ライフサイエンスコーパス: imatinib mesylate

1 (TKIs) may select for resistant clones (ie, imatinib mesylate).

2 ing those sensitive and resistant to STI571 (imatinib mesylate).

3 e activation loop mutants are insensitive to imatinib mesylate.

4 ing enhances targeting of CML progenitors by imatinib mesylate.

5 RECIST in assessing the response of GISTs to imatinib mesylate.

6 rongly inhibited by the Abl kinase inhibitor imatinib mesylate.

7 107-resistant mutants were also resistant to imatinib mesylate.

8 isorders, predicting a favorable response to imatinib mesylate.

9 d better defined the results of therapy with imatinib mesylate.

10 ent of chronic myelogenous leukemia (CML) by imatinib mesylate.

11 re sensitive to PKC412 despite resistance to imatinib mesylate.

12 rticipants from a clinical trial of adjuvant imatinib mesylate.

13 Administration of hydroxyurea and imatinib mesylate.

14 ; the gene products of both are inhibited by imatinib mesylate.

15 ssion of ABCG2 does not confer resistance to imatinib mesylate.

16 e to the targeted molecular therapeutic drug imatinib mesylate.

17 ession and protected cells from lethality of imatinib mesylate.

18 tration range found in patients treated with imatinib mesylate.

19 s inhibited by the tyrosine kinase inhibitor imatinib mesylate.

20 osis in association with the decision to use imatinib mesylate.

21 e of biologically targeted therapies such as imatinib mesylate.

22 spond to the tyrosine kinase inhibitor (TKI) imatinib mesylate.

23 pathway is targeted by the antifibrotic drug imatinib mesylate.

24 uding mutants resistant to the Kit inhibitor imatinib-mesylate.

25 The Bcr-Abl kinase inhibitor imatinib mesylate (1 microM) and two Jak2 kinase inhibit

26 nty different mutations were identified with imatinib mesylate, 10 with nilotinib (including only 1 n

27 Mice were treated with imatinib mesylate (100 mg/kg three times weekly) or with

28 feron-alpha (IFN-alpha) failure treated with imatinib mesylate 400 mg daily.

29 activity and tolerability of an oral dose of imatinib mesylate 400 mg twice daily in patients with re

30 Imatinib mesylate, 400 mg orally twice daily.

31 This in turn led to the development of imatinib mesylate, a clinically successful inhibitor of

32 The clinical application of imatinib mesylate, a selective inhibitor of the KIT kina

33 GISTs can be successfully treated with imatinib mesylate, a selective small-molecule protein ki

34 Imatinib mesylate, a small-molecule inhibitor against se

35 Targeting these activated proteins with imatinib mesylate, a small-molecule kinase inhibitor, ha

36 Imatinib mesylate, a specific Bcr-Abl tyrosine kinase in

37 enesis of this tumor, and the development of imatinib mesylate, a specific inhibitor of KIT tyrosine

38 Imatinib mesylate, a tyrosine kinase inhibitor, has revo

39 hat inhibition of BCR-ABL kinase activity by imatinib mesylate abrogates such activation.

40 chronic myeloid leukemia (CML) treated with imatinib mesylate achieve a complete cytogenetic respons

41 roximately 85% of GIST patients treated with imatinib mesylate achieve disease stabilization, however

42 Imatinib mesylate administered orally twice daily for AI

43 e c-Kit oncogene and a favorable response to imatinib mesylate [also known as STI571 (Gleevec)] thera

44 Inhibition of c-abl activity with imatinib mesylate ameliorates experimental renal fibrosi

45 hase II study to evaluate the combination of imatinib mesylate, an adenosine triphosphate mimetic, ty

46 igen, and lead to appropriate treatment with imatinib mesylate, an inhibitor of the KIT tyrosine kina

47 ete cytogenetic response rates were 87% with imatinib mesylate and 28% with interferon-alpha (P < .00

48 stimated 3-year survival rates were 96% with imatinib mesylate and 81% with interferon-alpha (P < .01

49 The PDGF receptor tyrosine kinase inhibitor imatinib mesylate and a monoclonal antibody against PDGF

50 The kinase inhibitors imatinib mesylate and dasatinib are the preferred treatm

51 t activation-loop mutants are insensitive to imatinib mesylate and have been largely resistant to tar

52 ding to the resistance to inhibitors such as imatinib mesylate and malignant progression of the disea

53 Imatinib mesylate and new TKIs along with allogeneic ste

54 ) with the tyrosine kinase inhibitors (TKIs) imatinib mesylate and nilotinib represents a successful

55 -Abl or Bcr-Abl in cells or cell extracts by imatinib mesylate and other Bcr-Abl targeted kinase inhi

56 tment of chronic myeloid leukemia (CML) with imatinib mesylate and other second- and/or third-generat

57 Imatinib mesylate and other tyrosine kinase inhibitors (

58 Emergence of imatinib mesylate and other, second-generation tyrosine

59 In silico profiling of Imatinib mesylate and PD-173955 kinase inhibitors with p

60 provide insights into the modes of action of imatinib mesylate and rapamycin in treatment of CML.

61 crucial for TGFbeta-induced EndoMT and that imatinib mesylate and rottlerin or similar kinase inhibi

62 The inhibitory effects of imatinib mesylate and rottlerin were mediated by inhibit

63 The efficacy of the inhibitors imatinib mesylate and sunitinib malate in GIST patients

64 ondrial dysfunction and apoptosis induced by imatinib mesylate and the topoisomerase inhibitor VP-16

65 reas the second slope of -0.0057 +/- 0.0038 (imatinib mesylate) and -0.0019 +/- 0.0013 (nilotinib) pe

66 mework, the first slope of -0.052 +/- 0.018 (imatinib mesylate) and -0.042 +/- 0.015 (nilotinib) per

67 tworks, differential sensitivity to the drug imatinib mesylate, and differential self-renewal capacit

68 o the PDGF receptor (PDGFR)/c-kit inhibitor, imatinib mesylate, and investigated the effect of this t

69 Pretreatment with specific c-Abl inhibitor, imatinib mesylate, and knock down of c-Abl significantly

70 f Bcl-2 protected K562 and LAMA84 cells from imatinib mesylate- and PP2-mediated lethality.

71 rthermore, accumulation and efflux of [(14)C]imatinib mesylate are unaltered between ABCG2-expressing

72 challenges raised by clinical resistance to imatinib mesylate as a paradigm for how resistance might

73 To investigate the potential of imatinib mesylate as a therapy for melanoma, we studied

74 Patients were treated with daily oral imatinib mesylate at 220 mg/m(2) twice a day for childre

75 idney disease and NSF were treated with oral imatinib mesylate at a dosage of 400 mg/day.

76 tients with newly diagnosed CML treated with imatinib mesylate at our institution (2000-2004) to 650

77 We found that pretreatment of CML cells with imatinib mesylate augments the antigrowth effects of IFN

78 Imatinib mesylate blocked activation of the Smad1 pathwa

79 Our data demonstrated that imatinib mesylate blocked both PDGFR-alpha and PDGFR-bet

80 rsed by SB431542 and by the c-Abl inhibitor, imatinib mesylate, but not by the p38 map kinase inhibit

81 phase 2 trial to test whether treatment with imatinib mesylate can decrease the volume burden of clin

82 We have therefore examined whether imatinib mesylate can delay relapse and postpone the req

83 Resistance to imatinib mesylate can occur in chronic myelogenous leuke

84 Imatinib mesylate clearance was decreased at day 28 comp

85 C1 inhibitor everolimus and PDGFRA inhibitor imatinib mesylate confirmed that this drug combination c

86 ffectiveness of small molecule drugs such as imatinib mesylate could be due to the inhibitor's abilit

87 Imatinib mesylate could be used to treat plexiform neuro

88 patients resistant to BCR-ABL suppression by Imatinib mesylate coupled with the crystallographic stru

89 Imatinib mesylate currently provides excellent hematolog

90 es of KD mutants emerging in the presence of imatinib mesylate, dasatinib, and nilotinib, alone and i

91 Interestingly, imatinib mesylate did not inhibit expression of T-cell a

92 together, our data demonstrate that IFNs and imatinib mesylate differentially regulate PI 3' kinase/m

93 son (c-Abl), and c-Abl inhibitors, including imatinib mesylate, diminishing the fibrogenic effects of

94 The imatinib mesylate dose was 500 mg twice a day for patien

95 In mice treated with imatinib mesylate, DTH was reduced in comparison to sham

96 f Abl expression or Abl kinase activity with imatinib mesylate enhanced HNSCC matrix degradation and

97 Moreover, imatinib mesylate enhanced rat cardiac allograft vasculo

98 is-inducing factor release) and apoptosis by imatinib mesylate exhibited a pronounced reduction in ex

99 Concurrent EIAED use lowered imatinib mesylate exposure.

100 as also done for those patients able to take imatinib mesylate for 6 months.

101 Of the 23 patients who received imatinib mesylate for at least 6 months, six (26%, 95% C

102 n improved in the patient who resumed taking imatinib mesylate for longer than 2 weeks.

103 on that the Smad1/CCN2 pathway is blocked by imatinib mesylate further clarifies the mechanism of the

104 Imatinib mesylate (Gleevec) is a small-molecule inhibito

105 Imatinib mesylate (Gleevec) is effective therapy against

106 Although the ABL kinase inhibitor imatinib mesylate (Gleevec) provides highly effective tr

107 ent with the small molecule kinase inhibitor imatinib mesylate (Gleevec), complete remissions are rar

108 he discovery of the BCR-ABL kinase inhibitor imatinib mesylate (Gleevec), thus showing how a molecula

109 not by a neutralizing antibody to PDGF or by imatinib mesylate (Gleevec).

110 lines treated with the targeted therapeutic imatinib mesylate (Gleevec).

111 mors (GIST) can be successfully treated with imatinib mesylate (Gleevec); however, complete remission

112 cient mice and the antileukemia drug STI571 [imatinib mesylate (Gleevec); Novartis], which potently a

113 uccess of the Kit tyrosine kinase inhibitor, imatinib mesylate (Gleevec, formerly STI-571), has caugh

114 Imatinib mesylate (Gleevec, STI-571) is an inhibitor of

115 Imatinib mesylate (Gleevec, STI571), a Bcr-Abl kinase in

116 Imatinib mesylate (Gleevec, STI571), a selective inhibit

117 Imatinib mesylate (Gleevec, STI571, or CP57148B) is a di

118 teins, which serve as therapeutic targets of imatinib mesylate (Gleevec; Novartis, Basel, Switzerland

119 The systemic administration of STI571 (imatinib mesylate, Gleevec), an inhibitor of phosphoryla

120 ges treated with the selective Abl inhibitor imatinib mesylate had a reduced capability to migrate in

121 Imatinib mesylate has also been shown to inhibit KIT, AR

122 eson protein tyrosine (Abl) kinase inhibitor imatinib mesylate has become a critical issue for patien

123 Imatinib mesylate has been shown to effectively block co

124 17F would achieve similar disease control as imatinib mesylate has produced in chronic myeloid leukem

125 The introduction of imatinib mesylate has started the era of molecular thera

126 ino-pyrimidine class of TKIs, exemplified by imatinib mesylate, has not been examined.

127 Kit/Pdgfra inhibitors such as imatinib mesylate have increased progression-free surviv

128 Inhibitors of Bcr-abl such as imatinib mesylate have replaced the cytokine IFNalpha as

129 The successes and limitations of Imatinib mesylate hold general lessons for the developme

130 -Abl-transduced Ba/F3 cells (IC(50) = 14 nM; imatinib mesylate IC(50) = 350 nM).

131 astocytosis, and seminoma are insensitive to imatinib mesylate (IC50 > 5-10 micromol/L), and acquired

132 ase inhibitor, exhibits greater potency than imatinib mesylate (IM) and inhibits the majority of kina

133 ogenous leukemia (CML) patients treated with imatinib mesylate (IM) become drug resistant by mutation

134 Imatinib mesylate (IM) binds to the BCR-ABL protein, inh

135 e chronic myeloid leukemia were treated with imatinib mesylate (IM) for 6 to 12 months to establish d

136 AMN107 was more potent than imatinib mesylate (IM) in inhibiting Bcr-Abl tyrosine ki

137 Previous studies demonstrated that imatinib mesylate (IM) induces autophagy in chronic myel

138 Imatinib mesylate (IM) is effective at inducing complete

139 Imatinib mesylate (IM) therapy for chronic myeloid leuke

140 ence supposedly contribute to the failure of imatinib mesylate (IM) to eradicate chronic myeloid leuk

141 The impact of imatinib mesylate (IM) treatment for chronic myeloid leu

142 L stem cell survival and self-renewal during imatinib mesylate (IM) treatment.

143 ctivity and nuclear import were increased by imatinib mesylate (IM), a selective ABL inhibitor, but p

144 leukemia cells, including those resistant to imatinib mesylate (IM), particularly those with the T315

145 Despite excellent responses to imatinib mesylate (IM), patients are relapsing.

146 In the imatinib mesylate (IM)-refractory leukemia cells express

147 ed in Bcr/Abl(+) leukemia cells resistant to imatinib mesylate (IM).

148 ls overexpress BcrAbl and are insensitive to imatinib mesylate (IM).

149 se domain play a major role in resistance to imatinib mesylate (IM).

150 Imatinib mesylate (IM, Gleevec) has largely supplanted a

151 sine kinase (ABL1) kinase inhibitors such as imatinib mesylate (imatinib) are effective in managing c

152 Imatinib mesylate (imatinib) is a tyrosine kinase inhibi

153 gion/ABL (BCR/ABL) tyrosine kinase inhibitor imatinib mesylate (imatinib) is highly effective in indu

154 Imatinib mesylate (imatinib) is highly effective in the

155 Adjuvant therapy with imatinib mesylate improves recurrence-free survival rate

156 ffect in vivo, PD166326 was also superior to imatinib mesylate in inhibiting the constitutive tyrosin

157 ous report of a randomized phase II trial of imatinib mesylate in patients with incurable GIST detail

158 act-a phase 2 study demonstrated efficacy of imatinib mesylate in patients with metastatic GIST harbo

159 nhibition was quantitatively as effective as imatinib mesylate in suppressing cell growth and inducin

160 Despite the success of imatinib mesylate in the treatment of CML, resistance is

161 e trial, 1- and 3-year durations of adjuvant imatinib mesylate in the treatment of patients with gast

162 explored the effects of KIT inhibition using imatinib mesylate in this molecular subset of disease.

163 r, these data suggest a possible utility for imatinib mesylate in treating smallpox or MPX infections

164 ts with rapamycin and the Bcr-Abl inhibitor, imatinib mesylate, in Bcr-Abl-expressing cell lines and

165 nts were randomized to 1 of 2 dose levels of imatinib mesylate, including 400 mg once daily (400 mg/d

166 rsist in most patients with CML treated with imatinib mesylate, indicating the need for novel therape

167 ent of animals with the ABL kinase inhibitor imatinib mesylate induced specific modulation of blasts

168 ide-dependent kinase-1 (PDK-1) inhibitor, on imatinib mesylate-induced apoptosis in 2 clinically rele

169 therapy, whereas IL-33 counteracts in vitro imatinib mesylate-induced growth arrest in CML CD34(+) p

170 tudies have shown that the BCR-ABL inhibitor imatinib mesylate induces both apoptosis and autophagy,

171 The BCR-ABL kinase inhibitor imatinib mesylate induces complete cytogenetic response

172 Imatinib mesylate inhibited Pdgfr-beta activation and Ac

173 ng that, similarly to in vitro observations, imatinib mesylate inhibited T-cell response, but did not

174 In these cells, PKC412, but not imatinib mesylate, inhibited autophosphorylation of c-KI

175 Imatinib mesylate inhibits several tyrosine kinases, inc

176 These results suggest that imatinib mesylate inhibits the function of ABCG2 but is

177 After imatinib mesylate initiation, metabolic response by (18)

178 rmed at baseline, 1-7 d, and 4 or 8 wk after imatinib mesylate initiation.

179 atients with PMR, and the biologic action of imatinib mesylate interacts with glycolysis and GLUT4 ex

180 urrent data evaluating the relative roles of imatinib mesylate, interferon-alpha, and allogeneic bloo

181 that the targeted tyrosine kinase inhibitor imatinib mesylate is a dramatically effective agent, but

182 The small-molecule tyrosine kinase inhibitor imatinib mesylate is a potent inhibitor of wild-type (WT

183 Imatinib mesylate is a small molecule drug that in vitro

184 Imatinib mesylate is a small molecule that inhibits acti

185 Imatinib mesylate is a tyrosine kinase inhibitor that wa

186 Resistance to imatinib mesylate is an emerging problem in the treatmen

187 Furthermore, we show that imatinib mesylate is effective in a mouse model of infec

188 However, resistance to imatinib mesylate is emerging as a major clinical proble

189 Imatinib mesylate is highly effective in newly diagnosed

190 The BCR/ABL tyrosine kinase inhibitor imatinib mesylate is highly effective in the treatment o

191 Imatinib mesylate is standard treatment for patients who

192 omal tumor (GIST) and treated long-term with imatinib mesylate is unknown.

193 Treatment with imatinib mesylate led to accumulation of the cells in G0

194 Treatment of mice with the c-KIT inhibitor imatinib mesylate limited effusion precipitation by mous

195 Furthermore, the BCR/ABL kinase inhibitor imatinib mesylate markedly inhibited proliferation of BC

196 The KIT tyrosine kinase inhibitor imatinib mesylate markedly prolongs the survival of pati

197 ; range, 1.3-53.2), decreasing after 1 wk of imatinib mesylate (mean, 5.5; range, -0.5-47.7, P < 0.00

198 w-up of 13 months after CCR (29 months after imatinib mesylate; median 6 RQ-PCR assays), 23 patients

199 e that long-term administration of high-dose imatinib mesylate might affect immunity.

200 The clinical applications of imatinib mesylate might thus be expanded with its use as

201 may impede the antiproliferative effects of imatinib mesylate on CD34(+) progenitors in CML.

202 study, we have investigated the influence of imatinib mesylate on CD4(+)CD25(+)FoxP3(+) regulatory T

203 of the suppressive effects of nilotinib and imatinib mesylate on leukemic progenitor colony formatio

204 apamycin enhanced the suppressive effects of imatinib mesylate on primary leukemic granulocyte macrop

205 We examined the effects of IFNs or imatinib mesylate on signaling pathways regulating initi

206 rowth factor receptor (PDGFR)-beta inhibitor imatinib mesylate on tissue repair.

207 togenetic response category was similar with imatinib mesylate or interferon-alpha, suggesting that t

208 ggests limited treatment success with either imatinib mesylate or other anti-KIT D816V kinase inhibit

209 Additionally, the near universal exposure to imatinib mesylate or other kinase inhibitors before tran

210 h either the c-Abl tyrosine kinase inhibitor imatinib mesylate or the protein kinase Cdelta (PKCdelta

211 atment of PDGF-BB-overexpressing tumors with imatinib mesylate (PDGFR inhibitor) resulted in increase

212 Imatinib mesylate plus hydroxyurea is well tolerated and

213 Here, we show that imatinib mesylate potently reverses ABCG2-mediated resis

214 Inhibition of the c-abl kinase with imatinib mesylate prevents increased proliferation after

215 Adjuvant imatinib mesylate prolongs recurrence-free survival (RFS

216 phosphate (ATP)-competitive kinase inhibitor imatinib mesylate prompted us to characterize 14 c-KIT m

217 derived growth factor receptor with Gleevec (imatinib mesylate) reduced overall contractile ability a

218 The potency of AP23464 against imatinib mesylate-refractory Bcr-Abl and its distinct bi

219 hronic myeloid leukemia (CML) often manifest imatinib mesylate resistance associated with point mutat

220 vation loop mutations can be associated with imatinib mesylate resistance in GIST.

221 ide a novel therapeutic strategy to overcome imatinib mesylate resistance, especially with the Abl mu

222 t leukemic cells exhibiting various forms of imatinib mesylate resistance, including Bcr/Abl overexpr

223 pathophysiologies of disease progression and imatinib mesylate resistance, leading to the development

224 role for this pathway in CML maintenance and imatinib mesylate resistance.

225 84) displaying a Bcr/Abl-independent form of imatinib mesylate resistance.

226 te Abl inhibitors with activity against many imatinib mesylate-resistant BCR-ABL kinase domain (KD) m

227 ies of AP23464 extend to frequently observed imatinib mesylate-resistant Bcr-Abl mutants, including n

228 oM), sorafenib potently induced apoptosis in imatinib mesylate-resistant cells expressing high levels

229 326 also prolonged the survival of mice with imatinib mesylate-resistant CML induced by the Bcr/Abl m

230 ctive drugs for the treatment of de novo and imatinib mesylate-resistant CML.

231 or c-KIT-positive malignancies harboring the imatinib mesylate-resistant D816V or D816Y activation mu

232 malignancies, particularly in the setting of imatinib mesylate-resistant disease.

233 Parallel studies were performed in imatinib mesylate-resistant LAMA84 cells exhibiting redu

234 The imatinib mesylate-resistant mutant TEL-PDGFRbeta T681I w

235 The mutations included 6 known imatinib mesylate-resistant mutations, including T315I,

236 Therapy with imatinib mesylate resulted in a dramatic improvement in

237 sure of chick embryos to the PDGFR inhibitor imatinib mesylate resulted in spina bifida in the absenc

238 ma harboring KIT alterations, treatment with imatinib mesylate results in significant clinical respon

239 Treatment with the tyrosine kinase inhibitor imatinib mesylate reversed the adhesion deficient phenot

240 was unknown, and recent clinical trials with imatinib mesylate showed limited success due to normal t

241 Furthermore, imatinib mesylate significantly enhanced antitumor immun

242 Imatinib mesylate, similar to many other tyrosine kinase

243 rc family tyrosine kinases and is blocked by imatinib mesylate (STI-571; Gleevec), an Abl family kina

244 The precise mechanisms by which imatinib mesylate (STI571) and interferon alpha (IFNalph

245 Imatinib mesylate (STI571) is effective in chronic phase

246 Imatinib mesylate (STI571), a specific inhibitor of the

247 l to treatment with the KIT kinase inhibitor imatinib mesylate (STI571, Gleevec).

248 Imatinib mesylate (STI571, imatinib) inhibited DNA synth

249 In contrast to the effects of IFNs, imatinib mesylate suppressed p70 S6 kinase activity, con

250 nts with advanced GIST who were treated with imatinib mesylate survived for more than 5 years, regard

251 f highly efficacious therapeutics that, like imatinib mesylate, target the oncogenic kinase activity

252 Imatinib mesylate targets mutated KIT oncoproteins in ga

253 Additionally, imatinib mesylate that inhibits release of VEGF induces

254 lso able to survive higher concentrations of imatinib mesylate, the Bcr/Abl tyrosine kinase inhibitor

255 in changes recurred after discontinuation of imatinib mesylate, the duration for which treatment may

256 mia (CML) occurred after the introduction of imatinib mesylate, the first tyrosine kinase inhibitor (

257 Within weeks of stopping imatinib mesylate, the skin changes recurred in each pat

258 nd new issues have arisen as the benefits of imatinib mesylate therapy are revealed.

259 l stromal tumor, GLUT4 levels decrease after imatinib mesylate therapy in most patients with PMR, and

260 By multivariate analysis, imatinib mesylate therapy was identified as an independe

261 , ST2 overexpression is normalized following imatinib mesylate therapy, whereas IL-33 counteracts in

262 Thus, (18)F-FDG PET is a better guide for imatinib mesylate therapy.

263 arable in staging GISTs before initiation of imatinib mesylate therapy.

264 estinal stromal tumor undergoing neoadjuvant imatinib mesylate therapy.

265 cells to the residual apoptotic activity of imatinib mesylate, thereby overcoming the resistance.

266 llustrated by the successful introduction of imatinib mesylate, these new treatments will interfere w

267 with targeted KIT/PDGFRA inhibitors such as imatinib mesylate, these treatments are rarely curative.

268 When T cells were washed free of imatinib mesylate, they proliferated in response to PHA,

269 ons reduce the kinase inhibitory activity of imatinib mesylate; thus, agents that target Bcr/Abl thro

270 0% inhibitory concentration (IC50) values of imatinib mesylate to inhibit the proliferation of Ba/F3p

271 The capacity of imatinib mesylate to reverse established pulmonary arter

272 uccessful development of drugs, particularly imatinib mesylate, to treat chronic myelogenous leukemia

273 n of splenomegaly, compared with none of the imatinib mesylate-treated animals.

274 icroL) at necropsy, compared with only 8% of imatinib mesylate-treated animals.

275 Imatinib mesylate treatment decreases fibrosis and resul

276 Imatinib mesylate treatment markedly reduces the burden

277 myelogenous leukemia (CML) and resistance to imatinib mesylate treatment remain poorly investigated.

278 ical modeling approach that used the 10-year imatinib mesylate treatment response of patients with CM

279 d less staining for type I procollagen after imatinib mesylate treatment, but essentially unchanged t

280 that conserve class I MHC expression despite imatinib mesylate treatment.

281 K cells that accumulated in tumor foci after imatinib mesylate treatment.

282 h activated Smad1 signaling may benefit from imatinib mesylate treatment.

283 ase in the MRSS, following the initiation of imatinib mesylate treatment.

284 A survival benefit for imatinib mesylate versus interferon-alpha therapy could

285 pha, suggesting that the survival benefit of imatinib mesylate (versus interferon-alpha in newly diag

286 bl and its distinct binding mode relative to imatinib mesylate warrant further investigation of AP234

287 patients treated with nonimatinib therapies, imatinib mesylate was associated with a better 4-year su

288 Imatinib mesylate was previously reported to have specif

289 Imatinib mesylate was well tolerated but had minimal sin

290 f ACAs in early CP CML patients treated with imatinib mesylate, we performed an analysis in a large s

291 went treatment in a clinical trial with oral imatinib mesylate were followed up for 29 months.

292 Variable sensitivities to PKC412 or imatinib mesylate were observed among other mutants.

293 Survival rates with imatinib mesylate were significantly better than with in

294 ecific therapy was developed, initially with imatinib mesylate, which has transformed our treatment a

295 In contrast, imatinib mesylate, which inhibits KIT kinase activity bu

296 Then, in 2002, imatinib mesylate, which was introduced for the treatmen

297 d CCR, we monitored 85 patients treated with imatinib mesylate who achieved a CCR.

298 lso support the concept that combined use of imatinib mesylate with mTOR inhibitors may be an appropr

299 to-treat basis, had an objective response to imatinib mesylate, with a 20% or more decrease in tumour

300 of crossover (90%) from interferon-alpha to imatinib mesylate within a year of study entry.