ライフサイエンスコーパス: STI571

1 tyrosine kinase inhibitor imatinib mesylate (STI571).

2 e ETV6-ABL fusion gene to imatinib mesylate (STI571).

3 t of patients who had initially responded to STI571.

4 as are possible mechanisms of resistance to STI571.

5 rom patients before beginning treatment with STI571.

6 We aimed to predict resistance to STI571.

7 mic cells that were secondarily resistant to STI571.

8 killed by STI571, the patient was started on STI571.

9 ment with the ABL tyrosine kinase inhibitor, STI571.

10 obtained from patients during treatment with STI571.

11 rch for a more specific partner compound for STI571.

12 re obtained before and during treatment with STI571.

13 t alter the sensitivity of the Abl kinase to STI571.

14 r 3 days with and without growth factors +/- STI571.

15 e even in the presence of growth factors and STI571.

16 to predict sensitivity of leukaemic cells to STI571.

17 human angiomyolipoma cells are sensitive to STI571.

18 d is inhibited by the PDGF beta R inhibitor, STI571.

19 th the in vitro acquisition of resistance to STI571.

20 to determine whether ARG can be inhibited by STI571.

21 c cell death after prolonged incubation with STI571.

22 he small molecule, tyrosine kinase inhibitor STI571.

23 with the selective tyrosine kinase inhibitor STI571.

24 PDGFR phosphorylation was inhibited by STI571.

25 ted during inhibition of BCR-ABL activity by STI571.

26 l(+) leukemias, including those resistant to STI571.

27 at confer resistance to apoptosis induced by STI571.

28 To identify mechanisms of resistance to STI571, 30 complementary DNAs (including 9 matched sampl

29 g pilot study, 58 patients were treated with STI571; 38 patients had a myeloid blast crisis and 20 ha

30 Imatinib mesylate (Gleevec, STI571), a Bcr-Abl kinase inhibitor, selectively inhibit

31 Imatinib mesylate (Gleevec, STI571), a selective inhibitor of a restricted number of

32 Imatinib mesylate (STI571), a selective inhibitor of the Bcr-Abl tyrosine k

33 Imatinib mesylate (STI571), a specific Bcr-Abl tyrosine-kinase signal-trans

34 Imatinib mesylate (STI571), a specific inhibitor of the BCR-ABL tyrosine ki

35 Through rational drug development, STI571, a Bcr-Abl tyrosine kinase inhibitor, has emerged

36 Through rational drug development, STI571, a bcr-abl tyrosine kinase inhibitor, has emerged

37 STI571, a c-Abl kinase inhibitor, only inhibited bFGF- b

38 A combination of the tumor stroma-reactive STI571, a potent platelet-derived growth factor receptor

39 STI571, a selective inhibitor of Bcr-Abl, has been a suc

40 Thus there are two sites of STI571 action of potential importance in Bcr-Abl express

41 The tyrosine kinase inhibitor STI571, active against the BCR-ABL fusion protein in chr

42 Moreover, the combination of STI571 + adaphostin induced more cytotoxicity in K562 ce

43 STI571 is via direct inhibition of BCR-ABL, STI571 additionally reduces the enhanced response to SCF

44 controls, in the presence of growth factors, STI571 affected neither cell cycle kinetics nor recovery

45 STI571 also appeared to exhibit antiproliferative activi

46 Coexposure of Bcr/Abl(+) cells to STI571 also blocked SAHA-mediated induction of p21(CIP1)

47 STI571 also shows activity against c-kit and platelet-de

48 at doing so when the cells are treated with STI571, an Abl kinase inhibitor.

49 Herein, we show that STI571, an inhibitor of Bcr-Abl in chronic myelogenous l

50 Both STI571 and a related compound, inhibitor 2, also reduce

51 ents with CML-BC, including one resistant to STI571 and BMS-354825 and carrying the T315I Abl kinase

52 cals, Basel, Switzerland), formerly known as STI571 and CGP57148B, demonstrated that designer kinase

53 ng reporter gene assays, we demonstrate that STI571 and FoxO3a activate Bim transcription through a F

54 investigate the molecular mechanisms whereby STI571 and FoxO3a regulate Bim expression and apoptosis.

55 of Bcr/Abl(+) cells to the kinase inhibitor STI571 and HDIs leads to diverse perturbations in signal

56 The combined treatment with STI571 and LMB also preferentially eliminates mouse bone

57 As a result, the combined treatment with STI571 and LMB causes the irreversible and complete kill

58 Both STI571 and LY294002 lead to a decrease in the activity o

59 systemic administration of zoledronate with STI571 and paclitaxel produced a significant preservatio

60 wever, synergistic induction of apoptosis by STI571 and PD184352 was not observed in human myeloid le

61 Interactions between the kinase inhibitor STI571 and pharmacological antagonists of the mitogen-ac

62 the combination of BCR/ABL kinase inhibitor STI571 and PI-3k inhibitor wortmannin (WT) or LY294002 (

63 STI571 and SAHA also interacted synergistically to induc

64 rationale for combination clinical trials of STI571 and SCH66336 in CML patients and suggest that com

65 essing wild-type or mutant KIT, 2 compounds, STI571 and SU9529, inhibited wild-type and RT mutant KIT

66 Coadministration of STI571 and Taxol also induced the activation of procaspa

67 The therapeutic combination of STI571 and Taxol may be a powerful tool for targeting tu

68 nsitivity of CML CD34(+) progenitor cells to STI571 and the degree to which cell death was dependent

69 ine triphosphate binding-site-directed agent STI571 and the tyrphostin adaphostin are undergoing eval

70 d phosphorylation of PLSCR1 was inhibited by STI571 and was not observed in Abl-/- fibroblasts.

71 induced massive apoptosis, in comparison to STI571 and WT alone.

72 ecise mechanisms by which imatinib mesylate (STI571) and interferon alpha (IFNalpha) exhibit antileuk

73 a as a key regulator of apoptosis induced by STI571, and show that Bim is a direct transcriptional ta

74 ells was, however, incompletely inhibited by STI571, and the acquisition of the high degree of resist

75 liary ganglion (CG) lysates and neurons, and STI571 application blocked endogenous Abl tyrosine kinas

76 Further experience with the use of STI571 as a single agent or in combination with other an

77 in LAMA84 cells and K562 cells resistant to STI571, as well as in CD34(+) cells isolated from the bo

78 reatment with DLI, and then was administered STI571 at a dose of 400 mg daily.

79 The results also show that STI571 attenuates H(2)O(2)-induced loss of the mitochond

80 dicate that inhibition of c-Abl signaling by STI571 attenuates mitochondrial dysfunction and cell dea

81 Instead, the cytotoxic effects of STI571 became more pronounced with prolonged exposure, w

82 However, resistance to STI571 because of enhanced expression or mutation of the

83 eukemia (BCR/ABL) kinase inhibitor imatinib (STI571) because of mutations in the kinase domain that i

84 Using a variety of models of STI571 binding to the Abl kinase, we have performed an e

85 specific amino acid residues as critical to STI571 binding, one of which, T315, has been characteriz

86 Moreover, inhibition of c-Abl with STI571 blocked DNA damage-induced autoprocessing of casp

87 atients (67%) following their treatment with STI571 but not in the samples from patients before begin

88 ne kinase, either by mutation or by the drug STI571, can stimulate its nuclear entry.

89 In contrast, 20 microM STI571 caused rapid inhibition of bcr/abl autophosphoryl

90 erved only at 72 hours in both KBM5 and KBM5-STI571 cells as shown by annexin V staining.

91 ion and cell viability in both KBM5 and KBM5-STI571 cells.

92 viability in KBM5, but much less so in KBM5-STI571 cells.

93 mia (CML), and imatinib-resistant KBM5 (KBM5-STI571) cells were found to express high levels of survi

94 In cells expressing BCR-ABL, STI571 cooperated with 2ME2 in reducing cell growth, and

95 lular fractionation studies demonstrate that STI571 decreases H(2)O(2)-induced targeting of c-Abl to

96 that render the Abl kinase less sensitive to STI571 demonstrate a broad range of possibilities for cl

97 known substrate of c-Abl, the Abl inhibitor STI571 did not substantially affect its EGF-dependent ph

98 STI571 does not inhibit the gamma-secretase-catalyzed S3

99 These findings demonstrate that STI571 down-regulates c-Abl-mediated signals that target

100 with STI571 (Gleevec, imatinib mesylate) in STI571 drug-sensitive and -resistant cell lines.

101 ave shown that the tyrosine kinase inhibitor STI571 effectively controls BCR-ABL-positive chronic mye

102 t treatment of Bcr-Abl-expressing cells with STI571 elicits a cytoprotective MAPK activation response

103 L was generally oligoclonal, suggesting that STI571 eliminated or severely suppressed certain leukemi

104 the ABL-selective tyrosine kinase inhibitor STI571, even in advanced disease phases, which are chara

105 STI571 exemplifies the successful development of a ratio

106 STI571 failed to activate caspase cascades or to suppres

107 s from patients taken prior to and following STI571 failure suggested that expression and/or activati

108 ports describe the potential use of Gleevec (STI571) for dermatofibrosarcoma protuberans and the use

109 STI571 (formerly CGP57148B), is an ABL-specific inhibito

110 patients in the chronic phase, we evaluated STI571 (formerly known as CGP 57148B), a specific inhibi

111 onducted a phase 1, dose-escalating trial of STI571 (formerly known as CGP 57148B), a specific inhibi

112 ng reporter gene assays, we demonstrate that STI571, FoxO3a, and BCL6 can repress cyclin D2 transcrip

113 the small molecule tyrosine kinase inhibitor STI571 (Gleevec) abrogates cell growth.

114 STI571 (Gleevec), a novel anti-leukemia drug targeting B

115 been used successfully in the development of STI571 (gleevec), an inhibitor of bcr-abl tyrosine kinas

116 leukemia cells in response to treatment with STI571 (Gleevec).

117 signaling with the tyrosine kinase inhibitor STI571 (Gleevec).

118 response to imatinib mesylate [also known as STI571 (Gleevec)] therapy.

119 covered that disrupting c-Abl activity using STI571 (Gleevec, a c-Abl inhibitor) or stable c-Abl knoc

120 STI571 (Gleevec, a c-Abl tyrosine kinase inhibitor) and

121 actions between the Bcr/Abl kinase inhibitor STI571 (Gleevec, imatinib mesylate) and histone deacetyl

122 We determined the interaction of 2ME2 with STI571 (Gleevec, imatinib mesylate) in STI571 drug-sensi

123 Inhibition of BCR/ABL kinase activity by STI571 (Gleevec, imatinib mesylate) reverses drug resist

124 the KIT kinase inhibitor imatinib mesylate (STI571, Gleevec).

125 Although imatinib mesylate (STI571, Gleevec, Novartis, Basal, Switzerland) produces

126 peutic use of the recently FDA-approved drug STI571 has been successful in the treatment of Philadelp

127 inical trials, the tyrosine kinase inhibitor STI571 has proven highly effective in reducing leukemic

128 The ABL inhibitor Imatinib (Gleevec, STI571) has remarkable efficacy for treating chronic pha

129 ntly being used in clinical trials, and one, STI571, has recently been approved by the United States

130 n conclusion, Ph(+) ALL samples resistant to STI571 have a unique mutation Glu255Lys of BCR-ABL.

131 c myelogenous leukemia patients treated with STI571 have durable responses; however, most responding

132 harmacologically achievable concentration of STI571 (i.e., 1-2 microM) in resistant K562 cells expres

133 D cells or attenuation of kinase activity by STI571 (imatinib mesylate) in 32D cells transduced with

134 e oncogenes to the tyrosine kinase inhibitor STI571 (imatinib mesylate) makes it a potentially attrac

135 STI571 (imatinib mesylate), an abl tyrosine kinase inhib

136 STI571 (imatinib mesylate), an inhibitor of c-Abl, block

137 , this regimen potently induced apoptosis in STI571 (imatinib mesylate)-resistant K562 cells and CD34

138 , including those sensitive and resistant to STI571 (imatinib mesylate).

139 The systemic administration of STI571 (imatinib mesylate, Gleevec), an inhibitor of pho

140 harmaceutical inhibitor of the c-Abl kinase, STI571 (imatinib), reduced serovar Typhimurium invasion

141 Therefore, inhibition of Abl by STI571 [imatinib (Gleevec)] treatment or down-regulation

142 Abl-deficient mice and the antileukemia drug STI571 [imatinib mesylate (Gleevec); Novartis], which po

143 Imatinib mesylate (STI571, imatinib) inhibited DNA synthesis in primary hum

144 d the effects of the PDGF receptor inhibitor STI571 in 2 different animal models of pulmonary hyperte

145 Cells exposed to STI571 in combination with PD184352 for 48 h demonstrate

146 lls (i.e., LAMA 84), and in cells exposed to STI571 in combination with the HDI sodium butyrate.

147 tions for the design of future studies using STI571 in leukemias involving ABL-encoded fusion protein

148 Lastly, the potential use of STI571 in other malignancies and the translation of this

149 n GIST and suggest therapeutic potential for STI571 in patients afflicted by this chemoresistant tumo

150 The efficacy of STI571 in reducing Abeta without affecting Notch-1 cleav

151 erapy were discovered after the inclusion of STI571 in the therapy regimen.

152 Despite the well established role of STI571 in the treatment of chronic myelogenous leukemia,

153 mors retain sensitivity to the ABL inhibitor STI571 in vitro and in vivo.

154 another PDGFR inhibitor, imatinib (Gleevec, STI571), in VSMCs indicated that BMS-354825 is 67-fold m

155 nses in vivo, such in vitro insensitivity to STI571, in combination with its demonstrated antiprolife

156 osed the expected side activities for Glivec/STI571, including cellular inhibition of c-kit and plate

157 Moreover, SCH66336 enhances STI571-induced apoptosis in STI571-sensitive cells and,

158 d Ba/F3 cells with IL-3 completely prevented STI571-induced apoptosis in these cells, similar to what

159 riptional target of FoxO3a that mediates the STI571-induced apoptosis.

160 RhoA downstream effector Rho kinase reverses STI571-induced dendritic simplification, demonstrating t

161 Thus, STI571 induces an accumulation of FoxO3a activity which

162 e newly introduced tyrosine kinase inhibitor STI571 induces complete hematologic remission in almost

163 Our data indicate that STI571 induces phosphorylation of the p38 and activation

164 t not PDGF-R, whereas oral administration of STI571 inhibited the phosphorylation of PDGF-R but not E

165 STI571 inhibited tyrosine phosphorylation and cell growt

166 The results further show that STI571 inhibits ara-C-induced loss of mitochondrial tran

167 The tyrosine kinase inhibitor STI571 inhibits BCR/ABL and induces hematologic remissio

168 In concert with these effects, STI571 inhibits the death response to H(2)O(2) exposure

169 Gleevec (STI571) inhibits the Abl kinase and has shown great util

170 The major mechanism of action of STI571 is a competitive interference with the ATP-bindin

171 The tyrosine kinase inhibitor STI571 is a promising agent for the treatment of advance

172 The ABL tyrosine kinase inhibitor STI571 is a promising agent for treatment of advanced Ph

173 STI571 is a small molecule inhibitor with activity again

174 Since STI571 is active against A-MuLV-transformed cells in vit

175 l of this specifically targeted therapy, and STI571 is emerging as an important new therapeutic agent

176 Furthermore, although the primary effect of STI571 is via direct inhibition of BCR-ABL, STI571 addit

177 STI571 is well tolerated and has significant antileukemi

178 The BCR-ABL tyrosine kinase inhibitor STI571 is well tolerated and has substantial activity in

179 Imatinib mesylate (Gleevec, STI571) is a kinase inhibitor selective for Bcr-Abl, act

180 Imatinib mesylate (STI571) is a promising new treatment for chronic myeloge

181 Imatinib (Glivec, formerly STI571) is a rationally developed, orally administered i

182 Imatinib (formerly STI571) is a rationally developed, orally administered i

183 Imatinib mesylate (STI571) is a specific inhibitor of BCR-ABL tyrosine kina

184 Imatinib mesylate (Gleevec, formerly STI571) is an effective therapy for all stages of chroni

185 Imatinib mesylate (STI571) is effective in chronic phase chronic myelogenou

186 Imatinib mesylate, formerly STI571, is a selective inhibitor of this kinase.

187 otected K562 cells from apoptosis induced by STI571, it did not protect cells from apoptosis induced

188 resistance, K562 cells resistant to 5 microM STI571 (K562-R) were cloned and compared to the parental

189 In the most sensitive cases, STI571 killed almost all dividing cells; however, a sign

190 found that the inhibition of Abl kinases by STI571 leads to a remarkable simplification of dendritic

191 In conclusion, combination of STI571+WT or STI571+LY may represent a novel approach against the Ph(

192 Moreover, the combinations of STI571+WT or STI571+LY were effective in the inhibition of clonogenic

193 These results suggest that STI571 may be an effective targeted therapy in patients

194 K1/2 inhibitor PD184352 (5 microM) prevented STI571-mediated activation of p42/44 MAPK.

195 K1/2 construct significantly attenuated SAHA/STI571-mediated apoptosis in K562 cells, implicating dis

196 FoxO3a in Bcr-Abl-expressing cells abolishes STI571-mediated Bim induction and apoptosis.

197 d BCL6 in BCR-ABL-expressing cells abolishes STI571-mediated effects on cyclin D2.

198 from STI571-treated animals, consistent with STI571-mediated inhibition of the Bcr/Abl tyrosine kinas

199 Synergistic potentiation of STI571-mediated lethality by PD184352 was associated wit

200 neoplastic cell and our results suggest that STI571 might be useful in the treatment of neoplasms com

201 on, treatment was commenced immediately with STI571 monotherapy, resulting in considerable initial im

202 kinase inhibitor imatinib mesylate (Gleevec, STI571; Novartis, Basel, Switzerland) has shown remarkab

203 e fibroblasts, indicating that the effect of STI571 on Abeta production does not involve Abl kinase.

204 The effects of STI571 on Ba/F3 cells transformed with BCR/ABL, TEL/ABL,

205 ant role in the generation of the effects of STI571 on BCR-ABL-expressing cells.

206 38 reverses the growth inhibitory effects of STI571 on primary leukemic colony-forming unit granulocy

207 stance to the ABL kinase inhibitor imatinib (STI571 or Gleevec) in chronic myeloid leukemia (CML) occ

208 e specific inhibitor imatinib (also known as STI571 or Gleevec).

209 py with either the tyrosine kinase inhibitor STI571 or placebo.

210 Imatinib mesylate (Gleevec, STI571, or CP57148B) is a direct inhibitor of ABL (ABL1)

211 cell treatment with the Abl kinase inhibitor STI571, or in Abl-/- mouse fibroblasts, suggesting that

212 ment of cells with the Abl kinase inhibitor, STI571, or silencing c-Abl and Arg expression with RNA i

213 Finally, because STI571 potently inhibits Abl kinase activity, the autono

214 caused very little cell death inhibition in STI571-pretreated cells and in Abl shRNA-expressing cell

215 n from individuals who did not to respond to STI571 (primary resistance).

216 umor growth, its combination with AEE788 and STI571 produced >80% inhibition of tumor growth and prol

217 In the resistant KBM5-STI571(R1.0) cells, 20% of the BCR/ABL transcripts and 1

218 ase in the tumor absorbed radiation doses in STI571 + radioimmunotherapy-treated mice compared with P

219 primary reason for the growth arrest of the STI571 + radioimmunotherapy-treated tumors.

220 crystallization studies of Abl kinase and an STI571-related compound identify specific amino acid res

221 STI571-sensitive cells and, in patients with STI571 resistance from gene amplification, cooperates wi

222 This review will highlight mechanisms of STI571 resistance in clinical samples as well as preclin

223 ted contact points are capable of conferring STI571 resistance in relapsed patients.

224 ogether, these results suggest that acquired STI571 resistance may be associated with BCR-ABL indepen

225 model may be a useful tool for the study of STI571 resistance, CML progression, and the anti-CML imm

226 o investigate possible mediators of acquired STI571 resistance, K562 cells resistant to 5 microM STI5

227 on therapy may be effective in patients with STI571 resistance.

228 6 (lonafarnib) inhibits the proliferation of STI571-resistant BCR-ABL-positive cell lines and hematop

229 CML-selective agent that retains activity in STI571-resistant cell lines.

230 rated with 2ME2 in reducing cell growth, and STI571-resistant cells were sensitive to 2ME2 treatment.

231 The mutation was present in all 10 STI571-resistant clones derived from low density clonoge

232 role for CDK6 inhibitors in the treatment of STI571-resistant CML or ALL.

233 nonuclear cells obtained from a patient with STI571-resistant disease, as well as in Bcr/Abl- leukemi

234 acted synergistically to induce apoptosis in STI571-resistant K562 and LAMA 84 cells that display inc

235 Additional experiments revealed that STI571-resistant K562 cells remained sensitive to adapho

236 y formation from peripheral blood samples of STI571-resistant patients with CML.

237 The contribution of this mutation to STI571-resistant phenotype remains unknown.

238 The emergence of the STI571-resistant phenotype was accompanied by only a mar

239 Inhibition of BCR/ABL tyrosine kinase with STI571 restores Lyn responsiveness to SDF-1 signaling.

240 the predicted contact points between Abl and STI571 result in a kinase-inactive protein, additional m

241 xposure of cells to HDIs in conjunction with STI571 resulted in multiple perturbations in signaling a

242 rived BCR-ABL-expressing leukemia cells with STI571 results in activation of the p38 mitogen-activate

243 Inhibition of BCR-ABL by STI571 results in down-regulation of cyclin D2 expressio

244 Inhibition of Bcr-Abl kinase by STI571 results in FoxO3a activation, induction of Bim ex

245 ith the small molecule Abl kinase inhibitor (STI571) results in their differentiation to a late pre-B

246 ulmonary vascular disease, administration of STI571 reversed pulmonary vascular changes.

247 ls who were classified as good responders to STI571 (sensitive), and seven from individuals who did n

248 lase inhibitors (HDIs) have been examined in STI571-sensitive and -resistant Bcr/Abl(+) human leukemi

249 CH66336 enhances STI571-induced apoptosis in STI571-sensitive cells and, in patients with STI571 resi

250 at the restoration of C/EBPalpha activity in STI571-sensitive or -resistant 32D-BCR/ABL cells induced

251 in 4 of 10 and in 6 of 7 mice injected with STI571-sensitive or -resistant 32D-BCR/ABL cells, respec

252 On this basis, all the STI571-sensitive samples could clearly be distinguished

253 In concert with these effects of STI571, similar findings were obtained in c-Abl-deficien

254 Treatment of NCI-H69 cells with STI571 specifically inhibited the c-Kit signaling events

255 With similar potency, STI571 specifically reduced whole-cell current responses

256 was inhibitable by in vitro incubation with STI571, suggesting that BCR-ABL was not coupled to proli

257 prevent the induction of CCL9 expression by STI571, suggesting that C/EBPalpha is involved in mainta

258 Sensitivity to the Abl inhibitor STI571 suggests differential utilization of the p53 and

259 Exposure of K562 cells to concentrations of STI571 that minimally induced apoptosis (e.g., approxima

260 selectively inhibiting PDGF-R signaling with STI571, the cells are rendered sensitive to Taxol treatm

261 ic fusion oncogene are efficiently killed by STI571, the patient was started on STI571.

262 atients with advanced CML that progressed on STI571 therapy also were analyzed for LYN kinase express

263 However, disease progression while on STI571 therapy has been reported, suggesting de novo or

264 some Bcr/Abl(+) cells that are resistant to STI571 through increased Bcr/Abl expression.

265 ar results were obtained after administering STI571 to a primary GIST cell culture that expressed a c

266 The addition of STI571 to cultures of bone endothelial cells blocked PDG

267 bitor PD0332991 can act synergistically with STI571 to enhance leukemic cell death, suggesting a pote

268 nce from gene amplification, cooperates with STI571 to induce apoptosis.

269 Clinical trials demonstrated the ability of STI571 to induce remissions in patients with chronic pha

270 ridization of polysomal RNA of untreated and STI571-treated 32D-BCR/ABL cells, we identified the beta

271 In some STI571-treated animals Bcr/Abl messenger RNA and protein

272 STAT5, Shc, and Crk-L in leukemic cells from STI571-treated animals, consistent with STI571-mediated

273 kemia of placebo-treated animals, 80% of the STI571-treated mice were alive on day 74, with marked im

274 None of the STI571-treated mice were cured of the CML-like myeloprol

275 polyclonal leukemia of placebo-treated mice, STI571-treated murine CML was generally oligoclonal, sug

276 ke myeloproliferative disorder, however, and STI571-treated murine CML was transplanted to secondary

277 STI571 treatment also decreased pericyte coverage on tum

278 50, greater than 20 microM), whereas 24-hour STI571 treatment had no effect on CML or normal CFU-G.

279 Similarly, STI571 treatment of Meg-01 cells, a P210(BCR-ABL)-expres

280 17 samples were obtained before STI571 treatment was started: ten from individuals who w

281 6A c-Myb led to enhanced proliferation after STI571 treatment.

282 32D-BCR/ABL cells and reinduced by imatinib (STI571) via a mechanism that appears to depend on expres

283 STI571 was administered orally to 83 patients with CML i

284 STI571 was recently combined with the standard cytostati

285 r absence of growth factors, the response to STI571 was variable.

286 ven that PDGFRbeta signaling is inhibited by STI571, we found that SV7tert human angiomyolipoma cells

287 e, production of Abeta and its inhibition by STI571 were demonstrated to occur to similar extents in

288 ore advanced stages of disease, responses to STI571 were less common and often transient.

289 Adverse effects of STI571 were minimal; the most common were nausea, myalgi

290 ed by imatinib mesylate (Gleevec, previously STI571) whereas D816V and D816H were both resistant to i

291 ase inhibitor imatinib mesylate (Gleevec, or STI571), which targets the ATP-binding site of Abl and s

292 ctivity or presence of the BCR-ABL inhibitor STI571, which also inhibits c-kit.

293 ced by the Bcr-abl tyrosine kinase inhibitor STI571, which was accompanied by caspase-dependent cleav

294 Combination therapy using oral PKI166 and STI571 with i.p. injections of paclitaxel induced a high

295 The interaction of STI571 with the stromal PDGFr-beta reduced tumor interst

296 r the treatment revealed that combination of STI571+WT caused a more pronounced activation of caspase

297 We showed that STI571+WT exerted a synergistic effect against the Ph(1)

298 In conclusion, combination of STI571+WT or STI571+LY may represent a novel approach ag

299 Moreover, the combinations of STI571+WT or STI571+LY were effective in the inhibition

300 ormal bone marrow cells after treatment with STI571+WT were selectively depleted of BCR/ABL-positive