ライフサイエンスコーパス: dasatinib

1 it prevented relapse when administered with dasatinib.

2 umor and normal bone occurred in response to dasatinib.

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

4 ptosis induced by the SFK inhibitors PP2 and dasatinib.

5 RTK-driven adaptive response associated with dasatinib.

6 he sensitivity of the mutant to imatinib and dasatinib.

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

8 ore sensitive to SRC family kinase inhibitor Dasatinib.

9 ular kinase engagement by the approved drug, dasatinib.

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

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

12 as initial treatment imatinib, nilotinib, or dasatinib.

13 re used to determine the retinal toxicity of dasatinib.

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

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

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

17 response to the anti-invasive Src inhibitor dasatinib.

18 ment is usually observed after withdrawal of dasatinib.

19 e profiling of potential cellular targets of Dasatinib.

20 3/4 thrombocytopenia were more frequent with dasatinib.

21 a treated with the tyrosine kinase inhibitor dasatinib.

22 uced after oral administration of 5 mg/kg of dasatinib.

23 tiating cells in combination with IM but not dasatinib.

24 rowth becomes sensitive to the Src inhibitor Dasatinib.

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

26 800 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

27 ic-phase (CP) CML were randomized to receive dasatinib 100 mg (n = 259) or imatinib 400 mg (n = 260)

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

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

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

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

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

33 1 international study) and were treated with dasatinib 140 mg/day (100 mg/day over 70 years) with int

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

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

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

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

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

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

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

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

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

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

44 Dasatinib, a Food and Drug Administration-approved inhib

45 Dasatinib, a potent and specific Src tyrosine kinase inh

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

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

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

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

50 These data suggest that dasatinib, akin to other small molecule kinase inhibitor

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

52 Dasatinib also abrogated the anti-apoptotic effect of pr

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

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

55 Dasatinib also prevented TRD caused by PVR in vivo.

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

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

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

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 ating cell assay and expansion on removal of dasatinib and addition of growth factors.

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

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

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

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

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

67 Combined treatment using dasatinib and chemotherapy provides a novel approach to

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

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

70 Dasatinib and ibrutinib were also found to counteract an

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

72 Dasatinib and imatinib both blocked binding of PKCdelta

73 to better understand the exact relevance of Dasatinib and its pharmacological effects in relation to

74 Second-generation inhibitors such as dasatinib and nilotinib can overcome the majority of the

75 l mutations, including those associated with dasatinib and nilotinib resistance, except T315I.

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

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

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

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

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

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

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

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

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

85 Maintenance therapy was dasatinib and vincristine/dexamethasone reinductions for

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

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

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

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

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

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

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

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

94 6-Mercaptopurine, 6-thioguanine and dasatinib are three important anticancer drugs with high

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

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

97 nalyzed the outcome of patients treated with dasatinib as first-line therapy to identify patients who

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

99 y was designed to describe incident cases of dasatinib-associated PH reported in the French PH regist

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

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

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

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

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

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

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

107 Dasatinib (BMS-354825), a dual Src/Abl inhibitor, is a p

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

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

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

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

112 Dasatinib caused a partial inhibition of neutrophil resp

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

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

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

116 Primary data showed superior efficacy for dasatinib compared with imatinib after 12 months, includ

117 , vomiting, and rash were less frequent with dasatinib compared with imatinib, whereas pleural effusi

118 ained statistically significantly higher for dasatinib compared with imatinib.

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

120 Dasatinib completely blocked integrin- and Fc-receptor-m

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

122 Overall, dasatinib continues to show faster and deeper responses

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

124 kinase inhibitor therapy with imatinib (IM), dasatinib (DAS), or nilotinib is very effective in chron

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

126 ibition of Aurora kinase and SRC potentiated dasatinib-dependent loss of activated (Y(416)-phosphoryl

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

128 Dasatinib did not cause any detectable toxicity of the r

129 Dasatinib did not have any major effect on phagocytosis

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 ALL cell sensitivity to the kinase inhibitor dasatinib due to its inhibition of the pre-B cell recept

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

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

136 Conversely, dasatinib enhanced tyrosine phosphorylation in a panel o

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

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

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

140 t(V558;T669I/+) mice with either imatinib or dasatinib failed to inhibit oncogenic Kit signaling and

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

142 The addition of dasatinib further inhibited p-CrkL and p-STAT5, yet only

143 Complete growth factor withdrawal plus dasatinib further reduced input cells to 10%; however, t

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 included diarrhoea (58 [8%] patients in the dasatinib group vs 27 [4%] patients in the placebo group

146 0.7 mum) followed by ponatinib > bosutinib > dasatinib > imatinib.

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

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 eral blood, and support the investigation of dasatinib in combination strategies.

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

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

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

157 with imatinib, supporting first-line use of dasatinib in patients with newly diagnosed CML-CP.

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

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

160 we tested the combination of plerixafor with dasatinib in the same as well as an attenuated CML model

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

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

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

164 At present, little is known about how dasatinib influences nonmalignant cells.

165 gether, our results suggest that AZD0530 and dasatinib inhibit DV at the step of viral RNA replicatio

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

167 Most kinase inhibitors, including Dasatinib, inhibit multiple cellular targets and do not

168 0.1 muM dasatinib inhibited nearly 80% of vitreous fluid-stimula

169 Whereas dasatinib inhibited neutrophil chemotaxis under static c

170 The tyrosine kinase inhibitor dasatinib inhibits migration of several cell lines from

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 highly potent BCR-ABL inhibitor with esta

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

176 Dasatinib is a tyrosine kinase inhibitor used to treat i

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

178 Dasatinib is effective therapy for newly diagnosed patie

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

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

181 Consequently, ROR1 silencing accentuates dasatinib killing of t(1;19) ALL cells.

182 Data suggests that dasatinib kinase inhibition leads to antitumour activity

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

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

185 Importantly, dasatinib markedly increases the elimination of AML stem

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

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

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

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

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

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

195 n the present study, we tested the effect of dasatinib on functional responses of normal mature human

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 t of clinically achievable concentrations of dasatinib on signaling induced by the chemokine CXCL12 t

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

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

202 vo antitumor effects of the c-KIT inhibitor, dasatinib, on the c-KIT mutant P815 mastocytoma tumor we

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

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

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

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

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

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

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

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

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

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

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

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

215 Dasatinib pediatric pharmacokinetic parameters were comp

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

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

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

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 eatment, but is partially restored following dasatinib potentiation of ROR1 expression.

223 Dasatinib pre-treatment inhibited Akt and ERK phosphoryl

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

225 Dasatinib prevented RPE sheet growth, cell migration, pr

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

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

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

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

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

231 e neutrophils and raise the possibility that dasatinib-related compounds may provide clinical benefit

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

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 Dasatinib significantly inhibited PVR-related RPE change

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

247 onal antibodies or tyrosine kinase inhibitor dasatinib significantly reduced KSHV entry and gene expr

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

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

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 predict failure of second-line nilotinib or dasatinib therapy in patients with chronic myeloid leuke

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

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

257 hase patients receiving imatinib followed by dasatinib therapy.

258 tant patients before they began nilotinib or dasatinib therapy.

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

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

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

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

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

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

265 onds to the reported serum concentrations in dasatinib-treated patients.

266 Dasatinib treatment also improved renal function, reduce

267 We found that dasatinib treatment attenuated hypoxic pulmonary vasocon

268 In vivo dasatinib treatment enhances chemotherapy-induced target

269 Furthermore, dasatinib treatment induced pulmonary endothelial cell a

270 Dasatinib treatment inhibited the elevated phosphorylati

271 Those results suggest that dasatinib treatment may affect the proinflammatory funct

272 Dasatinib treatment mediated endothelial cell dysfunctio

273 Furthermore, dasatinib treatment resulted in the improved physical ap

274 sphorylation is transiently eliminated after dasatinib treatment, but is partially restored following

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

276 therapy, the tyrosine kinase inhibitor (TKI) dasatinib, unexpectedly depends on antitumor T-cell resp

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

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

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

289 -targeting multikinase inhibitors PKC412 and dasatinib were also found to override TKI resistance in

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

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

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

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

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

295 erum was significantly inhibited by 50-100nM dasatinib, which corresponds to the reported serum conce

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

297 genitor cells when combined with IM, but not dasatinib, while sparing bcr-abl-negative cells.

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.