ライフサイエンスコーパス: sunitinib

1 alanine aminotransferase (60%, vs. 43% with sunitinib).

2 the antiangiogenic tyrosine kinase inhibitor sunitinib.

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

4 in patients with metastatic RCC treated with sunitinib.

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

6 r with cyclosporine or with cyclosporine and sunitinib.

7 e cells to tolerate the cytotoxic effects of sunitinib.

8 lified by the multitargeted kinase inhibitor sunitinib.

9 A total of 54 patients received sunitinib.

10 al benefit for the addition of trebananib to sunitinib.

11 treatment course of the antiangiogenic agent sunitinib.

12 ared with the TB immediately before stopping sunitinib.

13 a being the most cited reason for preferring sunitinib.

14 metastatic renal cell carcinoma treated with sunitinib.

15 observed with bevacizumab, estramustine, and sunitinib.

16 d 2 tyrosine kinase inhibitors, imatinib and sunitinib.

17 ring cediranib with another VEGFR inhibitor, sunitinib.

18 ssing after failure of at least imatinib and sunitinib.

19 show the noninferiority of pazopanib versus sunitinib.

20 ed fBV in tumors that acquired resistance to sunitinib.

21 arker of response to the antiangiogenic drug sunitinib.

22 hibitors, including erlotinib, lapatinib and sunitinib.

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

24 xenografts exhibiting acquired resistance to sunitinib.

25 s used to adjust for nonrandom assignment to sunitinib.

26 unitinib and TB increase while not receiving sunitinib.

27 drugs such as the tyrosine kinase inhibitor sunitinib.

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

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

30 ysicians also preferred pazopanib (61%) over sunitinib (22%); 17% expressed no preference.

31 more patients preferred pazopanib (70%) over sunitinib (22%); 8% expressed no preference (P < .001).

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

33 Sunitinib 37.5 mg per day (schedule 4/2) plus FOLFIRI is

34 ion were randomly assigned 1:1 to placebo or sunitinib 37.5 mg per day until progression.

35 herapy were randomly assigned 2:1 to receive sunitinib 37.5 mg/d continuously or placebo.

36 domly assigned to receive FOLFIRI and either sunitinib (37.5 mg per day) or placebo (4 weeks on treat

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

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

39 day for 10 weeks, a 2-week washout, and then sunitinib 50 mg per day (4 weeks on, 2 weeks off, 4 week

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

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

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

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

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

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

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

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

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

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

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

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

52 Sunitinib, a multi-target receptor tyrosine kinase inhib

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

54 pment of ovarian dysgerminoma and the use of Sunitinib, a receptor tyrosine kinase inhibitor with an

55 tested the efficacy of a combination of oral sunitinib, a small molecule multitargeted receptor tyros

56 Similarly, sunitinib, a small-molecule inhibitor of RET, blocked GD

57 Sunitinib, a vascular endothelial growth factor pathway

58 dy was conducted to evaluate trebananib plus sunitinib, a vascular endothelial growth factor receptor

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

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

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

62 growth delay compared with equimolar SAN1 or sunitinib alone.

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

64 Importantly, Sunitinib also increased engraftment and differentiation

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

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

67 Sunitinib, an inhibitor of key molecules involved in neo

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

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

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

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

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

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

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

75 Food and Drug Administration-approved drugs, sunitinib and dasatinib, prohibit brain metastases deriv

76 WI-38 fibroblasts, gemcitabine, bevacizumab, sunitinib and EMAP caused 79, 58, 80 and 29 percent inhi

77 owth inhibition in gemcitabine, bevacizumab, sunitinib and EMAP monotherapy was 43, 38, 94 and 46 per

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

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

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

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

82 Targeted therapy for pNET is limited to sunitinib and everolimus.

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

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

85 Three sunitinib and no placebo patients achieved complete resp

86 ry meningiomas as recently demonstrated with sunitinib and novel somatostatin analogues.

87 edian OS was 13.1 months and 11.8 months for sunitinib and placebo, respectively (hazard ratio [HR],

88 In contrast to sunitinib and sorafenib, axitinib did not affect the mit

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

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

91 valuated patient preference for pazopanib or sunitinib and the influence of health-related quality of

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

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

94 luded, with 2,856 from sorafenib, 1,388 from sunitinib, and 435 from pazopanib trials.

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

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

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

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

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

100 of bowel NETs; everolimus, streptozocin, and sunitinib are approved to treat pancreatic NETs.

101 PFS was significantly improved in the sunitinib arm (median 5.6 v 4.1 months; HR, 0.725; 95% C

102 Median PFS for the sunitinib arm was 7.8 months (95% CI, 7.1 to 8.4 months)

103 d treatment discontinuations occurred in the sunitinib arm.

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

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

106 red the efficacy and safety of pazopanib and sunitinib as first-line therapy.

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

108 Patients treated with sunitinib, as compared with those treated with pazopanib

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

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

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

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

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

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

115 Compared with sunitinib, cabozantinib treatment significantly increase

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

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

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

119 periments using treatment with tamoxifen and sunitinib confirmed the increased effectiveness of dual

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

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

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

123 Sunitinib decreased neointimal formation and smooth musc

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

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

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

127 This intermittent sunitinib dosing continued until Response Evaluation Cri

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

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

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

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

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

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

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

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

136 b for ERBB2 mutations or amplifications; and sunitinib for KIT or PDGFRA mutations or amplification.

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

138 metastatic renal cell carcinoma treated with sunitinib from October 1, 2008, to March 1, 2013, were e

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

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

141 g treatment with gemcitabine, cisplatin, and sunitinib (GCS) 37.5 mg per day.

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

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

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

145 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

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

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

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

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

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

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

152 In the sunitinib group, the mean change in tumor SUV(max) was -

153 let-derived growth factor receptor inhibitor sunitinib have noted improved progression-free survival

154 Until now, only imatinib and sunitinib have proven clinical benefit in patients with

155 Pazopanib and sunitinib have similar efficacy, but the safety and qual

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

157 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

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

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

160 as 6.9 months for placebo and 9.0 months for sunitinib (HR, 1.28; 95% CI, 0.79 to 2.10; one-sided P =

161 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

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

163 zopanib (800 mg once daily; 557 patients) or sunitinib in 6-week cycles (50 mg once daily for 4 weeks

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

165 Pazopanib was superior to sunitinib in HRQoL measures evaluating fatigue, hand/foo

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

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

168 n of VEGF signaling by anti-VEGF antibody or sunitinib in mice from the age of 14 to 17 weeks was acc

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

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

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

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

173 mTORC1 activity correlate with resistance to sunitinib in patients.

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

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

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

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

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

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

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

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

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

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 Sunitinib maintained its antiangiogenic and antimetastat

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

189 Systemic sunitinib malate may be useful in slowing progression of

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

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

192 ted juxtapapillary RCH treated with systemic sunitinib malate.

193 uxtapapillary RCH were treated with systemic sunitinib malate.

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

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

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

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

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

199 published animal efficacy experiments where sunitinib monotherapy was tested for effects on tumor vo

200 3 patients were randomly assigned to receive sunitinib (n = 584) or placebo (n = 289).

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

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

203 ceived maintenance therapy (placebo, n = 41; sunitinib, n = 44).

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

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

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

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

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

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

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

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

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

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

214 ither by gene knockdown or by treatment with sunitinib or vandetanib reduced RET-dependent growth of

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

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

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

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

219 ormed a randomized phase III trial comparing sunitinib plus capecitabine (2,000 mg/m2) with single-ag

220 s of 5.5 months (95% CI, 4.5 to 6.0) for the sunitinib plus capecitabine arm and 5.9 months (95% CI,

221 Sunitinib plus erlotinib may enhance antitumor activity

222 d, phase III study aimed to demonstrate that sunitinib plus FOLFIRI (fluorouracil, leucovorin, and ir

223 all, 768 patients were randomly assigned to sunitinib plus FOLFIRI (n = 386) or placebo plus FOLFIRI

224 Sunitinib plus FOLFIRI was associated with more grade >/

225 was stopped because of potential futility of sunitinib plus FOLFIRI.

226 .807), indicating a lack of superiority for sunitinib plus FOLFIRI.

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

228 116 (57%) of 202 patients in the sunitinib plus IMA901 group and 62 (47%) of 132 in the s

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

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

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

232 We used available sunitinib preclinical studies to evaluate relationships

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

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

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

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

237 Pazopanib and sunitinib provided a progression-free survival benefit,

238 tested the ability of cabozantinib to rescue sunitinib resistance.

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

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

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

242 lpha strongly decreases tumor uptake whereas sunitinib results in a modest reduction with an overshoo

243 2 weeks after daily treatment with 40 mg/kg sunitinib revealed a 71% (P < 0.01) reduction in fBV in

244 or many of these agents, including imatinib, sunitinib, rituximab, and cetuximab.

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

246 Trebananib plus sunitinib seemed to increase toxicity at the tested dose

247 Sunitinib sensitivity correlated with vascular endotheli

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

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

250 Bevacizumab, estramustine, and sunitinib should not be offered.

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

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

253 Sunitinib significantly increased progression-free survi

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

255 The multikinase inhibitors sunitinib, sorafenib, and axitinib have an impact not on

256 Sunitinib stimulated a VEGFC-dependent development of ly

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

258 rug Administration-approved PDGFR inhibitor, sunitinib, targets FOXC2-expressing tumor cells leading

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

260 rse events (AEs; 27% v 7%) were greater with sunitinib than placebo.

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

262 We evaluated angiogenesis-targeted sunitinib therapy in a randomized, double-blind trial of

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

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

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

266 The addition of sunitinib to capecitabine does not improve the clinical

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

268 The addition of sunitinib to prednisone did not improve OS compared with

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

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

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

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

273 Chronic sunitinib treatment of RCC cell lines activated both AXL

274 In addition, sunitinib treatment of tumor-bearing mice was associated

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

276 Sunitinib treatment was independently associated with pa

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

278 In CT26-bearing mice, anti-VEGF antibody and sunitinib treatments reduced Treg but masitinib, a TKI n

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

280 om assignment for maintenance placebo versus sunitinib using a one-sided log-rank test with alpha = .

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

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

283 Sunitinib was discontinued, and he completed four additi

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

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

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

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

288 Sunitinib was reinitiated for two cycles in those patien

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

290 Sunitinib was well tolerated and almost completely preve

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

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

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

294 th failure of at least previous imatinib and sunitinib were randomised in a 2:1 ratio (by computer-ge

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

296 iangiogenic tyrosine kinase inhibitor (TKI), sunitinib, which failed to meet primary or secondary sur

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

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

299 Pazopanib was noninferior to sunitinib with respect to progression-free survival (haz

300 ficant patient preference for pazopanib over sunitinib, with HRQoL and safety as key influencing fact