ライフサイエンスコーパス: sorafenib

1 r HBV and positive for HCV when treated with sorafenib.

2 connection with the immunological profile of sorafenib.

3 th as a single agent and in combination with sorafenib.

4 ical use, including imatinib, sunitinib, and sorafenib.

5 of the clinically approved kinase inhibitor, sorafenib.

6 fied SLC22A20 (OAT6) as an uptake carrier of sorafenib.

7 mutation responsive to targeted therapy with sorafenib.

8 fit from treatment with the kinase inhibitor sorafenib.

9 sustained treatment with the FLT3 inhibitor sorafenib.

10 the potential interaction between PTP1B and sorafenib.

11 us MK-2206, (3) MK-2206 plus AZD6244, or (4) sorafenib.

12 ing treatment with the multikinase inhibitor sorafenib.

13 hat undergo hepatic glucuronidation, such as sorafenib.

14 classes, including the multikinase inhibitor sorafenib.

15 906 to potentiate the anti-tumor activity of Sorafenib.

16 o and in vivo through continuous exposure to sorafenib.

17 s submitted cases of complete response under sorafenib.

18 carcinoma following first-line therapy with sorafenib.

19 ent with the tyrosine kinase inhibitor (TKI) sorafenib.

20 patient profile in the improved response to sorafenib.

21 of either its parent compound, amonafide, or sorafenib.

22 hepatocellular and renal cell carcinoma drug sorafenib.

23 MEK/ERK signaling, including regorafenib and sorafenib.

24 1% of patients with HCC who are treated with sorafenib.

25 tionally designed combination therapies with sorafenib.

26 and 6 mg/kg, 3 and 6 mg/kg/h for 1 h, i.v.), sorafenib (10 and 20 mg/kg, 10 and 20 mg kg/h for 1 h, i

27 -CD47 Ab (500 mug/mouse) in combination with sorafenib (100 mg/kg, orally) exerted synergistic effect

28 C (bevacizumab 5 mg/kg IV every 2 weeks and sorafenib 200 mg orally twice daily on days 1 to 5, 8 to

29 o 5, 8 to 12, 15 to 19, and 22 to 26), or D (sorafenib 200 mg twice daily and temsirolimus 25 mg IV w

30 hout the first 4 weeks of each 6 week cycle, sorafenib 400 mg twice per day orally throughout each cy

31 ed minimisation algorithm to continuous oral sorafenib (400 mg twice-daily) or matching placebo combi

32 patient intolerance to sunitinib (37.5 mg), sorafenib (400 mg) daily, or equivalent placebo with man

33 while 48 patients (22.3%) were treated with sorafenib, 42 patients (19.5%) with TACE and 23 patients

34 thy donors over a range of concentrations of sorafenib (5-20 muM), IL-2 (2-24 nM), and IFN-alpha (10(

35 ceived 1 year of adjuvant sunitinib (50 mg), sorafenib (800 mg) daily, or equivalent placebo.

36 who were prescribed standard starting dosage sorafenib (800 mg/d per os) versus that of patients who

37 9.2 months), 9.2 months for bevacizumab plus sorafenib (90% CI, 7.5 to 11.4 months), and 7.4 months f

38 Sorafenib, a broad tyrosine kinase inhibitor, is the onl

39 Sorafenib, a multikinase inhibitor approved for the trea

40 rming cells were sensitive to treatment with sorafenib, a multikinase inhibitor, that is used for HCC

41 antifolate drug, sensitizes cancer cells to sorafenib, a targeted therapy for HCC.

42 PHY906 may potentiate Sorafenib action by increasing hMCP1 expression and enha

43 g of an oncology drug library, we found that sorafenib activates recruitment of the ubiquitin E3 liga

44 igations into the intracellular mechanism of sorafenib activity through in situ kinome profiling iden

45 c reactions, and seven patients discontinued sorafenib after achieving complete response due to adver

46 reased survival times compared to vehicle or sorafenib alone.

47 fenib and AMD3100 and not when combined with sorafenib alone.

48 Pretreatment with sorafenib also inhibited PBMC expression of IFN-alpha- a

49 survival is 12.6 (11.15 to 13.8) months for sorafenib and 10.2 (8.88 to 12.2) months for "other" tre

50 ning patients were randomly assigned: 157 to sorafenib and 156 to placebo.

51 l antitumor activity only when combined with sorafenib and AMD3100 and not when combined with sorafen

52 fects on tumor suppression, as compared with sorafenib and anti-CD47 Ab alone.

53 Publications dealing with sorafenib and any of its common adverse effects were con

54 e ability of iRGD to improve the delivery of sorafenib and doxorubicin therapy in hepatocellular carc

55 gmented the individual inhibitory effects of sorafenib and doxorubicin without increasing systemic to

56 ed to explore the antifibrotic activities of sorafenib and its derivative SC-1 (devoid of Raf kinase

57 Purpose Sorafenib and lenvatinib are oral multikinase inhibitors

58 Combined therapy using both sorafenib and MEAN enhanced tumor growth inhibition over

59 Tissue and plasma sorafenib and metabolite levels, downstream antitumor ta

60 fail or who do not tolerate the sequence of sorafenib and regorafenib.

61 Sorafenib and SC-1 activated Src-homology protein tyrosi

62 In conclusion, sorafenib and SC-1 ameliorate liver fibrosis through STA

63 Both sorafenib and SC-1 ameliorated liver fibrosis in vivo an

64 downstream signals were down-regulated after sorafenib and SC-1 treatment in HSC.

65 tion and undermined the apoptotic effects of sorafenib and SC-1, whereas STAT3-specific inhibition pr

66 uct ligation in Balb/C mice and treated with sorafenib and SC-1.

67 A combination of sorafenib and stattic had a significantly stronger effec

68 res were highly sensitive to cell death from sorafenib and stattic treatment.

69 were treated with varying concentrations of sorafenib and stimulated with IFN-alpha or IL-2.

70 e confirmed previous reports that sunitinib, sorafenib and TNP-470 are teratogenic and demonstrate th

71 spective cohort of HCC patients treated with sorafenib and to describe the profile of the patients wh

72 n, local ablation, transarterial therapy, or sorafenib) and overall survival.

73 tients on sunitinib and 95 [15%] patients on sorafenib), and fatigue 110 [18%] patients on sunitinib

74 hemotherapeutic agents, including cisplatin, sorafenib, and 5-fluorouracil.

75 of last 28 days of treatment), progressed on sorafenib, and had Child-Pugh A liver function were enro

76 r levels of ERK1/2-P are more susceptible to Sorafenib, and the S component of PHY906 may increase ER

77 in HCC models; when used in combination with sorafenib, anti-PD-1 immunotherapy shows efficacy only w

78 udies suggested that nonclassical targets of sorafenib are important for the propagation of RVFV.

79 s of DeltaPsim and ROS production induced by sorafenib are independent of caspase activities and do n

80 results reveal a new mechanism of action for sorafenib as a mitocan and suggest that high Parkin acti

81 Radiological images taken before starting sorafenib, at first control, after starting sorafenib, a

82 sorafenib, at first control, after starting sorafenib, at the time of complete response, and at leas

83 end toward a decreased rate of discontinuing sorafenib because of adverse events.

84 nib cost and were less likely to discontinue sorafenib because of gastrointestinal adverse effects (8

85 may potentiate the anti-hepatoma activity of Sorafenib by multiple mechanisms targeting on the inflam

86 Thus, our mechanistic data indicate that sorafenib bypasses central resistance mechanisms through

87 of xenobiotics, such as the anticancer drug sorafenib, can also undergo hepatocyte hopping.

88 ission electron microscopy demonstrated that sorafenib caused virions to be present inside large vacu

89 Collectively, these data indicate that sorafenib causes a disruption in viral egress by targeti

90 established cancer-related protein kinases, sorafenib causes variable responses among human tumors,

91 ntly over time in mice treated with 30 mg/kg sorafenib, coinciding with the onset of resistance but a

92 2.6-35.8) and 577 mg per day (SD 212.8) for sorafenib, compared with 22.2 months (8.1-38.8) and 778.

93 r carcinoma, we demonstrated that ONC201 and sorafenib cooperatively and safely triggered tumor regre

94 rienced significantly lower total cumulative sorafenib cost and were less likely to discontinue soraf

95 peutic response, particularly in settings of sorafenib cotreatment to enhance anticancer responses.

96 Pretreatment of PBMCs with 10 muM sorafenib decreased STAT1 and STAT5 phosphorylation afte

97 Sorafenib dephosphorylated focal adhesion kinase (FAK) a

98 In contrast, sorafenib did not alter MMP activity or cell motility, s

99 However, the combination of AMD3100 and sorafenib did not significantly change cytotoxic CD8(+)

100 the end of treatment; one patient receiving sorafenib died from infectious colitis while on treatmen

101 Sorafenib down-regulated total FAK, inducing its proteas

102 ith hepatocellular carcinoma (HCC) receiving sorafenib, drug resistance is common.

103 n, diarrhea, and hypertension, compared with sorafenib experience in renal or hepatocellular cancer.

104 drive prognosis in patients who discontinued sorafenib for any reason may help to improve patient man

105 care following permanent discontinuation of sorafenib for any reason were included.

106 Administration hospitals who were prescribed sorafenib for hepatocellular carcinoma between January 2

107 nce of any improvement in OS attributable to sorafenib for patients positive for HBV and negative for

108 single-agent therapy or in combination with sorafenib for the management of HCC.

109 er-deficient mouse models, we show here that sorafenib-glucuronide can be extruded from hepatocytes i

110 We further demonstrate that sorafenib-glucuronide excreted into the gut lumen can be

111 eported for 497 (89%) of 559 patients in the sorafenib group and 206 (38%) of 548 patients in the pla

112 l was 238.0 days (95% CI 221.0-281.0) in the sorafenib group and 235.0 days (209.0-322.0) in the plac

113 reported in 65 (41%) of 157 patients in the sorafenib group and 50 (32%) of 156 in the placebo group

114 urvival was 8.5 months (IQR 2.9-19.5) in the sorafenib group and 8.4 months (2.9-19.8) in the placebo

115 ents were reported in total, 95 (52%) in the sorafenib group and 86 (48%) in the placebo group.

116 were attributed to study drug; three in the sorafenib group and one in the placebo group.

117 nce in progression-free survival between the sorafenib group and the placebo group (hazard ratio [HR]

118 e were four (<1%) drug-related deaths in the sorafenib group and two (<1%) in the placebo group.

119 ere fatigue (29 [18%] of 157 patients in the sorafenib group vs 21 [13%] of 156 patients in the place

120 l between the two groups (33.3 months in the sorafenib group vs 33.7 months in the placebo group; haz

121 n reaction (154 [28%] of 559 patients in the sorafenib group vs four [<1%] of 548 patients in the pla

122 red (270 in the placebo group and 194 in the sorafenib group).

123 Of 556 patients in the sorafenib group, 553 (>99%) received the study treatment

124 21 countries, adults with HCC who tolerated sorafenib (>/=400 mg/day for >/=20 of last 28 days of tr

125 Sorafenib had no effect on infarct size, fibrosis, or po

126 ients on sunitinib and 102 [16%] patients on sorafenib), hand-foot syndrome (94 [15%] patients on sun

127 ssessment Randomized Protocol (SHARP) trial, sorafenib has become the standard of care for patients w

128 ors of improved survival were treatment with sorafenib (hazard ratio [HR], 0.66; 95% confidence inter

129 Purpose Following the Sorafenib Hepatocellular Carcinoma Assessment Randomized

130 , 6.1 years (IQR 1.7-not estimable [NE]) for sorafenib (HR 0.97, 97.5% CI 0.80-1.17, p=0.7184), and 6

131 Sorafenib impaired HCC cell proliferation and induced ap

132 Escalation from 30 to 60 mg/kg sorafenib improved antitumor efficacy but worsened survi

133 We aimed to determine whether TACE with sorafenib improves progression-free survival versus TACE

134 r carcinoma, while the multikinase inhibitor sorafenib improves survival in patients with advanced di

135 nts (10.7%) received treatment with TACE and sorafenib in combination.

136 vival and cost-effectiveness associated with sorafenib in elderly patients with advanced HCC.

137 ate that 1l augments the cytotoxic action of sorafenib in murine hepatocellular carcinoma cells.

138 ported to enhance the anti-tumor activity of Sorafenib in nude mice bearing HepG2 xenografts.

139 Results Hazard ratios show improved OS for sorafenib in patients who are both HBV negative and HCV

140 The DECISION trial of sorafenib in patients with differentiated thyroid cancer

141 The clinical benefit of sorafenib in patients with hepatocellular carcinoma (HCC

142 ers and thereby an increased accumulation of sorafenib in the cancer cells.

143 HCC cells were challenged with sorafenib in the presence of Ln-332 and of HSC condition

144 B overexpression impaired the sensitivity of sorafenib in vitro and in vivo, implying that PTP1B has

145 d obtained first insights into the effect of sorafenib in vivo.

146 Finally, we demonstrate that sorafenib induced keratinocyte injury in vivo and that t

147 lying that PTP1B has a significant effect on sorafenib-induced apoptosis.

148 More intriguingly, we find that it is sorafenib-induced ROS accumulation that enables TRAIL to

149 atinocytes and explains the basis underlying sorafenib-induced skin toxicity, with important implicat

150 Instead, sorafenib induces rapid dissipation of the mitochondrial

151 -fumarate (MA/FA) ratio at days 2 to 5 after sorafenib infusion.

152 We show that sorafenib inhibits the activity of both complex II/III o

153 findings to identify the mechanism by which sorafenib inhibits the release of RVFV virions from the

154 Sorafenib is a new standard treatment for patients with

155 In conclusion, tumor CYP3A4 induction by sorafenib is a novel mechanism to account for variabilit

156 Sorafenib is a RAF inhibitor approved for several cancer

157 Sorafenib is a Raf kinase inhibitor that could have off-

158 ance, and targeting CD47 in combination with sorafenib is an attractive therapeutic regimen for the t

159 Sorafenib is an oral multikinase inhibitor that was orig

160 Sorafenib is approved by the US Food and Drug Administra

161 Sorafenib is associated with improved survival in elderl

162 Only the multikinase inhibitor sorafenib is available for the management of advanced ca

163 Purpose Sorafenib is currently the only Food and Drug Administra

164 In addition, sorafenib is described as an antiangiogenic drug, but it

165 Our data indicate that sorafenib is not an effective intervention in the adjuva

166 ents with advanced hepatocellular carcinoma, sorafenib is the only approved drug worldwide, and outco

167 Sorafenib is the only chemotherapeutic approved for trea

168 r carcinoma (HCC), the multikinase inhibitor sorafenib is the only systemic treatment that has been s

169 However, the therapeutic effect of sorafenib is transient, and patients invariably develop

170 kinase inhibitors (MKI) in oncology, such as sorafenib, is associated with a cutaneous adverse event

171 chanistically, the antiangiogenic effects of sorafenib led to increased bone marrow hypoxia, which co

172 Notably, combining ONC201 and sorafenib led to synergistic induction of TRAIL and its

173 mic drug levels; however, declining systemic sorafenib levels may only be a minor resistance mechanis

174 ts who were prescribed reduced starting dose sorafenib (< 800 mg/d per os).

175 3 (p-STAT3), and apoptosis, suggesting that sorafenib may affect SHP-1 by triggering a conformationa

176 Recent findings suggest that resistance to sorafenib may have a reversible phenotype.

177 expression and acts as a determinant of the sorafenib-mediated drug effect; targeting the PITX1-p120

178 experiments testing tumor volume response to sorafenib monotherapy in any cancer published until Apri

179 (n = 42), MK-2206 plus AZD6244 (n = 75), or sorafenib (n = 61).

180 were randomly assigned to sunitinib (n=647), sorafenib (n=649), or placebo (n=647).

181 Sorafenib (Nexavar) is a broad-spectrum multikinase inhi

182 Treatment with sorafenib of patients with advanced hepatocellular carci

183 re is consistent evidence that the effect of sorafenib on OS is dependent on patients' hepatitis stat

184 tion (D61A) of SHP-1 abolished the effect of sorafenib on SHP-1, phosphorylated signal transducer and

185 ndomly assigned (1:1) to receive 400 mg oral sorafenib or placebo twice a day, for a maximum of 4 yea

186 the VEGF receptor tyrosine kinase inhibitors sorafenib or sunitinib showed no survival benefit relati

187 epa129 or TC1 tumor cells when combined with sorafenib or with an antitumor vaccine, respectively.

188 ine, felodipine, nicardipine, nilotinib, and sorafenib) or low micromolar range (abiratone, candesart

189 Here we demonstrate that sorafenib overcomes TRAIL resistance in RCC by a mechani

190 tients (63%) and 1,809 reduced starting dose sorafenib patients (37%).

191 Results There were 3,094 standard dose sorafenib patients (63%) and 1,809 reduced starting dose

192 Reduced starting dose sorafenib patients experienced significantly lower total

193 Consequently, reduced starting dose sorafenib patients had lower OS (median, 200 v 233 days,

194 Reduced starting dose sorafenib patients had more Barcelona Clinic Liver Cance

195 eived only one prior VEGFR-targeted therapy (sorafenib, pazopanib, or cediranib), and four patients h

196 nuously for 4 weeks of every 6 week cycle or sorafenib placebo given twice per day throughout the stu

197 proposed to be due to a gradual decrease in sorafenib plasma levels in patients.

198 CI, 7.5 to 11.4 months), and 7.4 months for sorafenib plus temsirolimus (90% CI, 5.6 to 7.9 months).

199 eated or intolerant without viral hepatitis, sorafenib progressor without viral hepatitis, HCV infect

200 vestigate the underlying mechanisms by which sorafenib promotes keratinocyte cytotoxicity and subsequ

201 Here, we demonstrate that RAF inhibition by sorafenib rapidly leads to RAF dimerization and ERK acti

202 ients on sunitinib and 208 [33%] patients on sorafenib), rash (15 [2%] patients on sunitinib and 95 [

203 Sorafenib-related serious adverse events included hand-f

204 Sorafenib remains the only approved drug for treating pa

205 s transient, and patients invariably develop sorafenib resistance (SR).

206 This study unveils a novel mechanism of sorafenib resistance depending on the alpha3beta1/Ln-332

207 To examine whether sorafenib resistance was a result of the presence of liv

208 he possible mechanisms underlying reversible sorafenib resistance were investigated using a Hep3B-hCG

209 -kappaB-mediated CD47 up-regulation promotes sorafenib resistance, and targeting CD47 in combination

210 n of the Tec family kinase BMX occurs during sorafenib resistance.

211 urine FLT3-ITD-positive (FLT3-ITD+) model of sorafenib resistance.

212 significantly extended survival of mice in a sorafenib-resistant AML patient-derived xenograft model.

213 nes, as well as of blasts from patients with sorafenib-resistant AML, suggested an enrichment of the

214 Using these models, we found that sorafenib-resistant clones demonstrated enhanced T-IC pr

215 of the presence of liver T-ICs, we developed sorafenib-resistant HCC cells both in vitro and in vivo

216 Functional characterization of CD47 in sorafenib-resistant HCC cells was evaluated using a lent

217 Consistently, NF-kappaB was activated in sorafenib-resistant HCC cells, and this finding was conf

218 3 expression in both sorafenib-sensitive and sorafenib-resistant Huh-7 cells, inhibiting TYRO3/growth

219 tudy, we generated two functionally distinct sorafenib-resistant human Huh-7 HCC cell lines in order

220 els could make tumor cells more sensitive to sorafenib's actions, providing one possible explanation

221 HSC-CM or Ln-332 inhibited sorafenib's effectiveness in HCC cells expressing both a

222 y was to investigate the effect of Ln-332 on sorafenib's effectiveness.

223 ffectively silenced TYRO3 expression in both sorafenib-sensitive and sorafenib-resistant Huh-7 cells,

224 y hepatocarcinoma, the multikinase inhibitor Sorafenib (SFB) usually fails to eradicate liver cancer.

225 While FLT3 inhibitors like sorafenib show initial therapeutic efficacy, resistance

226 novel ARAF positive mutation, treatment with sorafenib showed regression of the choroidal lesions and

227 In addition, the multikinase inhibitor sorafenib significantly reduces FBP levels in HCC cells

228 rs, injection of xentuzumab, with or without sorafenib, slowed tumor growth and increased survival ti

229 There are few data examining how sorafenib starting dose may influence patient outcomes a

230 ce status of 0 or 1, had previously received sorafenib (stopped because of progression or intolerance

231 Mechanism-of-action studies indicated that sorafenib targeted a late stage in virus infection and c

232 The activity of sorafenib, temsirolimus, and bevacizumab administered in

233 protein kinase MAP3K7 (TAK1) as a target of sorafenib that induces cell death.

234 rch is in identifying the cellular target of sorafenib that inhibits RVFV propagation, so that this i

235 s on sunitinib, 199 [45%] of 441 patients on sorafenib), the starting dose of each drug was reduced a

236 ry limited survival benefits with the use of sorafenib, the current standard of care for advanced dis

237 Sorafenib, the first and only targeted drug approved for

238 ious in inhibiting tumor growth in mice than sorafenib, the only approved drug for HCC.

239 Continuous sorafenib therapy (400 mg twice daily) was started 1 wee

240 Combined continuous sorafenib therapy and on-demand DEB TACE provided excell

241 Conclusion The initiation of sorafenib therapy at reduced dosages was associated with

242 Long-term administration of sorafenib therapy in combination with DEB TACE may have

243 er "paradoxical" ERK activation occurs after sorafenib therapy in HCC, and if so, if it impacts the t

244 PBMCs from patients receiving sorafenib therapy showed decreased responsiveness to IL-

245 iver Cancer (BCLC) stage and the duration of sorafenib therapy.

246 INTERPRETATION: The addition of sorafenib to DEB-TACE does not improve progression-free

247 as no additional prognostic effect of adding sorafenib to TACE treatment in this patient cohort.

248 ctiveness ratios (ICERs) were calculated for sorafenib-treated and control patients.

249 We included 228 sorafenib-treated patients and 870 control patients.

250 The median survival of the sorafenib-treated patients was 150.5 days versus 62 days

251 In sorafenib-treated tumor samples, we further found inhibi

252 Microvessel density was inhibited by sorafenib treatment but remained suppressed over time an

253 She was commenced on sorafenib treatment but required early dose reductions d

254 Moreover, sorafenib treatment effectively blocked FLT3 activation

255 critical role of autocrine VEGF signaling on sorafenib treatment efficacy.

256 ility of dual RAF/MEK inhibition to overcome sorafenib treatment escape in HCC.

257 mall number of cases of complete response to sorafenib treatment have now been reported worldwide, ho

258 Moreover, in mouse models after sorafenib treatment intratumoral hypoxia is increased an

259 ls, we now show that increased hypoxia after sorafenib treatment promotes immunosuppression, characte

260 ciated HCC can attain excellent responses to sorafenib treatment that is durable.

261 one, which activates the mitophagy response, sorafenib treatment triggers PINK1/Parkin-dependent cell

262 Previous sorafenib treatment was allowed.

263 an immunosuppressive microenvironment after sorafenib treatment, inhibited tumor growth, reduced lun

264 imaging revealed progressive disease despite sorafenib treatment.

265 vival benefit in HCC patients progressing on sorafenib treatment.

266 patients with HCC who have progressed during sorafenib treatment.

267 assessed during standard and dose-escalated sorafenib treatment.

268 vival benefit in HCC patients progressing on sorafenib treatment.

269 oemoblisation treatment and was commenced on sorafenib treatment.

270 cinoma (HCC) whose disease progresses during sorafenib treatment.

271 ainst IGF1 and IGF2 (xentuzumab), along with sorafenib; tumor growth was measured and tissues were an

272 r patients before and after receiving 400 mg sorafenib twice daily.

273 We tested sunitinib and sorafenib, two oral anti-angiogenic agents that are effe

274 expansion phase to patients in four cohorts: sorafenib untreated or intolerant without viral hepatiti

275 proach and showed increased sensitization to sorafenib upon CD47 knockdown.

276 class occur at a noticeably higher rate with sorafenib use in thyroid cancer patients.

277 ting (HR, 1.45; 95% CI, 1.21-1.73.) Although sorafenib use was associated with a survival benefit (HR

278 therapy was 120.0 days (IQR 43.0-266.0) for sorafenib versus 162.0 days (70.0-323.5) for placebo.

279 dian daily dose was 660 mg (IQR 389.2-800.0) sorafenib versus 800 mg (758.2-800.0) placebo, and media

280 esigned to assess the efficacy and safety of sorafenib versus placebo as adjuvant therapy in patients

281 igh-risk patients randomized to sunitinib or sorafenib vs placebo among patients with stages comparab

282 ) in the ASSURE trial (adjuvant sunitinib or sorafenib vs placebo in resected unfavorable renal cell

283 Sorafenib was confirmed to inhibit MAPK signaling in the

284 Effect sizes were significantly smaller when sorafenib was tested against either a different active a

285 large prospective randomized trials in which sorafenib was the control arm.

286 the secretory pathway and a known target of sorafenib, was found to be important for RVFV egress.

287 les of these patients receiving sunitinib or sorafenib were also performed.

288 of 3,256 patients, 1,643 (50%) who received sorafenib were available.

289 t TACE and a combination therapy of TACE and sorafenib were significant prognostic factors in metasta

290 two inhibitors that inhibit RAF (PLX4032 and sorafenib) were studied further to determine whether cha

291 le transfected, cells acquired protection by sorafenib when plated on Ln-332-CM or HSCs.

292 the rate of occurrence of adverse effects of sorafenib when used in differentiated thyroid cancer com

293 le, except for fluticasone, nicardipine, and sorafenib which suffer from severe matrix suppression.

294 lumen can be cleaved by microbial enzymes to sorafenib, which is then reabsorbed, supporting its pers

295 resented in terms of hazard ratios comparing sorafenib with alternative therapies according to hepati

296 n P in increasing tumor apoptosis induced by Sorafenib with an increase of mouse(m)FasL and human(h)F

297 d CXCR4-targeted nanoparticles to co-deliver sorafenib with the MEK inhibitor AZD6244 in HCC.

298 mmittee on Cancer stage III/IV) who received sorafenib within 6 months of diagnosis (and were otherwi

299 ients as compared with the standard of care (sorafenib), without increasing liver toxicity.

300 We hypothesized that sorafenib would also have inhibitory effects on cytokine