ライフサイエンスコーパス: tyrosine kinase inhibitor

1 PL-504, volitinib) is a highly selective MET tyrosine kinase inhibitor.

2 epidermal growth factor receptor (EGFR)/HER2 tyrosine kinase inhibitor.

3 o entospletinib, a recently developed spleen tyrosine kinase inhibitor.

4 despite treatment with ibrutinib, a Bruton's tyrosine kinase inhibitor.

5 rats treated with imatinib, another BCR-ABL tyrosine kinase inhibitor.

6 ctivity of sunitinib, an orally administered tyrosine kinase inhibitor.

7 pan-fibroblast growth factor receptor (FGFR) tyrosine kinase inhibitor.

8 activity of oral BGJ398, a selective FGFR1-3 tyrosine kinase inhibitor.

9 inhibitor or who had been pretreated with a tyrosine kinase inhibitor.

10 astases who had been pretreated with an EGFR tyrosine kinase inhibitor.

11 ation of sunitinib, a multitargeted receptor tyrosine kinase inhibitor.

12 tured microglia by PP2, a Src family protein tyrosine kinase inhibitor.

13 ib is a second-generation, irreversible EGFR tyrosine kinase inhibitor.

14 itive disease who have progressed on an EGFR tyrosine-kinase inhibitor.

15 after previous therapy with an approved EGFR tyrosine-kinase inhibitor.

16 erations that are amenable to treatment with tyrosine kinase inhibitors.

17 ure, with the emergence of clinically useful tyrosine kinase inhibitors.

18 -2, and had not previously been treated with tyrosine kinase inhibitors.

19 ndothelial growth factor receptor 2 (VEGFR2) tyrosine kinase inhibitors.

20 ired resistance to the current clinical EGFR tyrosine kinase inhibitors.

21 t of chronic lymphocytic leukemia (CLL) with tyrosine kinase inhibitors.

22 loid leukemia (CP-CML) patients treated with tyrosine kinase inhibitors.

23 utic considerations, including new and novel tyrosine kinase inhibitors.

24 the number of previous treatments with VEGFR tyrosine-kinase inhibitors.

25 X-82 is an oral tyrosine kinase inhibitor active against vascular endoth

26 al decrease following cediranib (a pan-VEGFR tyrosine kinase inhibitor) administration.

27 cancer cells with both onapristone and IGF1R tyrosine kinase inhibitor AEW541 was more effective than

28 n NCI-H460 cells, which are resistant to the tyrosine kinase inhibitor AG1478, is also disrupted with

29 cell lung cancer (NSCLC) is sensitive to ALK tyrosine kinase inhibitors (ALK inhibitors) such as criz

30 (BIBF1120) is a potent, oral, small-molecule tyrosine kinase inhibitor, also known as a triple angiok

31 GFR*-driven gliomas were insensitive to EGFR tyrosine kinase inhibitors, although they could efficien

32 Combined treatment with an EGFR tyrosine kinase inhibitor and Akt inhibitor causes apopt

33 al metastases who had never received an EGFR tyrosine kinase inhibitor and patients with leptomeninge

34 This led to development of small-molecule tyrosine kinase inhibitors and inhibitors of mammalian t

35 to epidermal growth factor receptor-targeted tyrosine kinase inhibitors and may also be of interest t

36 umber of novel therapeutic agents, including tyrosine kinase inhibitors and monoclonal antibodies, ha

37 to be responsible for resistance to BCR-ABL tyrosine kinase inhibitors and relapse of chronic myelog

38 absence of ERBB3 remained sensitive to EGFR tyrosine kinase inhibitors and retained activation of th

39 ore potent BCR-ABL1 inhibitor than all other tyrosine-kinase inhibitors and selectively suppresses th

40 Terreic acid (a Bruton's tyrosine kinase inhibitor) and pergolide (a dopamine and

41 Ibrutinib is a Bruton tyrosine kinase inhibitor approved for the treatment of

42 Tyrosine kinase inhibitors are effective treatments for

43 ivo treatment studies suggested that pre-BCR tyrosine kinase inhibitors are useful for the treatment

44 cer (NSCLC) with acquired resistance to EGFR tyrosine-kinase inhibitors are undefined.

45 VEGF inhibitors, including receptor tyrosine kinase inhibitors, are used as adjunct therapie

46 ansplantation vs long-term administration of tyrosine-kinase inhibitors) as well as on MRD testing.

47 y blocker) with erlotinib (a reversible EGFR tyrosine kinase inhibitor), as second-line treatment for

48 on of skin toxicity in patients treated with tyrosine kinase inhibitors at levels not detectable via

49 e or parallel prospective clinical trials of tyrosine-kinase inhibitors at a single institution from

50 h structural analysis to establish the VEGFR tyrosine kinase inhibitor axitinib as a selective and ef

51 of EGFR, HER2, and HER3 signalling with the tyrosine kinase inhibitor AZD8931 will control growth of

52 hree-dimensional modeling suggests how these tyrosine kinase inhibitors bind and inhibit filarial pro

53 oid leukemia (CML) is currently treated with tyrosine kinase inhibitors, but these do not effectively

54 tly observed adverse effects associated with tyrosine kinase inhibitors, can significantly affect pat

55 However, adverse effects common to the tyrosine kinase inhibitor class occur at a noticeably hi

56 ve NSCLC and resistance to one previous EGFR tyrosine kinase inhibitor (cohort 3), other cancers with

57 ilic blocks and dasatinib (DAS, an oncogenic tyrosine kinases inhibitor) conjugated hydrophobic block

58 nation of PGE1/misoprostol with conventional tyrosine-kinase inhibitors could provide effective thera

59 Addition of the dual MET/RON tyrosine kinase inhibitor, crizotinib, restored cetuxima

60 Tivantinib, a MET receptor tyrosine kinase inhibitor, demonstrated increased antica

61 CP-196) is a highly selective, potent Bruton tyrosine kinase inhibitor developed to minimise off-targ

62 EGFR return as SCLC when resistance to EGFR tyrosine kinase inhibitors develops.

63 cent drug screening assays are essential for tyrosine kinase inhibitor discovery.

64 By contrast, the multi-targeted tyrosine kinase inhibitors dovitinib and vatalanib, whic

65 vercome the epidermal growth factor receptor tyrosine kinase inhibitor (EGFR TKI) resistance induced

66 The tyrosine kinase inhibitor erlotinib improves the outcome

67 The epidermal growth factor receptor tyrosine kinase inhibitor erlotinib in combination with

68 The tyrosine kinase inhibitor erlotinib poorly penetrates th

69 ce (EGFR(ptKO)) or administration of an EGFR tyrosine kinase inhibitor erlotinib.

70 g cancer, which is commonly treated with the tyrosine kinase inhibitor erlotinib.

71 ition when treated with chloroquine plus the tyrosine kinase inhibitors erlotinib or sunitinib, sugge

72 e cytotoxic chemotherapy (5-fluorouracil) or tyrosine kinase inhibitor (erlotinib), we show that thes

73 red resistance to an IGF-1 receptor (IGF-1R) tyrosine kinase inhibitor exhibited reduced expression o

74 lysis, and the classical ATP-analog class of tyrosine kinase inhibitors fail to inactivate it.

75 inib highlights the therapeutic potential of tyrosine kinase inhibitors for treatment of FSHD.

76 L LICs), thereby sensitizing them to BCR-ABL tyrosine kinase inhibitors, for example, Imatinib.

77 ily blocker afatinib and the reversible EGFR tyrosine kinase inhibitor gefitinib are approved for fir

78 and safety with that of the reversible EGFR tyrosine kinase inhibitor gefitinib in the first-line tr

79 the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor gefitinib relative to placebo

80 before and after treatment of cells with the tyrosine-kinase inhibitor Gefitinib.

81 Deregulation of ZAP-70 using tyrosine kinase inhibitors, gefitinib or ibrutinib, dimi

82 er substantiated by the rescue effect of the tyrosine kinase inhibitor genistein, and the more specif

83 CSF1R in APP/PS1 mice by an orally available tyrosine kinase inhibitor (GW2580) resulted in the block

84 methotrexate and high-dose cytarabine plus a tyrosine kinase inhibitor, had minimal residual disease

85 argeting the fusion oncoprotein BCR-ABL with tyrosine kinase inhibitors has significantly affected ch

86 Despite the fact that tyrosine kinase inhibitors have established targeted mol

87 used EGFR-targeted monoclonal antibodies and tyrosine kinase inhibitors have specific limitations rel

88 TZ), a monoclonal antibody, and lapatinib, a tyrosine kinase inhibitor, have proved highly beneficial

89 ibitors, including monoclonal antibodies and tyrosine kinase inhibitors, have achieved only modest su

90 ing with EGFR-specific antibodies or an EGFR tyrosine kinase inhibitor hindered HGF-stimulated pancre

91 The Bruton's tyrosine kinase inhibitor ibrutinib effectively inhibite

92 The novel Bruton's tyrosine kinase inhibitor ibrutinib has demonstrated hig

93 utations conferring resistance to the Bruton tyrosine kinase inhibitor ibrutinib in chronic lymphocyt

94 reducing toxicity of the single-agent Bruton tyrosine kinase inhibitor ibrutinib in chronic lymphocyt

95 lymphocytic leukemia (CLL) with the Bruton's tyrosine kinase inhibitor ibrutinib.

96 , immunomodulator lenalidomide, and Bruton's tyrosine kinase inhibitor ibrutinib.

97 vo and synergizes strongly with the Bruton's tyrosine kinase inhibitor ibrutinib.

98 ting us to combine AZD8835 with the Bruton's tyrosine kinase inhibitor ibrutinib.

99 tudy, we randomly compared high doses of the tyrosine kinase inhibitor imatinib combined with reduced

100 Finally, we demonstrated that the tyrosine kinase inhibitor imatinib induces lysosome acid

101 The PDGF receptor tyrosine kinase inhibitor imatinib mesylate and a monocl

102 ieve complete response when treated with the tyrosine kinase inhibitor imatinib.

103 The effects of the tyrosine kinase inhibitors imatinib, nilotinib, and dasa

104 Combining a tyrosine kinase inhibitor (imatinib) and a thiazolidined

105 ity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in h

106 Tyrosine-kinase inhibitors improve overall survival in p

107 limumab in combination, and nivolumab plus a tyrosine kinase inhibitor in metastatic renal cell carci

108 l transplant may be advisable; addition of a tyrosine kinase inhibitor in patients with t(9;22) trans

109 ions are important predictive biomarkers for tyrosine kinase inhibitors in lung cancer.

110 for epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in unselected patients with h

111 restores the sensitivity of glioma cells to tyrosine kinase inhibitors in vivo in preclinical combin

112 We investigated dasatinib, another potent tyrosine kinase inhibitor, in combination with low-inten

113 afety of bosutinib, an oral dual Src/Bcr-Abl tyrosine kinase inhibitor, in patients with ADPKD.

114 sistance to current and newly developed EGFR tyrosine kinase inhibitors, including AZD9291.

115 d that RCN2 knockout sensitized HCC cells to tyrosine kinase inhibitors, including erlotinib, lapatin

116 Epidermal growth factor receptor tyrosine kinase inhibitors, including gefitinib, erlotin

117 summary, we show that PI3Kdelta or Bruton's tyrosine kinase inhibitors increase genomic instability

118 dermal growth factor receptor (EGFR) by EGFR tyrosine kinase inhibitors is insufficient for effective

119 vival after initial treatment with different tyrosine kinase inhibitors is unknown.

120 Combination of chemotherapy with a tyrosine-kinase inhibitor is effective in the treatment

121 ral population by age, response, and type of tyrosine-kinase inhibitor is not known.

122 Ibrutinib, a Bruton tyrosine kinase inhibitor, is a new targeted agent appro

123 Sorafenib, a broad tyrosine kinase inhibitor, is the only approved systemic

124 b (ABT-869), a novel multi-targeted receptor tyrosine kinase inhibitor, markedly augments cytotoxicit

125 In this study, the mast cell-targeting tyrosine kinase inhibitor, masitinib, was released from

126 ereas the off-target effect of multitargeted tyrosine kinase inhibitors may be mediated by disruption

127 the bloodstream, we decided to explore which tyrosine kinase inhibitors might block the kinase-induce

128 Tyrosine kinase inhibitors might still have potential in

129 wn EMT reversal and resensitization to other tyrosine kinase inhibitors, mitotic inhibitors, and plat

130 However, similar to other tyrosine kinase inhibitors, most patients achieve diseas

131 With access to tyrosine-kinase inhibitors, most patients with chronic m

132 multimodal strategy combining multitargeted tyrosine kinase inhibitors (MTKIs) and microRNA (miRNA)

133 s, we used prospectively collected data from tyrosine kinase inhibitor-naive patients with EGFR mutat

134 e standard neoadjuvant chemotherapy plus the tyrosine kinase inhibitor neratinib with control.

135 ion of novel targets for two clinically used tyrosine kinase inhibitors, nilotinib and osimertinib.

136 Imatinib (Gleevec), a non-receptor tyrosine kinase inhibitor (nRTKI), is one of the most su

137 Cediranib is a potent tyrosine kinase inhibitor of VEGFR1, 2, and 3.

138 Vandetanib is a novel tyrosine kinase inhibitor of VEGFR2, RET, and EGFR, all

139 e safety and activity of dovitinib, a potent tyrosine-kinase inhibitor of fibroblast growth factor re

140 Neratinib, an irreversible tyrosine-kinase inhibitor of HER1, HER2, and HER4, has c

141 Effects of 4 multitargeted receptor tyrosine kinase inhibitors on regional hemodynamics in c

142 S metastases who had either never received a tyrosine kinase inhibitor or who had been pretreated wit

143 nhibitors alone or in combination with other tyrosine kinase inhibitors or chemotherapeutic agents.

144 t the NOXA promoter in TT cells treated with tyrosine kinase inhibitors or the ATF4 inducer eeyaresta

145 In the era of treatment with tyrosine-kinase inhibitors, patients diagnosed with CML-

146 had progressed after treatment with an EGFR tyrosine kinase inhibitor received AZD3759 at 50 mg, 100

147 Because receptor tyrosine kinase inhibitors render JHCO3 in the PT insens

148 ivity using Sunitinib, a clinically-approved tyrosine kinase inhibitor, rescued differentiation in bo

149 The diversity and unpredictability of EGFR tyrosine kinase inhibitor resistance mechanisms presents

150 apeutically combat the heterogeneity of EGFR tyrosine kinase inhibitor resistance mechanisms.EGFR-mut

151 tually all patients succumb to acquired EGFR tyrosine kinase inhibitor resistance that occurs via div

152 ession of chronic myeloid leukemia (CML) and tyrosine kinase inhibitor resistance through poorly unde

153 ion is a convergent feature of acquired EGFR tyrosine kinase inhibitor resistance, across a spectrum

154 r developing new treatments to overcome EGFR tyrosine kinase inhibitor resistance.

155 cell lung cancer patients with acquired EGFR tyrosine kinase inhibitor resistance.

156 ten initially sensitive to imatinib or other tyrosine kinase inhibitors, resistance generally develop

157 In tyrosine kinase inhibitor-resistant lung tumors, rocilet

158 nergistic growth inhibition in multiple EGFR tyrosine kinase inhibitor-resistant non-small-cell lung

159 cquired and intrinsic resistance to receptor tyrosine kinase inhibitors (RTKi) represents a major hur

160 D9291) is an oral, potent, irreversible EGFR tyrosine-kinase inhibitor selective for EGFR tyrosine-ki

161 tyrosine-kinase inhibitor selective for EGFR tyrosine-kinase inhibitor sensitising mutations, and the

162 1 year of neratinib, an irreversible pan-HER tyrosine kinase inhibitor, significantly improves 2-year

163 Novel therapies include tyrosine kinase inhibitors, small-molecule inhibitors (e

164 Adjuvant treatment with the VEGF receptor tyrosine kinase inhibitors sorafenib or sunitinib showed

165 Treatment with the KDR tyrosine kinase inhibitor SU1498 or the KDR ligand VEGFA

166 ntagonist in polystyrene microspheres (PE) + tyrosine kinase inhibitor SU5416 (SU) group.

167 nitially respond to treatment with the multi-tyrosine kinase inhibitor sunitinib eventually relapse.

168 -C or VEGFR3 deletion, administration of the tyrosine kinase inhibitor sunitinib, or expression of VE

169 esis is the main target of drugs such as the tyrosine kinase inhibitor sunitinib.

170 odel of mBC resistance to the antiangiogenic tyrosine kinase inhibitor sunitinib.

171 is aggressive tumor, a multi-target receptor tyrosine kinase inhibitor, sunitinib base, was efficient

172 ly approved vandetanib and cabozantinib, the tyrosine kinase inhibitors targeting RET, vascular endot

173 The latest examples are tyrosine kinase inhibitors targeting the Philadelphia Ch

174 For the past 10 years, tyrosine kinase inhibitors targeting vascular endothelia

175 Cabozantinib, a small molecule tyrosine kinase inhibitor, targets MET, VEGFR, RET, ROS1

176 tor receptor 2, c-MET, and RET multitargeted tyrosine kinase inhibitor that has antiangiogenic and an

177 Erlotinib is an EGFR tyrosine kinase inhibitor that has shown a significant b

178 Ibrutinib is a clinically approved Bruton's tyrosine kinase inhibitor that inhibits mast cells and t

179 inetic analysis identified Pz-1 as a type II tyrosine kinase inhibitor that is able to bind the "DFG-

180 induced by dasatinib, a dual Src and BCR-ABL tyrosine kinase inhibitor that is used to treat chronic

181 posed by the introduction of trastuzumab and tyrosine kinase inhibitors that revolutionized cancer th

182 RNA or inhibition by cabozantinib, the multi-tyrosine kinases inhibitor that targets vascular endothe

183 impressive additional value when combining a tyrosine kinase inhibitor, that is, the Bruton tyrosine

184 In addition to tyrosine kinase inhibitors, therapeutic strategies that

185 Studies of resistance to tyrosine kinase inhibitor therapy have not fully reflect

186 ls at CML diagnosis on molecular response to tyrosine kinase inhibitor therapy in early chronic-phase

187 first-line epidermal growth factor receptor tyrosine kinase inhibitor therapy, and T790M mutation, o

188 reatment may increase patients' adherence to tyrosine kinase inhibitor therapy.

189 IB/IV) NSCLC who progressed on previous EGFR tyrosine-kinase inhibitor therapy received osimertinib 8

190 We tested both rapamycin and a TIE2 tyrosine kinase inhibitor (TIE2-TKI) for their effects o

191 leukemia (ALL) who progress after failure of tyrosine kinase inhibitor (TKI) -based therapy.

192 the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) AZD9291.

193 STOP second generation (2G)-tyrosine kinase inhibitor (TKI) is a multicenter observa

194 efitinib (Iressa, ZD-1839), a small molecule tyrosine kinase inhibitor (TKI) of the epidermal growth

195 The third-generation tyrosine kinase inhibitor (TKI) ponatinib shows activity

196 eport on the discovery of a new mechanism of tyrosine kinase inhibitor (TKI) resistance, which is med

197 erally associated with decreased response to tyrosine kinase inhibitor (TKI) therapy and adverse surv

198 n chronic myeloid leukemia (CML) patients on tyrosine kinase inhibitor (TKI) therapy and may promote

199 Because children with CML may receive tyrosine kinase inhibitor (TKI) therapy for many decades

200 Although tyrosine kinase inhibitor (TKI) therapy has improved cli

201 Tyrosine kinase inhibitor (TKI) therapy has led to subst

202 Discontinuation of tyrosine kinase inhibitor (TKI) therapy is feasible for

203 ll-cell lung cancer (NSCLC) are sensitive to tyrosine kinase inhibitor (TKI) therapy, but resistance

204 might have a central role in the response to tyrosine kinase inhibitor (TKI) therapy, we analyzed if

205 radiotherapy [WBRT]), and 86 of 90 received tyrosine kinase inhibitor (TKI) therapy.

206 on, have emerged over many years, the use of tyrosine kinase inhibitor (TKI) to counteract FGFR3 hype

207 Tyrosine kinase inhibitor (TKI) treatment of chronic mye

208 Their prevalence, response to tyrosine kinase inhibitor (TKI) treatment, and prognosti

209 ents at diagnosis and following conventional tyrosine kinase inhibitor (TKI) treatment.

210 so suspected with nilotinib, another BCR-ABL tyrosine kinase inhibitor (TKI) used in patients with CM

211 elatin nanocore encapsulated with gefitinib (tyrosine kinase inhibitor (TKI)) and surface functionali

212 data acquired in the presence of erlotinib-a tyrosine kinase inhibitor (TKI)-in cancer cells expressi

213 introduction of imatinib mesylate, the first tyrosine kinase inhibitor (TKI).

214 also enabled monitoring cell sensitivity to tyrosine kinase inhibitors (TKI) - a common drug used fo

215 olid tumors and clinical trials of selective tyrosine kinase inhibitors (TKI) are underway.

216 The BCR-ABL specific tyrosine kinase inhibitors (TKI) changed the outcome of

217 onic myelogenous leukemia (CML) with BCR-ABL tyrosine kinase inhibitors (TKI) fails to eliminate leuk

218 FMS-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibitors (TKI) have been tested extens

219 glioblastoma (GBM), but small-molecule EGFR tyrosine kinase inhibitors (TKI) have failed to yield du

220 Imatinib and other tyrosine kinase inhibitors (TKI) have improved treatment

221 h(+) ALL) is currently treated with BCR-ABL1 tyrosine kinase inhibitors (TKI) in combination with che

222 Antiangiogenic tyrosine kinase inhibitors (TKI) that target VEGF recept

223 g EGFR-mutant lung cancer patients with EGFR tyrosine kinase inhibitors (TKI), all patients eventuall

224 ctivating EGFR mutations become resistant to tyrosine kinase inhibitors (TKI), often through second-s

225 Mutant-selective EGFR tyrosine kinase inhibitors (TKI), such as osimertinib, a

226 tumor cells sensitive to treatment with EGFR tyrosine kinase inhibitors (TKI).

227 ion to the antiproliferative effects of EGFR tyrosine kinase inhibitors (TKI).

228 Tyrosine-kinase inhibitor (TKI) therapy for human cancer

229 xamined rates of initiation and adherence to tyrosine kinase inhibitors (TKIs) among Medicare benefic

230 as a novel pathway of acquired resistance to tyrosine kinase inhibitors (TKIs) and cytotoxic drugs in

231 the effect of ATP-competitive small molecule tyrosine kinase inhibitors (TKIs) and phosphatase-based

232 Tyrosine kinase inhibitors (TKIs) are anticancer drugs t

233 Several tyrosine kinase inhibitors (TKIs) are available for trea

234 Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are standard treatment

235 and epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) are treatment options

236 Tyrosine kinase inhibitors (TKIs) are used in the clinic

237 fers intrinsic resistance to small molecular tyrosine kinase inhibitors (TKIs) by concurrently stimul

238 Tyrosine kinase inhibitors (TKIs) directed against BCR-A

239 ermal growth factor receptor (EGFR)-directed tyrosine kinase inhibitors (TKIs) gefitinib, erlotinib a

240 The dramatic success of tyrosine kinase inhibitors (TKIs) has led to the widespr

241 omarkers to tailor patient therapy with EGFR tyrosine kinase inhibitors (TKIs) has revolutionised tre

242 The introduction of highly selective ABL-tyrosine kinase inhibitors (TKIs) has revolutionized the

243 cond- and/or third-generation c-Abl-specific tyrosine kinase inhibitors (TKIs) has substantially exte

244 Tyrosine kinase inhibitors (TKIs) have been used to trea

245 tion epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) have demonstrated pote

246 Tyrosine kinase inhibitors (TKIs) have increased surviva

247 most patients with chronic myeloid leukemia, tyrosine kinase inhibitors (TKIs) have turned a fatal di

248 BCR-ABL tyrosine kinase inhibitors (TKIs) imatinib and dasatinib

249 The introduction of protein tyrosine kinase inhibitors (TKIs) in 1998 transformed th

250 escribe how to detect changes in response to tyrosine kinase inhibitors (TKIs) in the phosphorylation

251 CML therapy based on tyrosine kinase inhibitors (TKIs) is highly effective in

252 Tyrosine kinase inhibitors (TKIs) of the EGF receptor (E

253 The development of BCR/ABL1 tyrosine kinase inhibitors (TKIs) over the past 20 years

254 ratification and response assessment between tyrosine kinase inhibitors (TKIs) sensitive and resistan

255 Imatinib mesylate and other tyrosine kinase inhibitors (TKIs) that target the kinase

256 Although tyrosine kinase inhibitors (TKIs) that target the kinase

257 (LSC)-directed therapy which may compliment tyrosine kinase inhibitors (TKIs) to eradicate LSC in ch

258 PM-ALK-amplified cell lines resistant to ALK tyrosine kinase inhibitors (TKIs) underwent apoptosis up

259 FLT3 tyrosine kinase inhibitors (TKIs) used as monotherapy al

260 The introduction of tyrosine kinase inhibitors (TKIs), a treatment of chroni

261 espite remarkable progress in treatment with tyrosine kinase inhibitors (TKIs), only 5% of patients a

262 Therapeutic benefits offered by tyrosine kinase inhibitors (TKIs), such as gefitinib (Ir

263 nt interaction between drug transporters and tyrosine kinase inhibitors (TKIs), which has uncovered w

264 lopment of resistance against promising EGFR tyrosine kinase inhibitors (TKIs).

265 efficacy of all targeted therapies including tyrosine kinase inhibitors (TKIs).

266 t alone or in combination with a low dose of tyrosine kinase inhibitors (TKIs).

267 s resistant to crizotinib and other anti-ALK tyrosine kinase inhibitors (TKIs).

268 chronic myeloid leukemia (CML) treated with tyrosine kinase inhibitors (TKIs).

269 c myeloid leukemia (CP-CML) are treated with tyrosine kinase inhibitors (TKIs).

270 hocytic leukemia/lymphoma 2 (BCL2), and many tyrosine kinase inhibitors (TKIs).

271 SCs that is enriched following therapy with tyrosine kinase inhibitors (TKIs).

272 IRC5) and attenuation of sensitivity to EGFR tyrosine kinase inhibitors (TKIs).

273 EGFR tyrosine-kinase inhibitors (TKIs) are given as a primary

274 with epidermal growth factor receptor (EGFR) tyrosine-kinase inhibitors (TKIs).

275 Imatinib was the first targeted tyrosine kinase inhibitor to be approved for clinical us

276 se inhibitor to block Notch activation and a tyrosine kinase inhibitor to inhibit ERBB3/2 elicits syn

277 ndings indicated that targeted delivery of a tyrosine kinase inhibitor to tumors can be used in a nov

278 Trials comparing the addition of tyrosine kinase inhibitors to conventional therapy are r

279 ly focused on the development of more potent tyrosine kinase inhibitors to suppress oncogenic signall

280 nd previous treatment with one or more VEGFR tyrosine-kinase inhibitors to receive 60 mg cabozantinib

281 xpression had reduced sensitivity to BCR-ABL tyrosine kinase inhibitor treatment but increased sensit

282 cell lung cancer are often resistant to EGFR tyrosine kinase inhibitor treatment.

283 (EGFR) mutations typically benefit from EGFR tyrosine kinase inhibitor treatment.

284 spectroscopy to predict skin toxicity due to tyrosine kinase inhibitors treatment.

285 leukemia (Ph(+) ALL) undergoing maintenance tyrosine-kinase inhibitor treatment, little is known abo

286 arcinoma who progressed after previous VEGFR tyrosine-kinase inhibitor treatment.

287 the emergence of mutant clones arising from tyrosine kinase inhibitor treatments.

288 We show that the known tyrosine kinase inhibitor tyrphostinA23, which is routin

289 eted antibody therapy (but not EGFR-targeted tyrosine-kinase inhibitors) was allowed.

290 Dasatinib, a potent and specific Src tyrosine kinase inhibitor, was found to decrease the lev

291 reening algorithms, bafetinib, a Bcr-Abl/Lyn tyrosine kinase inhibitor, was found to have inhibitory

292 With use of data from trials of tyrosine kinase inhibitors, we compared overall survival

293 Bruton tyrosine kinase inhibitors were active in progressive CL

294 ses of previous chemotherapy with or without tyrosine-kinase inhibitors were also eligible.

295 HER3 mAb) and erlotinib (EGFR small-molecule tyrosine kinase inhibitor) were marginal.

296 were co-treated with cisplatin plus an EGFR tyrosine kinase inhibitor, where receptor activation was

297 Sunitinib is a tyrosine kinase inhibitor which inhibits both VEGF and P

298 ed the possibility of therapeutic use of Bmx tyrosine kinase inhibitors, which we have addressed here

299 AZD3759 is a novel EGFR tyrosine kinase inhibitor with high capability to penetr

300 l glioma mouse model, we assessed a panel of tyrosine kinase inhibitors with different selectivity pr