ライフサイエンスコーパス: imatinib

1 f either Hsp90 (geldanamycin) or Abl kinase (imatinib).

2 ash (ten [6%] of 154 vs two [1%] of 152 with imatinib).

3 e frequently with dasatinib (28% v 0.8% with imatinib).

4 d neoplasms has been dramatically altered by imatinib.

5 Dutch GIST registry treated with neoadjuvant imatinib.

6 r later TKIs and intolerant or refractory to imatinib.

7 rs (GISTs) treated with surgery and adjuvant imatinib.

8 valuate for an early response to neoadjuvant imatinib.

9 it most from the longer duration of adjuvant imatinib.

10 ne or fentanyl with the PDGFR-beta inhibitor imatinib.

11 e disease in a patient who had received only imatinib.

12 ts who had been randomly assigned to receive imatinib.

13 nib, compared with CML patients treated with imatinib.

14 ents with suboptimal cytogenetic response on imatinib.

15 ificantly higher for dasatinib compared with imatinib.

16 n treated with the tyrosine kinase inhibitor imatinib.

17 ABL tyrosine kinase inhibitors, for example, Imatinib.

18 lowed by ponatinib > bosutinib > dasatinib > imatinib.

19 py results in longer survival than 1 year of imatinib.

20 chronic phase (CP) treated with dasatinib or imatinib.

21 ent occurred in three or more patients given imatinib.

22 ib and 95 patients were randomly assigned to imatinib.

23 nded well after initiation of treatment with imatinib.

24 ranscripts regularly observed in patients on imatinib.

25 e allocated nilotinib and 320 were allocated imatinib.

26 a series of phosphorus-containing analogs of imatinib.

27 rsued since the discovery and development of imatinib.

28 second-generation TKIs compared with generic imatinib.

29 e of resistance to first-line treatment with imatinib.

30 patients, positive for EBF1-PDGFRB, received imatinib; 1 died 6 months after a matched unrelated bone

31 pants received half their standard TKI dose (imatinib 200 mg daily, dasatinib 50 mg daily, or nilotin

32 cts with clinically-defined HES who received imatinib (300-400 mg daily >/= 1 month) were classified

33 ive dasatinib 100 mg once daily (n = 259) or imatinib 400 mg once daily (n = 260).

34 nt, all patients had received 3-18 months of imatinib 400 mg once daily and had a suboptimal cytogene

35 :1) via a randomisation list to receive oral imatinib 400 mg once daily or oral nilotinib 400 mg twic

36 ies were randomly assigned to receive either imatinib 400 mg or 800 mg daily.

37 system to receive oral ponatinib (45 mg) or imatinib (400 mg) once daily until progression, unaccept

38 GNP-HCIm decreased LFs viability compared to Imatinib (44.4 +/- 1.8% vs. 91.8 +/- 3.2%, p < 0.001), i

39 CR-ABL1 </= 10% at 3 months (dasatinib, 84%; imatinib, 64%), improvements in progression-free and ove

40 years, respectively) than in those receiving imatinib (8 per 1000 person-years), although data are li

41 was performed at day 22 and if <1000 ng/mL, imatinib 800 mg/day was given.

42 of-principle trial to evaluate the effect of imatinib, a KIT inhibitor, on airway hyperresponsiveness

43 Imatinib, a selective BCR-ABL1 kinase inhibitor, improve

44 hase with suboptimal cytogenetic response to imatinib according to the 2009 European LeukemiaNet crit

45 and, surprisingly, only a modestly decreased imatinib affinity.

46 pment of the tyrosine kinase inhibitor (TKI) imatinib allows patients with CML to experience near-nor

47 Imatinib also reduced levels of serum tryptase, a marker

48 kemia (CML) cells elicited by treatment with imatinib, an ABL kinase inhibitor approved by the FDA fo

49 ent tissues and driving development of novel imatinib analogs.

50 hese chiral tertiary piperazines resulted in imatinib analogues which exhibited comparable antiprolif

51 t in chronic phase was estimated at 26% with imatinib and 44% with second-generation TKIs.

52 m of this study was to assess the effects of imatinib and anakinra on PTF and TBF in colorectal cance

53 BCR-ABL tyrosine kinase inhibitors (TKIs) imatinib and dasatinib inhibit fludarabine and cytarabin

54 Treatments using imatinib and JAK2 pathway inhibitors can be effective on

55 Importantly, imatinib and nilotinib increased tyrosine phosphorylatio

56 We investigated the effects of imatinib and nilotinib on human NK cells, monocytes, and

57 bition of FAK activity both strongly reduced imatinib and nilotinib stimulated invasion.

58 Imatinib and nilotinib treatment increased two dimension

59 Imatinib and nilotinib-induced tyrosine phosphorylation

60 th other mutations that either progressed on imatinib and one or more tyrosine kinase inhibitor, or o

61 useful in patients who develop resistance to imatinib and other TKIs used to treat this disease.

62 a effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias ex

63 oblastoma multiforme (GBM) tumour cells with imatinib and the closely-related drug, nilotinib, striki

64 We also show that combination treatment with imatinib and tigecycline, an antibiotic that inhibits mi

65 Combining a tyrosine kinase inhibitor (imatinib) and a thiazolidinedione (pioglitazone) is prop

66 ell line (EA.hy926 cells) and pharmacologic (imatinib) and genetic (short hairpin RNA knockdown of IL

67 vy metal drugs (cisplatin), targeted agents (imatinib), and cytotoxic agents (docetaxel).

68 At 2 years, 55% of patients remained on imatinib, and 30% on nilotinib.

69 d to imatinib completed study treatment with imatinib, and 82.8% had a complete cytogenetic response.

70 ep molecular responses compared with generic imatinib, and the associated cost of each modality.

71 the USA using second-generation TKIs versus imatinib (annual price $4400 per year) with the potentia

72 ese effects were absent in rats treated with imatinib, another BCR-ABL tyrosine kinase inhibitor.

73 -up of 4.7 years, 5-year IFFS was 87% in the imatinib arm versus 84% in the control arm (hazard ratio

74 n 5% and 7% of patients in the dasatinib and imatinib arms, respectively.

75 p in patients with CML who were treated with imatinib as initial therapy.

76 se inhibitors, including the anticancer drug imatinib, as inhibitors of both SARS-CoV and MERS-CoV in

77 e of resistance to first-line treatment with imatinib at six institutions (teaching hospitals and dis

78 ith more arterial occlusive events than with imatinib at the doses studied.

79 These findings demonstrate that imatinib attenuates multiple cytoskeletal changes associ

80 Adjuvant therapy with imatinib benefits patients with a high risk of recurrenc

81 ase inhibitors, such as the anti-cancer drug Imatinib, bind.

82 novel c-Src allosteric sites associated with imatinib binding and kinase activation and provide a fra

83 n functional regulatory sites, distal to the imatinib binding pocket, show similarities to structural

84 Our results demonstrate that imatinib binding to the kinase domain effects dynamics o

85 the transient conformation to which the drug imatinib binds enabled the elucidation of drug-resistanc

86 We also showed that imatinib blocked tolerance to other clinically used opio

87 We found that imatinib blocked tolerance without altering receptor int

88 y GIST patients respond to the Kit inhibitor imatinib, but this drug often becomes ineffective becaus

89 ng ALKBH2-benzaldehyde, AKT3-vandetanib, BCR-imatinib, CDK1 and 20-palbociclib, CASP1-imexon, and FGF

90 ts (48.3%) who had been randomly assigned to imatinib completed study treatment with imatinib, and 82

91 hase chronic myeloid leukaemia compared with imatinib could not be assessed due to trial termination,

92 tive activity to that of their corresponding imatinib counterparts.

93 ctivity was shown by nintedanib, followed by imatinib, dasatinib, and acetylcysteine.

94 ast decade, several targeted therapies (e.g. imatinib, dasatinib, nilotinib) have been developed to t

95 In patients with severe asthma, imatinib decreased airway hyperresponsiveness, mast-cell

96 apoptosis in a dose-dependent manner, while imatinib did not.

97 ty and efficacy of switching to nilotinib vs imatinib dose escalation for patients with suboptimal cy

98 ponses with switching to nilotinib than with imatinib dose escalation, although the difference was no

99 nib 400 mg twice per day or an escalation of imatinib dose to 600 mg once per day (block size of 4).

100 n the absence of the drug, therefore halting imatinib during pregnancy endangers the mother.

101 ronous recurrence/metastases (MET), and also imatinib era (before and after it became available).

102 OS was longer in the imatinib era compared with the pre-imatinib era in each

103 Patients treated in the imatinib era had prolonged OS across all presentations.

104 er in the imatinib era compared with the pre-imatinib era in each presentation group, including in Mi

105 PRIM patients in the imatinib era who received imatinib (neoadjuvant and/or a

106 In the imatinib era, among site, size, and mitotic rate, high-r

107 In the pre-imatinib era, primary tumor site, size, and mitotic rate

108 Among PRIM patients from the pre-imatinib era, tumor site, size, and mitotic rate were in

109 (ALL) in the elderly has improved during the imatinib era.

110 he placenta and implantation after long-term imatinib exposure.

111 currence were randomized to receive adjuvant imatinib for 1 or 3 years.

112 The trail blazed by imatinib for chronic myelogenous leukemia and GIST has b

113 NK cells and monocytes of patients receiving imatinib for chronic myeloid leukemia.

114 e patients were randomly assigned to receive imatinib for either 1 or 3 years.

115 namics, in the presence and absence of bound imatinib, for full-length human c-Src using hydrogen-deu

116 Imatinib (Gleevec), a non-receptor tyrosine kinase inhib

117 p (50%, 95.18% CI 40-61) and 40 of 95 in the imatinib group (42%, 32-53%; difference 7.9% in favour o

118 nib group and 34 (36%) of 95 patients in the imatinib group achieved complete cytogenic response at 6

119 nse at 12 months, as only 13 patients in the imatinib group and ten patients in the ponatinib group c

120 and hypophosphatemia were more common in the imatinib group than in the placebo group.

121 th groups was abdominal pain (11 [4%] in the imatinib group, 14 [4%] in the nilotinib group).

122 (+/-SD) of 1.73+/-0.60 doubling doses in the imatinib group, as compared with 1.07+/-0.60 doubling do

123 In the imatinib group, grade 3 or 4 adverse events observed in

124 QT prolongation (nilotinib group, n=1 [1%]; imatinib group, n=1 [1%, after crossover to nilotinib]).

125 last cell crisis (nilotinib group, n=1 [1%]; imatinib group, n=1 [1%]), and QT prolongation (nilotini

126 %, including 1 after crossover to imatinib]; imatinib group, n=1 [1%]), blast cell crisis (nilotinib

127 Among the patients in the imatinib group, the estimated overall survival rate at 1

128 In the imatinib group, the most common grade 3-4 adverse events

129 b group and nine (10%) of 93 patients in the imatinib group.

130 oup and five (5%) of 93 patients died in the imatinib group; no deaths were treatment-related.

131 natinib and three (2%) of 152 patients given imatinib had arterial occlusive events (p=0.052); arteri

132 Imatinib has radically changed the management of GIST, y

133 atus more quickly and for more patients than imatinib; however, with the availability and lower cost

134 However, the Az and imatinib hybrids have weak inhibitory activities towards

135 Purpose Imatinib (IM) can safely be discontinued in patients wit

136 tailor the fate of anticancer drugs such as imatinib (IM) to the tumor site resulting in efficient t

137 oup, n=2 [2%, including 1 after crossover to imatinib]; imatinib group, n=1 [1%]), blast cell crisis

138 The Evaluation of Ponatinib versus Imatinib in Chronic Myeloid Leukemia (EPIC) study was a

139 ic and recurrent tumors after treatment with Imatinib in most cases a decrease in size and contrast e

140 inhibitor, was markedly more effective than imatinib in multiple preclinical models of imatinib-sens

141 (OR, 3.47; 95% CI, 1.23-9.78) compared with imatinib in patients with CML.

142 400 mg/d) versus a higher dose (800 mg/d) of imatinib in patients with metastatic or locally advanced

143 -blind, placebo-controlled, 24-week trial of imatinib in patients with poorly controlled severe asthm

144 ld result in superior outcomes compared with imatinib in previously untreated patients with chronic m

145 explain the failure of Abl kinase inhibitor imatinib in prostate cancer clinical trials.

146 e used different price scenarios for generic imatinib in the USA (average price $35 000 per year; low

147 eginning of the learning curve of the use of imatinib, in a large population of patients with advance

148 icacy and safety of ponatinib, compared with imatinib, in newly diagnosed patients with chronic-phase

149 Treatment with imatinib increased TNT formation in both Kcl-22 and K562

150 se data suggest SERT polymorphisms influence imatinib-induced diarrhoea but not that of dasatinib.

151 onstrated that the tyrosine kinase inhibitor imatinib induces lysosome acidification and antimicrobia

152 known about whether the duration of adjuvant imatinib influences the prognostic significance of KIT p

153 Imatinib inhibited hCNT2 with an IC50 value of 2.3 mum P

154 The small molecule imatinib inhibits KIT and has been a mainstay of therapy

155 Imatinib-insensitive leukemia stem cells (LSCs) are beli

156 Encapsulation of Imatinib into targeted nanoparticles could be considered

157 Imatinib is an oral chemotherapeutic used primarily to t

158 e, the antitumor effect of the Kit inhibitor imatinib is partially mediated by CD103(+)CD11b(-) DCs,

159 ation of the transporter, and establish that imatinib is particularly effective in stabilizing the in

160 kinase domain in the BCR-ABL fusion protein, imatinib is strikingly effective in the initial stage of

161 sease: imatinib, sunitinib, and regorafenib; imatinib is usually the best tolerated of the three and

162 romal tumors (GISTs), and the KIT inhibitor, imatinib, is therefore standard of care for patients wit

163 Imatinib mesylate (IM) blocks the CSF-1 receptor.

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

165 tance of CML stem cells (CMLSCs) to the drug imatinib mesylate (IM).

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

167 Imatinib mesylate and new TKIs along with allogeneic ste

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

169 Moreover, imatinib mesylate enhanced rat cardiac allograft vasculo

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

171 Imatinib mesylate, 1a, inhibits production of beta-amylo

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

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

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

175 ted with the tyrosine kinase inhibitor (TKI) imatinib mesylate.

176 The duration of adjuvant imatinib modifies the risk of GIST recurrence associated

177 ed entry inhibitors of SARS-CoV-2, including imatinib, mycophenolic acid and quinacrine dihydrochlori

178 Treatment at entry was imatinib (n=148), nilotinib (n=16), or dasatinib (n=10),

179 mly assigned to receive ponatinib (n=155) or imatinib (n=152).

180 and without diarrhoea on the SPIRIT2 trial (imatinib, n = 319; and dasatinib, n = 297) were genotype

181 IM patients in the imatinib era who received imatinib (neoadjuvant and/or adjuvant) had higher risk t

182 he effects of the tyrosine kinase inhibitors imatinib, nilotinib, and dasatinib on B. malayi adult ma

183 sessed interactions of bosutinib, dasatinib, imatinib, nilotinib, and ponatinib with recombinant hNTs

184 CML patients at diagnosis (n = 21), on TKI (imatinib, nilotinib, dasatinib) before achieving major m

185 he De-Escalation and Stopping Treatment with Imatinib, Nilotinib, or sprYcel (DESTINY) study is a non

186 o Here we show that the anti-CoV activity of imatinib occurs at the early stages of infection, after

187 developing nations, with a price of generic imatinib of $2100 per year and a willingness to pay of $

188 The effects of imatinib on future fertility are unknown.

189 ults indicate potential long-term effects of imatinib on pregnancy and implantation.

190 ssible long-term (post-treatment) effects of imatinib on reproduction have not been studied.

191 used a mouse model to examine the effects of imatinib on the placenta and implantation after long-ter

192 e the outstanding success of the cancer drug imatinib, one obstacle in prolonged treatment is the eme

193 d CML in the chronic phase to receive either imatinib or interferon alfa plus cytarabine.

194 ased the rate of MMR at 1 year compared with imatinib (overall OR, 2.22; 95% CI, 1.87 to 2.63).

195 atinib and in one (1%) of 152 patients given imatinib (p=0.010).

196 onatinib and five [38%] of 13 patients given imatinib; p=0.074).

197 ars of follow-up showed that the efficacy of imatinib persisted over time and that long-term administ

198 Imatinib plasma trough level was performed at day 22 and

199 tyrosine kinase inhibitor, or only received imatinib previously.

200 ed anaphylaxis with the ABL kinase inhibitor imatinib protected the mice from severe IgE-mediated ana

201 nia (19 [12%] of 154 vs ten [7%] of 152 with imatinib), rash (ten [6%] of 154 vs two [1%] of 152 with

202 However, Abl kinase inhibition by imatinib reduces rapid redistribution of the important c

203 f low-level BCR-ABL1 mutations present after imatinib resistance has prognostic significance for subs

204 dentified known and new mutations conferring imatinib resistance in chronic myeloid leukemia cells.

205 common second-site mutation associated with imatinib resistance in GIST and the first in vivo demons

206 However, most GISTs develop imatinib resistance through secondary KIT mutations.

207 CL1 combination, which was also effective in imatinib-resistant cells.

208 IT expression and relative cell viability of imatinib-resistant GIST cells.

209 In imatinib-resistant GIST with a secondary Kit mutation, K

210 preclinical models of imatinib-sensitive and imatinib-resistant GIST.

211 ficantly better growth inhibitory effects on imatinib-resistant GIST48 and GIST430 cells in vitro, an

212 nctive biologic features in KIT-independent, imatinib-resistant GISTs as a step towards identifying d

213 n, and may offer a new strategy for treating imatinib-resistant GISTs.

214 Both imatinib-sensitive and imatinib-resistant Kit (Kit(mut)) become fully auto-phos

215 I3K and MEK inhibition was effective against imatinib-resistant Kit(V558Delta;T669I/+) tumors.

216 effective in vitro and in vivo, including in imatinib-resistant models.

217 However, imatinib-resistant mutations are increasingly prevalent

218 r developing combination therapy to overcome imatinib-resistant of KIT-expressing GISTs.

219 r responses in both previously untreated and imatinib-resistant patients with CML.

220 bserved with nilotinib/dasatinib therapy for imatinib-resistant patients with multiple mutations were

221 e data also identify imatinib-sensitive, and imatinib-resistant, mutation sites.

222 LSCs, aberrantly expressed proteins, in both imatinib-responder and non-responder patients, are modul

223 on gene, little is known about predictors of imatinib response in clinically-defined hypereosinophili

224 Clinical features of MHES predict imatinib response in PDGFRA-negative HES.

225 Overall, imatinib response rates were 100% in the FP group (n = 1

226 A biosynthesis, where pathway inhibition via imatinib results in marked PPP impairment and an accumul

227 Targeting of KIT and PDGFRA with imatinib revolutionised treatment in gastrointestinal st

228 umulate in an order of magnitude increase in imatinib's half-maximal inhibitory concentration (IC(50)

229 ts recently identified to be responsible for imatinib's high selectivity toward Abl.

230 characteristic intracellular accumulation of imatinib-sensitive and -resistant Kit protein is well do

231 n imatinib in multiple preclinical models of imatinib-sensitive and imatinib-resistant GIST.

232 Both imatinib-sensitive and imatinib-resistant Kit (Kit(mut))

233 These data also identify imatinib-sensitive, and imatinib-resistant, mutation sit

234 Imatinib should be prescribed for high-risk features.

235 Imatinib should still be prescribed for patients with hi

236 tumors such as stage 4 neuroblastomas (NB), imatinib showed benefits that might depend on both on-ta

237 Combining valproic acid with imatinib showed significantly better growth inhibitory e

238 tumor-bearing mice with the c-Kit inhibitor imatinib significantly reduced tumor growth and phospho-

239 We report the final results of the Stop Imatinib (STIM1) study with a long follow-up.

240 analysis from the phase III Dasatinib Versus Imatinib Study in Treatment-Naive Chronic Myeloid Leukem

241 stromal tumours with progression on at least imatinib, sunitinib, and regorafenib or documented intol

242 oved for the management of advanced disease: imatinib, sunitinib, and regorafenib; imatinib is usuall

243 gonists currently in clinical use, including imatinib, sunitinib, and sorafenib.

244 CML, with over 80% of patients treated with imatinib surviving for more than 10 years.

245 We specifically identified the imatinib target, Abelson tyrosine-protein kinase 2 (Abl2

246 nd FAK activity and was independent of known imatinib targets including Abl, platelet derived growth

247 Diarrhoea was more prevalent in imatinib, than in dasatinib treated patients (P = 0.015)

248 hod was applied to a three-step synthesis of imatinib, the API of Gleevec, in good yield without the

249 Imatinib, the first and arguably the best targeted thera

250 Imatinib, the first BCR-ABL1 TKI granted regulatory appr

251 Similar to imatinib, the partial response rate for regorafenib by C

252 underexpression predicts a worse response to imatinib, the standard treatment for Ph(+) CML.

253 h the availability and lower cost of generic imatinib, the value of second-generation TKIs as frontli

254 = 5) were enrolled in a prospective study of imatinib therapy (NCT00044304: registered at clinicaltri

255 Three years of adjuvant imatinib therapy are recommended for patients with GI st

256 However, in both mice and humans, chronic imatinib therapy decreases intratumoral DCs and effector

257 Imatinib therapy drives the leukemic population into the

258 Right from the start of Imatinib therapy in inoperable and disseminated GIST pat

259 Three years of adjuvant imatinib therapy results in longer survival than 1 year

260 Neoadjuvant imatinib therapy should be considered for patients requi

261 any patients who otherwise responded well to imatinib therapy still showed variations in their BCR-AB

262 issue in GIST patients receiving front-line imatinib therapy.

263 e (22 [14%] of 154 vs three [2%] of 152 with imatinib), thrombocytopenia (19 [12%] of 154 vs ten [7%]

264 onal dynamics associated with the binding of Imatinib to the proto-oncogene c-Src.

265 rprisingly, immunofluorescence microscopy of imatinib-treated cells revealed a marked colocalization

266 ained the occurrence of diarrhoea in ~10% of imatinib-treated female CML patients.

267 Fifteen dasatinib-treated and 19 imatinib-treated patients had BCR-ABL1 mutations identif

268 study closure, 61% and 63% of dasatinib- and imatinib-treated patients remained on initial therapy, r

269 Unfortunately, imatinib-treated patients typically relapse, most often

270 Stimulants that expand and mature DCs during imatinib treatment improve antitumor immunity.

271 Furthermore, the absence of SCF or imatinib treatment prevents progenitors from developing

272 the 62 patients who underwent randomization, imatinib treatment reduced airway hyperresponsiveness to

273 ding affinities are markedly diminished upon imatinib treatment, including CHK1, a checkpoint kinase

274 umor high-risk features were associated with imatinib treatment, only tumor size >10 cm remained asso

275 KIT mutants, including a mutant resistant to imatinib treatment, responded well to a combination of T

276 took place after insulin/IGF1 stimulation or imatinib treatment, suggesting that the direct SHP2-p85

277 Imatinib treatment, which inhibits KIT signaling, deplet

278 ogenitors are present in patients undergoing imatinib treatment.

279 ces durable, long-term overall survival with imatinib treatment.

280 s in the neoplastic tissue of GIST following Imatinib treatment.

281 f gastrointestinal stromal tumors (GISTs) to imatinib treatment.

282 BCR-ABL signaling, reducing the efficacy of imatinib treatment.

283 ATP-binding affinities of kinases induced by imatinib treatment.

284 ces of second-generation TKIs and of generic imatinib under different pricing scenarios in the USA, E

285 GNP-HCIm reduced cAbl-p (0.41 GNP-HCIm, 0.24 Imatinib vs. to control; p < 0.001).

286 Imatinib was loaded in gold nanoparticles (GNP) function

287 er time and that long-term administration of imatinib was not associated with unacceptable cumulative

288 fects on placental growth occurred even when imatinib was stopped prior to pregnancy.

289 After >/= 18 months in complete remission, imatinib was tapered and discontinued in 8 FP and 1 MHES

290 Imatinib was the first targeted tyrosine kinase inhibito

291 Imatinib was the first-line treatment for 111 patients,

292 Among 142 long-term survivors, imatinib was the sole therapy administered in 69 (48.6%)

293 cal, molecular, and bone marrow responses to imatinib were assessed.

294 idered by the investigators to be related to imatinib were uncommon and most frequently occurred duri

295 ncial toxicity," the burden of drugs such as imatinib, where a year's supply can easily cost as much

296 f kinases in K-562 cells upon treatment with imatinib, which is accompanied by substantial decreases

297 Treating mice with dasatinib or imatinib, which target c-Kit, resulted in complete tumor

298 In addition to imatinib, which was approved for pediatric CML in 2003,

299 ;V653A Kit double mutation were resistant to imatinib, while cabozantinib was more effective in overc

300 itized Ba/F3 BCR-ABL1 cells to inhibition by imatinib, while demonstrating no toxicity toward Ba/F3 p