parameters correlating with TACE response.

291 (ART score: Assessment for Retreatment with TACE) in the training cohort (n = 107, Vienna) by using

292 compared with those of patients treated with TACE MWA.

293 epatocellular carcinoma lesions treated with TACE transarterial chemoembolization .

294 mean age, 61.9 years +/- 10.7) treated with TACE with drug-eluting beads.

295 l of patients with HCC who were treated with TACE.

296 with unresectable HCC who were treated with TACE.

297 ) with multifocal, bilobar NELM treated with TACE.

298 23 patients (10.7%) received treatment with TACE and sorafenib in combination.

299 epatic HCC progression, local treatment with TACE may result in improved OS, although it is not recom

300 iseases who were eligible for treatment with TACE were enrolled.

301 sis (PVTT), and time between treatments with TACE and RT were performed.