ライフサイエンスコーパス: sunitinib

1 ared with the TB immediately before stopping sunitinib.

2 ed fBV in tumors that acquired resistance to sunitinib.

3 arker of response to the antiangiogenic drug sunitinib.

4 hibitors, including erlotinib, lapatinib and sunitinib.

5 bozantinib versus 18% (95% CI, 10 to 28) for sunitinib.

6 more effective in overcoming resistance than sunitinib.

7 xenografts exhibiting acquired resistance to sunitinib.

8 s used to adjust for nonrandom assignment to sunitinib.

9 unitinib and TB increase while not receiving sunitinib.

10 drugs such as the tyrosine kinase inhibitor sunitinib.

11 nues to have superior clinical outcomes over sunitinib.

12 X-241) but not when CVX-060 is combined with sunitinib.

13 in patients with metastatic RCC treated with sunitinib.

14 interquartile range, $12,102 to $12,262) for sunitinib.

15 r with cyclosporine or with cyclosporine and sunitinib.

16 al benefit for the addition of trebananib to sunitinib.

17 treatment course of the antiangiogenic agent sunitinib.

18 seful adjuvant antiangiogenesis therapy with sunitinib.

19 rylation, responsive to the kinase inhibitor sunitinib.

20 profile of nivolumab plus ipilimumab versus sunitinib.

21 lified by the multitargeted kinase inhibitor sunitinib.

22 the antiangiogenic tyrosine kinase inhibitor sunitinib.

23 e cells to tolerate the cytotoxic effects of sunitinib.

24 A total of 54 patients received sunitinib.

25 b and included diarrhea (cabozantinib, 10% v sunitinib, 11%), fatigue (6% v 15%), hypertension (28% v

26 discontinued by 193 [44%] of 438 patients on sunitinib, 199 [45%] of 441 patients on sorafenib), the

27 Twenty-three of the 65 patients who received sunitinib (35%) showed at least 3% pancreatic volume los

28 study was amended for patient intolerance to sunitinib (37.5 mg), sorafenib (400 mg) daily, or equiva

29 sequentially onto two cohorts that received sunitinib 50 mg once per day for 4 weeks on and 2 weeks

30 15 mg/kg intravenously once every 3 weeks or sunitinib 50 mg orally once daily for 4 weeks on, 2 week

31 omly assigned (1:1:1) to receive 54 weeks of sunitinib 50 mg per day orally throughout the first 4 we

32 lowed by nivolumab 3 mg/kg every 2 weeks, or sunitinib 50 mg/day for 4 weeks of each 6-week cycle.

33 lpha (3-9 million IU 3 times/wk) (n = 11) or sunitinib (50 mg daily, 4 of every 6 wk) (n = 11).

34 r cell mRCC were treated with four cycles of sunitinib (50 mg once per day, 4 weeks of receiving trea

35 atio to cabozantinib (60 mg once per day) or sunitinib (50 mg once per day; 4 weeks on, 2 weeks off).

36 ab (3 mg/kg intravenously) every 2 weeks; or sunitinib (50 mg orally) once daily for 4 weeks (6-week

37 -cell renal-cell carcinoma to receive either sunitinib (50 mg per day) or placebo on a 4-weeks-on, 2-

38 Sunitinib (50 mg) was given orally once daily, with each

39 Patients received 1 year of adjuvant sunitinib (50 mg), sorafenib (800 mg) daily, or equivale

40 d (1:1) to receive everolimus (10 mg/day) or sunitinib (50 mg/day; 6-week cycles of 4 weeks with trea

41 mly assigned to nivolumab plus ipilimumab or sunitinib (550 vs 546 in the intention-to-treat populati

42 -mum unloaded beads, and seven received oral sunitinib (6 mg every day).

43 treated with unloaded beads (+42%) and oral sunitinib (6 mg every day; +1853%; P = .044).

44 uable after cross-over had stable disease on sunitinib (6 to 27 weeks).

45 Suppressing RET activity using Sunitinib, a clinically-approved tyrosine kinase inhibit

46 Sunitinib, a multi-receptor tyrosine kinase (RTK) inhibi

47 y concurrent or sequential administration of sunitinib, a multitargeted receptor tyrosine kinase inhi

48 Here we report incorporation of sunitinib, a tyrosine kinase inhibitor that blocks VEGF

49 Sunitinib, a vascular endothelial growth factor pathway

50 In addition, sunitinib activated p38 MAPK, which resulted in the upre

51 Sunitinib administered once weekly at 300 mg or once eve

52 o the liver, lungs, and spleen revealed that sunitinib administration enhances metastasis, but only i

53 orted by the ability of the kinase inhibitor sunitinib alone and in combination with the MEK inhibito

54 growth delay compared with equimolar SAN1 or sunitinib alone.

55 before the first vaccination, or to receive sunitinib alone.

56 Importantly, Sunitinib also increased engraftment and differentiation

57 Sunitinib also inhibited chronic PDGF-A and -B and VEGF-

58 ibitor of the mammalian target of rapamycin; sunitinib, an angiogenesis inhibitor; and cytotoxic regi

59 to understand the mechanism of resistance to sunitinib, an antiangiogenic small molecule, and to expl

60 We investigated the activity of sunitinib, an orally administered tyrosine kinase inhibi

61 nts were hypertension (105 [17%] patients on sunitinib and 102 [16%] patients on sorafenib), hand-foo

62 b), hand-foot syndrome (94 [15%] patients on sunitinib and 208 [33%] patients on sorafenib), rash (15

63 nts on sorafenib), rash (15 [2%] patients on sunitinib and 95 [15%] patients on sorafenib), and fatig

64 ated 65 patients with GIST treated with oral sunitinib and a control group of 30 patients with GIST w

65 ression analysis, interaction between use of sunitinib and age as a dichotomous variable was highly s

66 cell line 786-O was chronically treated with sunitinib and assayed for AXL, MET, epithelial-mesenchym

67 While sunitinib and atezolizumab + bevacizumab are effective i

68 r targets underlying the antiviral effect of sunitinib and erlotinib (in addition to EGFR), respectiv

69 Last, in addition to affecting assembly, sunitinib and erlotinib inhibited HCV entry at a postbin

70 In cultured cells, treatment with sunitinib and erlotinib, approved anticancer drugs that

71 ors, including the approved anticancer drugs sunitinib and erlotinib, could block HCV assembly.

72 cytes (7%), and decreased platelets (7%) for sunitinib and fatigue (10%) for placebo; grade 4 adverse

73 events were 67% for cabozantinib and 68% for sunitinib and included diarrhea (cabozantinib, 10% v sun

74 Three sunitinib and no placebo patients achieved complete resp

75 microvessels were most sensitive to combined sunitinib and PI3Kbeta inactivation.

76 We tested sunitinib and sorafenib, two oral anti-angiogenic agents

77 ooth pattern of TB reduction while receiving sunitinib and TB increase while not receiving sunitinib.

78 ated lipase (n = 1; all in same patient) for sunitinib and thrombocytopenia (n = 1) and hypernatremia

79 L receptors is associated with resistance to sunitinib and with more aggressive tumor behavior.

80 duction in tumor blood volume in response to sunitinib, and acquired resistance to sunitinib was not

81 mours with progression on at least imatinib, sunitinib, and regorafenib or documented intolerance to

82 he management of advanced disease: imatinib, sunitinib, and regorafenib; imatinib is usually the best

83 rrently in clinical use, including imatinib, sunitinib, and sorafenib.

84 We validated sunitinib- and erlotinib-mediated inhibition of AAK1 and

85 ib], one cardiac arrest [possibly related to sunitinib], and one myocardial infarction) and eight (6%

86 benefit in PFS and ORR over standard-of-care sunitinib as first-line therapy in patients with interme

87 r trial evaluated cabozantinib compared with sunitinib as first-line therapy in patients with mRCC.

88 d not improve overall survival when added to sunitinib as first-line treatment in patients with metas

89 identifies an already FDA-approved compound, Sunitinib, as a possible DMD therapeutic with the potent

90 Conclusion Pancreatic atrophy is a sunitinib-associated toxicity detected at imaging.

91 ic mutant (T165E,S171E), each complexed with sunitinib at 2.17-3.00- angstrom resolutions.

92 i-target receptor tyrosine kinase inhibitor, sunitinib base, was efficiently encapsulated into a targ

93 Patients were not eligible for intermittent sunitinib because of progressive disease (n = 13), toxic

94 nsitive to the targeted anti-angiogenic drug sunitinib but resistant to cytotoxic chemotherapy.

95 that is intrinsically resistant to the RTKi sunitinib, but not to the VEGF therapeutic antibody beva

96 ells respond to clinically relevant doses of sunitinib by enhancing the stability of the antiapoptoti

97 Compared with sunitinib, cabozantinib treatment significantly increase

98 In this study, we found that sunitinib can stimulate vegfc gene transcription and inc

99 r efficacy of nivolumab plus ipilimumab over sunitinib comes with the additional benefit of improved

100 nitinib concentration (PSC) and intratumoral sunitinib concentration (ITSC) after transcatheter arter

101 Purpose To measure plasmatic sunitinib concentration (PSC) and intratumoral sunitinib

102 orafenib), and fatigue 110 [18%] patients on sunitinib [corrected].

103 kidney transplantation which indicates that sunitinib could be a potential intervention also in clin

104 angiogenic drugs such as Vegf morpholino and sunitinib could potentially interfere with tumor invasiv

105 Sunitinib decreased neointimal formation and smooth musc

106 Treatment of mdx mice with Sunitinib demonstrated decreased membrane leakiness and

107 ile on treatment and four patients receiving sunitinib died, with one death due to each of neurologic

108 tients in cohorts A and B, respectively, had sunitinib dose interruptions (dose decrease, withholding

109 t aortic denudation model was used to define sunitinib dose.

110 This intermittent sunitinib dosing continued until Response Evaluation Cri

111 ility and clinical outcome with intermittent sunitinib dosing in patients with mRCC was explored.

112 0) value that is 9-fold more potent than the sunitinib drug tested under the same conditions.

113 verse events (AEs) and dose interruptions of sunitinib during the first 12 weeks of treatment.

114 of these compounds, VX-680, Roscovitine and Sunitinib, each eliminate >85% of infection.

115 olization (TACE) with two different sizes of sunitinib-eluting beads (SEBs) in rabbits with VX2 hepat

116 Pretreatment with sunitinib enhanced angiogenesis in 786-0/human umbilical

117 murine models of dengue and Ebola infection, sunitinib/erlotinib combination protected against morbid

118 ent with the multi-tyrosine kinase inhibitor sunitinib eventually relapse.

119 Sunitinib exerts its regenerative effects via transient

120 of patients who intended to receive adjuvant sunitinib for 6 months was compared with institutional h

121 linical trial evaluating the use of systemic sunitinib for ocular VHL lesions during a period of 9 mo

122 nctival (SCT) injection in comparison to its sunitinib free base formulation.

123 ty <5%, and good accuracy in the recovery of sunitinib from spiked samples.

124 nically established antiangiogenic compound (sunitinib), from which a lead candidate (SAN1) was conju

125 r 4 adverse events were more frequent in the sunitinib group (48.4% for grade 3 events and 12.1% for

126 s bevacizumab group versus 7.7 months in the sunitinib group (hazard ratio [HR] 0.74 [95% CI 0.57-0.9

127 l infarction) and eight (6%) patients in the sunitinib group (one case each of renal failure, oesopha

128 There were 51 deaths, 14 (26%) in the sunitinib group and 37 (50%) in the control group.

129 ce interval [CI], 5.8 to not reached) in the sunitinib group and 5.6 years (95% CI, 3.8 to 6.6) in th

130 plus IMA901 group and 62 (47%) of 132 in the sunitinib group had grade 3 or worse adverse events, the

131 In the univariate analysis, the sunitinib group had longer overall survival (hazard rati

132 ab plus bevacizumab group and 37 (8%) in the sunitinib group had treatment-related all-grade adverse

133 b group and 240 (54%) of 446 patients in the sunitinib group had treatment-related grade 3-4 adverse

134 Patients in the sunitinib group had worse cytogenetic or molecular featu

135 of adverse events were more frequent in the sunitinib group than in the placebo group (34.3% vs. 2%)

136 ree survival was significantly longer in the sunitinib group than in the placebo group, at a cost of

137 e aminotransferase (28 [5%]), whereas in the sunitinib group they were hypertension (90 [17%] of 535)

138 hypertension (12 [24%] of 51 patients in the sunitinib group vs one [2%] of 57 patients in the everol

139 plus ipilimumab group and four deaths in the sunitinib group were reported as treatment-related.

140 nib group vs 84 [20%] of 425 patients in the sunitinib group), alanine aminotransferase increase (54

141 izumab plus bevacizumab group and 461 to the sunitinib group.

142 r receptor (VEGFR) tyrosine kinase inhibitor sunitinib have shown positive results, but these have be

143 Antiangiogenic therapies, such as sunitinib, have revolutionized renal cell carcinoma (RCC

144 ree survival was 5.8 years (IQR 1.6-8.2) for sunitinib (hazard ratio [HR] 1.02, 97.5% CI 0.85-1.23, p

145 s 35.7 months [95% CI 33.3-not reached] with sunitinib); hazard ratio [HR] 0.68 [95% CI 0.55-0.85], p

146 n in tumor burden (TB) after four cycles had sunitinib held, with restaging scans performed every two

147 Rescue of DUX4-induced pathology by Sunitinib highlights the therapeutic potential of tyrosi

148 as 2.1 months for placebo and 3.7 months for sunitinib (HR, 1.62; 70% CI, 1.27 to 2.08; 95% CI, 1.02

149 astatic non-clear cell renal cell carcinoma, sunitinib improved progression-free survival compared wi

150 ) with first-line avelumab + axitinib versus sunitinib in advanced renal cell carcinoma (aRCC).

151 mparing atezolizumab plus bevacizumab versus sunitinib in first-line metastatic renal cell carcinoma.

152 RCC-induced EC survival was sensitive to sunitinib in half of the tumors and was refractory in tu

153 The direct detection of sunitinib in human plasma was successfully demonstrated

154 sunitinib in vitro and was synergistic with sunitinib in impairing tumor growth in vivo, indicating

155 ain RTKs, restoring the antitumor effects of sunitinib in models of acquired or intrinsically resista

156 P = 0.022), gender (P = 0.040), and adjuvant sunitinib in patients aged <60 years (P = 0.004).

157 eads to fewer symptoms and better HRQoL than sunitinib in patients at intermediate or poor risk with

158 umab improved overall survival compared with sunitinib in patients with intermediate or poor risk, pr

159 ught to determine the efficacy and safety of sunitinib in patients with locoregional renal-cell carci

160 val for atezolizumab plus bevacizumab versus sunitinib in patients with metastatic renal cell carcino

161 b prolonged progression-free survival versus sunitinib in patients with metastatic renal cell carcino

162 r everolimus and the VEGF receptor inhibitor sunitinib in patients with non-clear cell renal cell car

163 lus ipilimumab showed superior efficacy over sunitinib in patients with previously untreated intermed

164 ce every 2 weeks administration of high-dose sunitinib in patients with refractory solid malignancies

165 mTORC1 activity correlate with resistance to sunitinib in patients.

166 and Met activation to acquired resistance to sunitinib in renal cell carcinoma (RCC), providing a pre

167 ocalized and maintains therapeutic levels of sunitinib in retinal pigmented epithelium/choroid and re

168 ERK) activation in EC which was inhibited by sunitinib in sensitive but not in resistant tumors.

169 served with pembrolizumab plus axitinib over sunitinib in terms of overall survival (median not reach

170 plus ipilimumab continued to be superior to sunitinib in terms of overall survival (median not reach

171 mumab showed improved efficacy compared with sunitinib in terms of overall survival (median not reach

172 In this retrospective study, the use of sunitinib in the adjuvant setting was associated with be

173 enal cancer, however, combining CVX-060 with sunitinib in the adjuvant setting was superior to CVX-24

174 benefit of nivolumab plus ipilimumab versus sunitinib in this setting.

175 itized cells to clinically relevant doses of sunitinib in vitro and was synergistic with sunitinib in

176 l culture and rescued acquired resistance to sunitinib in xenograft models.

177 eived 0.05 mL of 100-300-mum SEBs (1.5 mg of sunitinib) in the hepatic artery, and six animals receiv

178 esign, patients received escalating doses of sunitinib, in 100 mg increments, starting at 200 mg once

179 ly correlated (R(2) = 0.92, P < 0.0001) with sunitinib-induced changes in tumor fBV across the cohort

180 ut (EpsilonC-betaKO) in mice potentiated the sunitinib-induced reduction in subcutaneous growth of LL

181 We hypothesized that sunitinib-induced upregulation of the prometastatic MET

182 aken together, EC PI3Kbeta inactivation with sunitinib inhibition reduces microvessel turnover and de

183 Purpose Sunitinib is a standard initial therapy in metastatic re

184 Sunitinib is a tyrosine kinase inhibitor which inhibits

185 Sunitinib is active in previously treated patients with

186 Sunitinib is an antiangiogenic therapy given as a first-

187 dministration (FDA)-approved small molecule, Sunitinib, is a potent alpha7 integrin enhancer capable

188 Sunitinib maintained its antiangiogenic and antimetastat

189 Sunitinib malate (Sunb-malate) targeting against multipl

190 s lost vision during therapy, treatment with sunitinib malate did not improve visual acuity or reduce

191 Systemic sunitinib malate may be useful in slowing progression of

192 d its use in this small series, and systemic sunitinib malate may not be safe for treatment of RCH wh

193 l-Lindau (VHL) disease treated with systemic sunitinib malate, an agent that inhibits both anti-vascu

194 uxtapapillary RCH were treated with systemic sunitinib malate.

195 ted juxtapapillary RCH treated with systemic sunitinib malate.

196 tion of an anti-VEGF antibody-based drug and sunitinib markedly promotes liver metastasis.

197 for many patients, combination therapy with sunitinib may significantly improve the therapeutic effi

198 Results Seventeen participants received sunitinib (mean age, 59 years +/- 7.0 [standard deviatio

199 A single intravitreous injection of sunitinib microparticles potently suppresses choroidal n

200 Intravitreous injection of sunitinib microparticles provides a promising approach t

201 After intravitreous injection in rabbits, sunitinib microparticles self-aggregate into a depot tha

202 flammatory biodegradable polymer to generate sunitinib microparticles specially formulated to self-ag

203 Mechanistically, we determined that sunitinib modulates MCL-1 stability by affecting its pro

204 to receive sunitinib plus IMA901 (n=204) or sunitinib monotherapy (n=135).

205 ceive pembrolizumab plus axitinib (n=432) or sunitinib monotherapy (n=429).

206 up vs not reached [33.67-not reached] in the sunitinib monotherapy group; hazard ratio 1.34 [0.96-1.8

207 safety of pembrolizumab plus axitinib versus sunitinib monotherapy in patients with advanced renal ce

208 efficacy of pembrolizumab plus axitinib over sunitinib monotherapy in treatment-naive, advanced renal

209 us 5 mg axitinib orally twice daily or 50 mg sunitinib monotherapy orally once daily for 4 weeks per

210 gned to nivolumab plus ipilimumab (n=425) or sunitinib (n=422).

211 nts were randomly assigned to receive either sunitinib (n=51) or everolimus (n=57).

212 cal Trials Network were randomly assigned to sunitinib (n=647), sorafenib (n=649), or placebo (n=647)

213 ere randomly assigned (cabozantinib, n = 79; sunitinib, n = 78).

214 Compared with sunitinib, nivolumab plus ipilimumab reduced risk of det

215 aluate the effect and clinical importance of sunitinib on pancreatic volume in patients with gastroin

216 udies were done to investigate the effect of sunitinib on smooth muscle cell proliferation and migrat

217 eal varices haemorrhage [possibly related to sunitinib], one cardiac arrest [possibly related to suni

218 nd circulatory collapse [possibly related to sunitinib], one oesophageal varices haemorrhage [possibl

219 dministration of mimics of these miRNAs with sunitinib or axitinib resulted in decreased tumour cell

220 was measured with ASL MRI before and during sunitinib or pazopanib therapy between October 2008 and

221 can be combined with VEGFR2-targeting TKIs (sunitinib or regorafenib) to successfully treat postsurg

222 S) in ccRCC high-risk patients randomized to sunitinib or sorafenib vs placebo among patients with st

223 cancer (ccRCC) in the ASSURE trial (adjuvant sunitinib or sorafenib vs placebo in resected unfavorabl

224 y dose quartiles of these patients receiving sunitinib or sorafenib were also performed.

225 inistration of the tyrosine kinase inhibitor sunitinib, or expression of VEGF-C/D trap, which also co

226 -defined disease progression while receiving sunitinib, or unacceptable toxicity occurred.

227 Patients received 50 mg of sunitinib orally once a day, in 6-week cycles (ie, 4 wee

228 ipilimumab versus -3.14 (-6.03 to -0.25) for sunitinib (p<0.0001), and for FACT-G total score being 4

229 ipilimumab versus -4.32 (-8.54 to -0.11) for sunitinib (p=0.0005).

230 lus ipilimumab and 6.40 (-1.36 to 14.16) for sunitinib (p=0.45).

231 Placebo could be sunitinib placebo given continuously for 4 weeks of ever

232 f whom 339 were randomly assigned to receive sunitinib plus IMA901 (n=204) or sunitinib monotherapy (

233 116 (57%) of 202 patients in the sunitinib plus IMA901 group and 62 (47%) of 132 in the s

234 ps (33.17 months [95% CI 27.81-41.36] in the sunitinib plus IMA901 group vs not reached [33.67-not re

235 t frequent IMA901-related side-effect in the sunitinib plus IMA901 group.

236 noma were randomly assigned (3:2) to receive sunitinib plus up to ten intradermal vaccinations of IMA

237 We used available sunitinib preclinical studies to evaluate relationships

238 d routinely every 4 months while on systemic sunitinib prescribed by her oncologist for metastatic pa

239 periments were used to examine the effect of sunitinib pretreatment on endothelial cell growth.

240 at combined inhibition of PGDF and VEGF with sunitinib prevents chronic rejection changes in experime

241 eater activity than sunitinib, was active in sunitinib-progressing tumours, and was better tolerated.

242 ng the stability of AXL mRNA to increase the sunitinib resistance in RCC.

243 However, the occurrence of sunitinib resistance in the clinical application has cur

244 e found TR4 nuclear receptor might alter the sunitinib resistance to RCC via altering the TR4/lncTASR

245 tested the ability of cabozantinib to rescue sunitinib resistance.

246 ional target for therapeutic intervention in sunitinib-resistant ccRCC as well as a predictive marker

247 ltures, including several from patients with sunitinib-resistant RCC, were established.

248 Normalization of tumor vasculature with sunitinib resulted in objective response to cytotoxic ch

249 2 weeks after daily treatment with 40 mg/kg sunitinib revealed a 71% (P < 0.01) reduction in fBV in

250 deeper understanding of the contribution of sunitinib's numerous targets to the clinical response or

251 Sunitinib sensitivity correlated with vascular endotheli

252 GF-dependent and -independent pathways, that sunitinib sensitivity correlates with VEGF-mediated ERK

253 rmin, or TR4-shRNAs, all led to increase the sunitinib sensitivity to better suppress the RCC progres

254 had a better synergistic effect to increase sunitinib sensitivity to suppress RCC progression.

255 ceived 0.05 mL of 70-150-mum SEBs (1.5 mg of sunitinib), seven received 0.05 mL of 70-150-mum unloade

256 ptor tyrosine kinase inhibitors sorafenib or sunitinib showed no survival benefit relative to placebo

257 ects can be amplified by coadministration of sunitinib.Significance: These findings reveal multiple u

258 Sunitinib significantly increased progression-free survi

259 We confirmed previous reports that sunitinib, sorafenib and TNP-470 are teratogenic and dem

260 Sunitinib (ST), a multitargeted receptor tyrosine kinase

261 Sunitinib stimulated a VEGFC-dependent development of ly

262 the tyrosine kinase inhibitors erlotinib or sunitinib, suggesting that the antiproliferative effects

263 the receptor tyrosine kinase (RTK) inhibitor sunitinib, target vascular endothelial growth factor (VE

264 hich can be counteracted more efficiently by sunitinib than by ibrutinib or idelalisib.

265 mine the clinical effect of adding IMA901 to sunitinib, the standard first-line treatment in metastat

266 may overcome resistance induced by prolonged sunitinib therapy in metastatic RCC.

267 nd the CT images obtained after one cycle of sunitinib therapy were evaluated in comparison with base

268 lly approved antiangiogenic kinase inhibitor sunitinib, three novel dual conjugates were synthesized

269 vourable with nivolumab plus ipilimumab than sunitinib throughout the first 103 weeks after baseline,

270 family, which coordinately act with the MTKI sunitinib to decrease GBM cell viability.

271 Using sunitinib to improve the survival has become the first-l

272 present study, tissue microarrays containing sunitinib-treated and untreated RCC tissues were stained

273 single-agent sunitinib treatment, tumors in sunitinib-treated EpsilonC-betaKO mice showed a marked d

274 invasion and new metastatic sites in 30% of sunitinib-treated patients and increased lymphatic vesse

275 Conclusion Periodic extended sunitinib treatment breaks are feasible and clinical eff

276 In summary, chronic sunitinib treatment induces the activation of AXL and ME

277 Chronic sunitinib treatment of RCC cell lines activated both AXL

278 on of patient samples prior to and following sunitinib treatment suggested that increases in MCL-1 le

279 Sunitinib treatment was independently associated with pa

280 Compared to single-agent sunitinib treatment, tumors in sunitinib-treated Epsilon

281 ion using cabozantinib both impaired chronic sunitinib treatment-induced prometastatic behavior in ce

282 published results of a 750-patient adjuvant sunitinib trial showing improved disease-free survival (

283 adverse events in the two groups (21.9% for sunitinib vs. 17.1% for placebo); no deaths were attribu

284 median increase in TB during the periods off sunitinib was 1.6 cm (range, -2.9 to 3.4 cm) compared wi

285 MCL-1 stability at different dose ranges of sunitinib was due to differential effects on ERK and GSK

286 for which KIs were effective; nevertheless, sunitinib was identified as the most common clinically a

287 31.LM2-4 human breast cancer model, adjuvant sunitinib was ineffective, whereas adjuvant CVX-060 dela

288 r efficacy of nivolumab plus ipilimumab over sunitinib was maintained in intermediate-risk or poor-ri

289 nse to sunitinib, and acquired resistance to sunitinib was not associated with a parallel increase in

290 Sunitinib was reinitiated for two cycles in those patien

291 Maintenance sunitinib was safe and improved PFS in extensive-stage S

292 Sunitinib was well tolerated and almost completely preve

293 PT2399 had greater activity than sunitinib, was active in sunitinib-progressing tumours,

294 Sunb-malate, the water-soluble form of sunitinib, was shown to have higher intraocular penetrat

295 Furthermore, higher doses of sunitinib were cytotoxic, triggered a decline in MCL-1 l

296 s and metastatic clear-cell RCC treated with sunitinib were included (n = 275).

297 els for the detection of the anticancer drug sunitinib were synthesized and characterized.

298 two FDA-approved drugs, Oxytetracycline and Sunitinib, were identified to dissociate Abeta oligomers

299 giogenic response of 786-0 RCC xenografts to sunitinib, which revealed that pretreatment tumor fBV wa

300 primary uveal melanoma who received adjuvant sunitinib with institutional controls.