ライフサイエンスコーパス: dasatinib

1 rowth becomes sensitive to the Src inhibitor Dasatinib.

2 )F-fluoride PET imaging before initiation of dasatinib.

3 it prevented relapse when administered with dasatinib.

4 umor and normal bone occurred in response to dasatinib.

5 ib, 105 received nilotinib, and 107 received dasatinib.

6 e inhibition constants of both bosutinib and dasatinib.

7 ptosis induced by the SFK inhibitors PP2 and dasatinib.

8 RTK-driven adaptive response associated with dasatinib.

9 ynergism and increased tumor accumulation of dasatinib.

10 he sensitivity of the mutant to imatinib and dasatinib.

11 CK1 by small molecule inhibitors, AIM-100 or Dasatinib.

12 ore sensitive to SRC family kinase inhibitor Dasatinib.

13 bitor AZD2014 and the multi-kinase inhibitor dasatinib.

14 e imatinib-induced diarrhoea but not that of dasatinib.

15 value for response to the Src/Abl inhibitor dasatinib.

16 red RPE sheets in the presence or absence of dasatinib.

17 as initial treatment imatinib, nilotinib, or dasatinib.

18 re used to determine the retinal toxicity of dasatinib.

19 odies, and the small-molecules gefitinib and dasatinib.

20 se (CCyR) rates in CML patients treated with dasatinib.

21 response to the anti-invasive Src inhibitor dasatinib.

22 ular kinase engagement by the approved drug, dasatinib.

23 a high-fat diet and treated with vehicle or dasatinib.

24 800 mg (HR 0.51, 95% CI 0.29-0.88, p=0.016), dasatinib (0.28, 0.12-0.66, p=0.004), or nilotinib (0.42

25 sed CML-CP were randomly assigned to receive dasatinib 100 mg once daily (n = 259) or imatinib 400 mg

26 from the DASISION trial continue to support dasatinib 100 mg once daily as a safe and effective firs

27 erant CML in chronic phase (CML-CP) received dasatinib 100 mg once daily, 50 mg twice daily, 140 mg o

28 PET before and 12 weeks after initiation of dasatinib (100 mg daily).

29 al prednisone 5 mg twice daily), plus either dasatinib (100 mg orally once daily) or placebo until di

30 1 international study) and were treated with dasatinib 140 mg/day (100 mg/day over 70 years) with int

31 Like dasatinib, (18)F-SKI underwent extensive metabolism afte

32 adverse event reported more frequently with dasatinib (28% v 0.8% with imatinib).

33 higher in patients treated with nilotinib or dasatinib (29 and 19 per 1000 person-years, respectively

34 ir standard TKI dose (imatinib 200 mg daily, dasatinib 50 mg daily, or nilotinib 200 mg twice daily)

35 daily (n=68), imatinib 800 mg daily (n=200), dasatinib 50 mg twice daily or 100 mg daily (n=106), or

36 Dasatinib 60 mg/m(2) and 80 mg/m(2) once-daily dosing we

37 s who achieved BCR-ABL1 </= 10% at 3 months (dasatinib, 84%; imatinib, 64%), improvements in progress

38 Pretreatment with dasatinib, a broad spectrum tyrosine kinase inhibitor, b

39 e-threatening disease that can be induced by dasatinib, a dual Src and BCR-ABL tyrosine kinase inhibi

40 We tested the efficacy of dasatinib, a Food and Drug Administration (FDA)-approved

41 se Inhibitor Resource database revealed that dasatinib, a Food and Drug Administration-approved drug,

42 Dasatinib, a Food and Drug Administration-approved inhib

43 Dasatinib, a multikinase inhibitor, was effective agains

44 Dasatinib, a potent and specific Src tyrosine kinase inh

45 amic assessment for systemic therapy such as dasatinib, a potent SRC kinase inhibitor, with activity

46 owth, but clinical trials using single agent dasatinib, a SRC family kinase inhibitor, have failed in

47 ibitor), CHIR99021 (GSK-3beta inhibitor) and Dasatinib (Abl, Src and c-Kit inhibitor) were found to c

48 nhibition with the tyrosine kinase inhibitor Dasatinib abrogates HS1-Y397 phosphorylation.

49 ated with imatinib and patients treated with dasatinib according to their transcript levels at 3 mont

50 nd/or compensatory signals exist that dampen dasatinib activity.

51 of human EGFR-2-positive (HER2(+)) disease, dasatinib alone is ineffective, but potentiates the effi

52 Treatment with dexamethasone and dasatinib also impaired engraftment of leukemia cells in

53 Although we observed that dasatinib also inhibits DV2 particle assembly and/or sec

54 Dasatinib also prevented TRD caused by PVR in vivo.

55 h dasatinib reduced the expression of Col1a1 Dasatinib also reduced proliferation and alpha-SMA expre

56 Likewise, pretreatment with dasatinib also suppressed etoposide and radiation induce

57 of transgene expression, and treatment with dasatinib, an inhibitor of Src family kinases, also mimi

58 plifications presented a high sensitivity to dasatinib, an SFK inhibitor, pointing out YES1 status as

59 Notably, dasatinib, an U.S. Food and Drug Administration-approved

60 to treatment; 762 patients were assigned to dasatinib and 760 to placebo.

61 ression by mTORC2 inhibition synergized with dasatinib and abolished resistance in vitro and in vivo.

62 mixture of four drugs (axitinib, erlotinib, dasatinib and AZD4547) at low doses, inhibiting 90% of c

63 and consolidation first-line treatment with dasatinib and blinatumomab that was based on a targeted

64 Furthermore, dasatinib and BMS-754807 inhibited in vivo growth of the

65 ro and in vivo by small molecule inhibitors (dasatinib and BMS-754807, against SFK and IGF-1R/Insulin

66 hallenging, and FDA-approved SRC inhibitors, dasatinib and bosutinib, are multitargeted kinase inhibi

67 of this approach, two kinase-targeted drugs, Dasatinib and Brigatinib (AP26113), were simultaneously

68 Concurrent exposure of cells to dasatinib and chemotherapeutic agents resulted in additi

69 Whereas dasatinib and CNX-774 were found to inhibit the growth o

70 ected tyrosine kinase inhibitors (Ibrutinib, Dasatinib and Crizotinib) that substantially impaired in

71 is study does not support the combination of dasatinib and docetaxel in this population of patients.

72 t PDGFRalpha-driven glioma were treated with dasatinib and everolimus.

73 significantly improved the CNS retention of dasatinib and extended the survival of PPK tumor-bearing

74 Dasatinib and ibrutinib were also found to counteract an

75 ase occurred in 5% and 7% of patients in the dasatinib and imatinib arms, respectively.

76 Dasatinib and imatinib both blocked binding of PKCdelta

77 tric CML in 2003, the second-generation TKIs dasatinib and nilotinib were recently approved for use i

78 a (CML) patients on imatinib, or second-line dasatinib and nilotinib, and 24 controls.

79 pecific sensitivity of group 2 ATRT cells to dasatinib and nilotinib, and suggest that these are prom

80 further investigate the cellular effects of dasatinib and other comparable KIs with varying risks of

81 pertension, suggesting a direct link between dasatinib and podocytes.

82 nt with a combination of the senolytic drugs dasatinib and quercetin (D+Q) reduces overall hepatic st

83 Furthermore, the combination of dasatinib and rapamycin delays tumor recurrence followin

84 In a luminal disease model, combined dasatinib and rapamycin is more effective at inducing re

85 CR-ABL kinase and Janus kinase 2 (JAK2) with dasatinib and ruxolitinib, respectively.

86 oved by the US Food and Drug Administration (dasatinib and ruxolitinib, which inhibit BCR-ABL and Jan

87 use cardiac transplant with atorvastatin and dasatinib and showed reduction of the CRM genes, signifi

88 tion: by suppressing Src using the inhibitor dasatinib and siRNA, we could increase AQP2 membrane acc

89 commercial drug and type I kinase inhibitor Dasatinib and the type II inhibitor RL45, respectively f

90 Maintenance therapy was dasatinib and vincristine/dexamethasone reinductions for

91 eceiving imatinib 800 mg, 23 (21%) receiving dasatinib, and 27 (25%) receiving nilotinib discontinued

92 re 6.06 microM for imatinib, 3.72 microM for dasatinib, and 81.35 microM for nilotinib; for L3 larvae

93 s shown by nintedanib, followed by imatinib, dasatinib, and acetylcysteine.

94 ses by the second-generation TKIs nilotinib, dasatinib, and bosutinib.

95 he inhibition of RNA replication by AZD0530, dasatinib, and Fyn RNAi.

96 o kinase inhibitor (Y27632), Cytochalasin D, Dasatinib, and Lysophosphatidic acid to modulate YAP loc

97 At the time of study closure, 61% and 63% of dasatinib- and imatinib-treated patients remained on ini

98 We investigated dasatinib, another potent tyrosine kinase inhibitor, in

99 The resulting dasatinib-antibody conjugate suppresses T-cell-receptor

100 hat two FDA-approved drugs (atorvastatin and dasatinib), approved for nontransplant indications, coul

101 6-Mercaptopurine, 6-thioguanine and dasatinib are three important anticancer drugs with high

102 L transcript levels </=10% was higher in the dasatinib arm.

103 The use of imatinib or dasatinib as a c-Kit inhibitor reduced the level of sphe

104 repurposing approach in DLBCL, and point to dasatinib as an attractive strategy for further clinical

105 or AZD2014 and the tyrosine kinase inhibitor dasatinib as monotherapies and in combination.

106 e for subsequent treatment with nilotinib or dasatinib as second-line therapy.

107 e effects of four BTK inhibitors (ibrutinib, dasatinib, AVL-292, and CNX-774) on IgE-dependent activa

108 nosis (n = 21), on TKI (imatinib, nilotinib, dasatinib) before achieving major molecular response (pr

109 er endpoints included differential effect of dasatinib between (18)F-fluoride incorporation in tumor

110 The data revealed saturable dasatinib binding to a small subset of kinase targets at

111 calculations find that the type I inhibitor Dasatinib binds favorably to the wild type but unfavorab

112 tment with a broad-spectrum kinase inhibitor dasatinib blocked protein aggregate accumulation and res

113 In vivo, pre-treatment of mice with dasatinib blocked radiation-induced apoptosis in the sal

114 d STAT1, as the application of SFK inhibitor Dasatinib blocks neutrophil exhaustion triggered by the

115 and Drug Administration (FDA)-approved drugs dasatinib, bosutinib, and saracatinib that target ABL, S

116 We showed that LCK inhibitors, such as dasatinib, bosutinib, nintedanib, and WH-4-023, are able

117 d the more specific Src/Abl kinase inhibitor dasatinib: both reduced ROS-induced degradation of beta-

118 ated senescence, and promoted sensitivity to dasatinib by targeting the proto-oncogene c-SRC.

119 Taken together, our findings indicate that dasatinib causes pulmonary vascular damage, induction of

120 In conclusion, dasatinib combined with low-intensity chemotherapy was w

121 We found that dasatinib combined with MET and insulin-like growth fact

122 ained statistically significantly higher for dasatinib compared with imatinib.

123 serum of CML patients who were treated with dasatinib, compared with CML patients treated with imati

124 Addition of the Src/c-Abl inhibitor, dasatinib, completely blocks this feedback activation, c

125 Hck is a key mediator of renal fibrosis and dasatinib could be developed as an antifibrotic drug.

126 methacrylate) (POEG) hydrophilic blocks and dasatinib (DAS, an oncogenic tyrosine kinases inhibitor)

127 We developed a first-of-kind dasatinib-derivative imaging agent, (18)F-SKI-249380 ((1

128 es seen in patients treated with the ABL TKI dasatinib despite its much shorter plasma half-life and

129 Dasatinib did not cause any detectable toxicity of the r

130 izing the drug dasatinib, we have shown that dasatinib-directed NEDDylation occurs for known endogeno

131 Escalating once-daily dasatinib doses (60 to 120 mg/m(2)) were administered to

132 ork, we show that ibrutinib, idelalisib, and dasatinib, drugs that block B cell receptor (BCR) signal

133 In vivo, while AZD2014 and dasatinib each inhibit tumor growth alone, the effect of

134 We found that dasatinib effectively inhibited the proliferation of mou

135 All drugs except one (dasatinib) elicited a spectral response in CYP27A1 and h

136 The SFK inhibitor dasatinib enhanced the antitumor effect of BKM120 and fu

137 Conversely, dasatinib enhanced tyrosine phosphorylation in a panel o

138 nd PDGFRB fusions were sensitive in vitro to dasatinib, EPOR and JAK2 rearrangements were sensitive t

139 y, Tg-C73A mice and non-Tg mice treated with dasatinib exhibited improved behavioral outcomes in moto

140 Dasatinib exhibited synergy with everolimus in the treat

141 d global tyrosine phosphorylation (pY) after dasatinib exposure using a mass spectrometry-based quant

142 ation of 6-mercaptopurine, 6-thioguanine and dasatinib for the first time.

143 patients, nilotinib for seven patients, and dasatinib for three patients.

144 al was 21.5 months (95% CI 20.3-22.8) in the dasatinib group and 21.2 months (20.0-23.4) in the place

145 0.7 mum) followed by ponatinib > bosutinib > dasatinib > imatinib.

146 ing rank order of potency: ibrutinib>AVL-292>dasatinib>CNX-774.

147 onatinib vs sham therapy (P < .001), whereas dasatinib had no effect.

148 er (SCC) where the tyrosine kinase inhibitor dasatinib has emerged as a new therapeutic option.

149 and of pulmonary arterial hypertension with dasatinib have raised concerns about long-term sequelae

150 ologic targeting of the EGFR, was blocked by Dasatinib, highlighting the central role of SFKs in uPAR

151 lpha, alemtuzumab, bendamustine, bortezomib, dasatinib, imatinib, lenalidomide, rituximab alone or in

152 We assessed interactions of bosutinib, dasatinib, imatinib, nilotinib, and ponatinib with recom

153 oride PET to delineate treatment response of dasatinib in CRPC bone metastases with borderline correl

154 AKT phosphorylation was weakly inhibited by dasatinib in DDR2-mutant lung SCC cells, suggesting that

155 Furthermore, chronic administration of dasatinib in mice causes reversible glomerular dysfuncti

156 Retinoids potentiated the activity of dasatinib in mouse and human BCR-ABL1 ALL, providing an

157 rget and predictive biomarker of response to dasatinib in NSCLC.Methods: Functional significance was

158 with everolimus may improve the efficacy of dasatinib in PDGFRalpha-driven glioma through combinator

159 electivity of the clinical BCR-ABL inhibitor dasatinib in peripheral blood mononuclear cell (PBMC) ly

160 lysis of 6-mercaptopurine, 6-thioguanine and dasatinib in pharmaceutical formulations and urine sampl

161 RPE cells was used to assess the efficacy of dasatinib in preventing traction retinal detachment (TRD

162 nografts were treated with the SRC inhibitor dasatinib in vivo.

163 Despite the lack of S256 phosphorylation, dasatinib increased phosphorylation of S269, even in S25

164 ling to identify the molecular mechanisms of dasatinib-induced injury to the actin cytoskeleton, and

165 MET rescued DDR2-mutant lung SCC cells from dasatinib-induced loss of cell viability.

166 sms involved in the long-term development of dasatinib-induced PAH.

167 We conclude that dasatinib induces nephrotoxicity through altered podocyt

168 At the end of dasatinib induction therapy (day 85), 29% of the patient

169 rosine kinase inhibitors (TKIs) imatinib and dasatinib inhibit fludarabine and cytarabine uptake.

170 0.1 muM dasatinib inhibited nearly 80% of vitreous fluid-stimula

171 DDR2-mutant lung SCC cells, suggesting that dasatinib inhibits survival signals distinct from other

172 Dasatinib inhibits tyrosine kinases, including Src kinas

173 Pharmacologic uptake of dasatinib into tumor was enhanced after alpha-particle t

174 Dasatinib is a potent BCR-ABL inhibitor with proven effi

175 of FDA Adverse Event Reporting System, that dasatinib is associated with high risk for glomerular to

176 Dasatinib is clinically used for the treatment of bcr/ab

177 ation of 6-mercaptopurine, 6-thioguanine and dasatinib is facilitated as a novel voltammetric sensor.

178 ow that combination therapy with AZD2014 and dasatinib is more effective at reducing metabolic activi

179 hat Fyn kinase, a target of both AZD0530 and dasatinib, is involved in DV2 RNA replication and is pro

180 ibited by combinatorial therapy of DNMTi and dasatinib, laying the groundwork for future clinical inv

181 Treatment of synovial sarcoma cells with dasatinib led to apoptosis and inhibition of cellular pr

182 , serial passaging of DV2 in the presence of dasatinib led to the identification of a mutation in the

183 Importantly, dasatinib markedly increases the elimination of AML stem

184 Our data suggested that dasatinib may be effective in the prevention of PVR.

185 ER-family inhibitors with other TKIs such as dasatinib may have therapeutic advantages in certain bre

186 identify the cellular target of AZD0530 and dasatinib mediating this anti-DV2 activity, we examined

187 sed CML-CP were randomized to receive 100 mg dasatinib (n = 259) or 400 mg imatinib (n = 260) once da

188 d with chemotherapy + imatinib (n = 54) or + dasatinib (n = 68).

189 y was imatinib (n=148), nilotinib (n=16), or dasatinib (n=10), for a median of 6.9 years (IQR 4.8-10.

190 on the SPIRIT2 trial (imatinib, n = 319; and dasatinib, n = 297) were genotyped for the promoter 5-HT

191 , several targeted therapies (e.g. imatinib, dasatinib, nilotinib) have been developed to treat Chron

192 Conclusions and Relevance: Dasatinib, nilotinib, and ponatinib increase vascular oc

193 ar range (abiratone, candesartan, celecoxib, dasatinib, nilvadipine, nimodipine, and regorafenib).

194 269A mutant in LLC-PK1 cells, and found that dasatinib no longer induced AQP2 membrane accumulation.

195 e kinase inhibitors imatinib, nilotinib, and dasatinib on B. malayi adult males, adult females, L3 la

196 igated the role of the dual kinase inhibitor dasatinib on human myeloid cells.

197 ion assay were used to examine the effect of dasatinib on migration, proliferation, and extracellular

198 The effect of dasatinib on RPE sheet growth was determined by measurin

199 the inhibitory effect of the anticancer drug dasatinib on Src kinase oncogenic potential in vivo We f

200 tient with refractory T-ALL was treated with dasatinib on the basis of drug profiling information and

201 Inhibition of SFK signaling with dasatinib or another SFK inhibitor, sarcatinib, suppress

202 ns of HER-family inhibitors with NVP-AEW541, dasatinib or crizotinib (inhibitors of IGF-1R, Src and c

203 Treating mice with dasatinib or imatinib, which target c-Kit, resulted in c

204 mia (CML) in chronic phase (CP) treated with dasatinib or imatinib.

205 istance to or unacceptable side effects from dasatinib or nilotinib and 70% of patients with the T315

206 istance to or unacceptable side effects from dasatinib or nilotinib or who had the BCR-ABL T315I muta

207 matinib 800 mg or the second-generation TKIs dasatinib or nilotinib resulted in superior and deeper r

208 Patients receiving first-line or subsequent dasatinib or nilotinib who stopped therapy after at leas

209 atinib 800 mg or second-generation TKIs (ie, dasatinib or nilotinib) achieved complete cytogenetic re

210 vascular occlusive events was increased with dasatinib (OR, 3.86; 95% CI, 1.33-11.18), nilotinib (OR,

211 a from CML patients on TKI or with imatinib, dasatinib, or nilotinib induced significant and dose-dep

212 e other TKI groups (imatinib 800 mg p=0.029, dasatinib p=0.003, nilotinib p=0.031).

213 ent inhibitors of the BCR-ABL kinase such as dasatinib, patients in remission frequently relapse due

214 Dasatinib pediatric pharmacokinetic parameters were comp

215 monary hypertension in patients treated with dasatinib, peripheral arterial occlusive disease and oth

216 We present long-term follow-up of a dasatinib phase 3 study of patients with imatinib-resist

217 We assessed whether dasatinib plus docetaxel in chemotherapy-naive men with

218 Dasatinib plus glucocorticoids were administered, follow

219 selectively killed by a senolytic cocktail, dasatinib plus quercetin (DQ), is fibrogenic.

220 lly important ABL TKIs (imatinib, nilotinib, dasatinib, ponatinib, and DCC-2036), we interrogated res

221 r varying resistance to imatinib, nilotinib, dasatinib, ponatinib, rebastinib, and bosutinib.

222 he direct inhibition of T-cell activation by dasatinib, pretreatment of maturing dendritic cells (DCs

223 Dasatinib prevented RPE sheet growth, cell migration, pr

224 Administration-approved drugs, sunitinib and dasatinib, prohibit brain metastases derived from breast

225 senescent HSCs by 'senolytic' treatment with dasatinib/quercetin or ABT-263 inhibits tumour progressi

226 sistently, the Src kinase inhibitors PP2 and dasatinib reduced chemokine secretion by neutrophils and

227 uch as the SRC family kinase (SFK) inhibitor dasatinib reduced pPLCgamma2 and inhibited proliferation

228 Treatment of tubular cells with dasatinib reduced the expression of Col1a1 Dasatinib als

229 -protein interaction relationships upon this dasatinib-regulated pY network revealed decreased phosph

230 Tumors exhibiting dasatinib resistance were commonly characterized by acti

231 may be exploited as a predictive marker for Dasatinib response in cancer patients.

232 ES1 status as a stratification biomarker for dasatinib response.

233 Conversely, inhibition of ACK1 by AIM-100 or Dasatinib restored dimethyl H3K9 methylation marks and c

234 or c-Src that are active in the presence of dasatinib restored phosphorylation of PKCdelta at Tyr-15

235 le inhibition of both PDGFRbeta and EphB4 by dasatinib resulted in a significant decrease in tumor ce

236 reas treatment with the SRC kinase inhibitor dasatinib resulted in equalization of GM-CSFR betac phos

237 First-line dasatinib resulted in faster and deeper responses compar

238 The combination of dasatinib, ruxolitinib, and the corticosteroid dexametha

239 To gain better insight into dasatinib's action in these cells, we assessed altered g

240 We find that Dasatinib's impotency against gatekeeper residue mutatio

241 for Children with Cancer Consortium assessed dasatinib safety and efficacy in pediatric patients.

242 Dasatinib safety and efficacy profiles compared favorabl

243 Treatment with the SFK and c-KIT inhibitor dasatinib selectively inhibits human AML stem/progenitor

244 plete remission continued consolidation with dasatinib, sequentially with cytarabine, asparaginase, a

245 ination of kinase inhibitors (vandetanib and dasatinib) showed enhanced sensitivity compared with eit

246 ment of nude mice with SYO-1 xenografts with dasatinib significantly inhibited tumor growth in vivo.

247 eral ureteric obstruction, pretreatment with dasatinib significantly reduced the upregulation of prof

248 tment of maturing dendritic cells (DCs) with dasatinib strongly enhanced their stimulatory activity.

249 Combined treatment with DNMTi and dasatinib targeted both Hippo-dependent and Hippo-indepe

250 ons were more sensitive to the SFK inhibitor dasatinib than those with WT DDR2.

251 served in a higher proportion of patients on dasatinib therapy and were associated with better 3-year

252 Here, we demonstrated that chronic dasatinib therapy causes pulmonary endothelial damage in

253 responses previously observed with nilotinib/dasatinib therapy for imatinib-resistant patients with m

254 ne requirement of immature leukemic B cells, dasatinib therapy restores cytokine dependency and sensi

255 CML-CP can experience long-term benefit with dasatinib therapy, particularly if achieving BCR-ABL </=

256 hase patients receiving imatinib followed by dasatinib therapy.

257 The addition of dasatinib to docetaxel did not improve overall survival

258 at can selectively deliver the Lck inhibitor dasatinib to human T lymphocytes.

259 chanisms of resistance to the Src inhibitor, dasatinib, to identify key pathways to target in combina

260 suppression of ACK1 signaling by AIM-100 or Dasatinib, to mitigate HOXA1 up-regulation in breast can

261 c-SRC or treatment with the c-SRC inhibitor dasatinib together with FBXL7 depletion prevents metasta

262 hoea was more prevalent in imatinib, than in dasatinib treated patients (P = 0.015), which when strat

263 Dasatinib treated podocytes show significant changes in

264 Fifteen dasatinib-treated and 19 imatinib-treated patients had B

265 by both duration and distance of swimming of dasatinib-treated fish compared with control animals.

266 death, were markedly reduced in Tg-C73A and dasatinib-treated non-Tg animals.

267 ction in mTOR signaling that persisted after dasatinib treatment alone.

268 Dasatinib treatment also improved renal function, reduce

269 We found that dasatinib treatment attenuated hypoxic pulmonary vasocon

270 In vivo dasatinib treatment enhances chemotherapy-induced target

271 ovide support for the clinical evaluation of dasatinib treatment in a selected subset of patients usi

272 Furthermore, dasatinib treatment induced pulmonary endothelial cell a

273 Dasatinib treatment mediated endothelial cell dysfunctio

274 Our results show that the efficacy of dasatinib treatment of PDGFRalpha-driven HGG was enhance

275 Furthermore, dasatinib treatment resulted in the improved physical ap

276 antiviral mechanism of action of AZD0530 and dasatinib, two pharmacological inhibitors of host kinase

277 asone reinductions for 18 months followed by dasatinib until relapse or death.

278 We found that post-HCT dasatinib use increased the risk of cytomegalovirus reac

279 Viral infections have been reported with dasatinib use, but its cytomegalovirus risk after hemato

280 eport the 5-year analysis from the phase III Dasatinib Versus Imatinib Study in Treatment-Naive Chron

281 mia in chronic phase (CML-CP) in the phase 3 DASatinib versus Imatinib Study In treatment-Naive CML p

282 for imatinib 800 mg, vs 100 [96%] of 104 for dasatinib vs 99 [93%] of 107 for nilotinib), major molec

283 cytogenetic response was 3 vs 6 months with dasatinib vs imatinib.

284 The results demonstrate that sensitivity to dasatinib was associated with a progenitor subtype.

285 Dasatinib was effective at inducing cell cycle arrest an

286 Dasatinib was more broadly active than the Bruton kinase

287 uperior efficacy of combined gedatolisib and dasatinib was observed in ABL/PDGFR-mutant models (P < .

288 Utilizing the drug dasatinib, we have shown that dasatinib-directed NEDDyla

289 were previously developed to be resistant to dasatinib, we identified a switch to a more invasive phe

290 Upon treatment with dasatinib, we observed a switch in activity at the invas

291 ceived 400 or 800 mg imatinib, nilotinib, or dasatinib were analyzed.

292 ents for 6-mercaptopurine, 6-thioguanine and dasatinib were found to vary linearly with their concent

293 istically significant changes in response to dasatinib were identified by the SUVmaxavg (average of m

294 tion of IGF-1-induced Akt1 phophorylation by dasatinib, whereas Akt2 phosphorylation was SFK independ

295 to FAK or Src specific inhibitors (PF-228 or Dasatinib), which inhibited only VCAM-1 expression.

296 were sensitive to the multikinase inhibitor dasatinib, which antagonizes TNK2 kinase activity, as we

297 Only 1/11 eyes had a TRD in the presence of dasatinib, while all 11 controls eyes had a TRD.

298 targeting of AML cells by the combination of dasatinib with daunorubicin may be related to inhibition

299 Unexpected sensitivity to dasatinib with half maximal inhibitory concentration val

300 ences of pleural effusion were reported with dasatinib, with the highest incidence in year 1.