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

1 mutant KIT and have durable response to KIT tyrosine kinase inhibitor.

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

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

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

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

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

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

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

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

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

11 ify previously unknown targets of a receptor tyrosine kinase inhibitor.

12 growth factor receptor (EGFR)-directed oral tyrosine kinase inhibitor.

13 ablated P-S6 and restored sensitivity to the tyrosine kinase inhibitor.

14 Acalabrutinib is a selective, potent Bruton tyrosine-kinase inhibitor.

15 7-ethyl-10-hydroxycamptothecin, and certain tyrosine kinase inhibitors.

16 ltimately indicate a class characteristic of tyrosine kinase inhibitors.

17 of dual ABCB1/ABCG2 substrate drugs, such as tyrosine kinase inhibitors.

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

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

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

21 stinal stromal tumour is highly resistant to tyrosine kinase inhibitors.

22 leukemia (ALL) have improved with the use of tyrosine kinase inhibitors.

23 lass fusions can be targeted successfully by tyrosine-kinase inhibitors.

24 PFS than those without these mutations after tyrosine kinase inhibitors (2.1 vs 3.7 months, p < 0.001

25 y and safety of ripretinib, a switch-control tyrosine kinase inhibitor active against a broad spectru

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

27 endothelial growth factor receptor (VEGF-R) tyrosine kinase inhibitors, although no prospective data

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

29 ng both BCRs and TLR-MyD88 by using Bruton's tyrosine kinase inhibitor and histone deacetylase inhibi

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

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

32 vascular endothelial growth factor receptor tyrosine kinase inhibitors and may help detect early evi

33 ositive) previously treated with one or more tyrosine kinase inhibitors and patients with baseline li

34 nges in ctDNA during systemic treatment with tyrosine kinase inhibitors and serves an unmet clinical

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

36 lphia chromosome-like ALL cases to ABL-class tyrosine kinase inhibitors, and CD19-positive and CD22-p

37 ic myeloid leukaemia treated with first-line tyrosine kinase inhibitors, and patients identified at t

38 nib is a novel second-generation oral Bruton tyrosine kinase inhibitor approved by the US Food and Dr

39 Tyrosine kinase inhibitors are widely used in the clinic

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

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

42 harboured alterations in genes targetable by tyrosine kinase inhibitors, as EGFR and MET.

43 The Janus kinase/spleen tyrosine kinase inhibitor ASN002 significantly suppresse

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

45 to assess the activity of the VEGF receptor tyrosine-kinase inhibitor axitinib plus the anti-PD-1 im

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

47 hese nine patients received one or more EGFR tyrosine kinase inhibitor before SCLC transformation.

48 tor (PI3K-deltai), umbralisib, plus a Bruton tyrosine kinase inhibitor (BTKi), ibrutinib, in relapsed

49 long-term follow-up data showing that Bruton tyrosine kinase inhibitors (BTKi's) are effective in chr

50 at COVID-19 diagnosis, most commonly Bruton tyrosine kinase inhibitors (BTKi's; n = 68/90 [76%]).

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

52 emonstrate that combination of IMC-targeting tyrosine kinase inhibitor cabozantinib and immune checkp

53 In this study, we discovered a multitargeted tyrosine kinase inhibitor, compound 15a, with potent inh

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

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

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

57 amplification received the irreversible EGFR tyrosine kinase inhibitor dacomitinib.

58 the dual mTORC1/2 inhibitor AZD2014 and the tyrosine kinase inhibitor dasatinib as monotherapies and

59 s differentiation step with an anti-fibrotic tyrosine kinase inhibitor decreases post-myocardial infa

60 o a subset of EGFR-mutant NSCLC to attenuate tyrosine kinase inhibitor delivery to the tumors by limi

61 eks of acalabrutinib, a more specific Bruton tyrosine kinase inhibitor, demonstrating that AF is an o

62 treated with regimens that do not contain a tyrosine-kinase inhibitor, despite the use of high-risk

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

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

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

66 sible, oral epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) that potently and s

67 Although new generations of EGFR-tyrosine kinase inhibitors (EGFR-TKI) have been develope

68 progressed epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) resistant LA patie

69 profile of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs).

70 -cell acute lymphocytic leukaemia in the pre-tyrosine-kinase inhibitor era.

71 The tyrosine kinase inhibitor erlotinib improves the outcome

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

73 The tyrosine kinase inhibitor erlotinib poorly penetrates th

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

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

76 genic drivers because administration of FGFR tyrosine kinase inhibitors (F-TKIs) can elicit meaningfu

77 clinical activity of small-molecule receptor tyrosine kinase inhibitors for oncogene-addicted subgrou

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 ween Oct 3, 2000, and Aug 28, 2018, in which tyrosine-kinase inhibitors had not been given as a first

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

85 Sunitinib (ST), a multitargeted receptor tyrosine kinase inhibitor, has been demonstrated to be e

86 Nintedanib, a tyrosine kinase inhibitor, has been shown to have antifi

87 Cediranib, a tyrosine-kinase inhibitor, has shown substantial activit

88 eral epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors have been developed and appro

89 Subsequent generations of tyrosine kinase inhibitors have improved these agents.

90 Tyrosine kinase inhibitors have provided an illustrative

91 in patients with EGFR mutations treated with tyrosine kinase inhibitors, HES1 protein levels increase

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

93 most patients now includes either the Bruton tyrosine kinase inhibitor ibrutinib or the B-cell lympho

94 on of targeted therapies, such as the Bruton tyrosine kinase inhibitor ibrutinib.

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

96 argeting drugs and found three host-directed tyrosine kinase inhibitors (Ibrutinib, Dasatinib and Cri

97 herapy, FGF/FGFR blockade by FGF trapping or tyrosine kinase inhibitor impaired the growth and dissem

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

99 The clinical evidence for the success of tyrosine kinase inhibitors in combination with microtubu

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

101 sequencing approaches to assess responses to tyrosine kinase inhibitors in patients with advanced lun

102 n BCR-ABL1 are associated with resistance to tyrosine kinase inhibitors in patients with chronic myel

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

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

105 y and safety of nintedanib, an intracellular tyrosine kinase inhibitor, in patients with idiopathic p

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

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

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

109 and schedule optimization of treatment with tyrosine kinase inhibitors is of utmost importance.

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

111 nib, a mutant-specific third-generation EGFR tyrosine kinase inhibitor, is emerging as the preferred

112 phase II trial evaluating the multitargeted tyrosine kinase inhibitor lenvatinib in patients with R/

113 Among those, the tyrosine kinase inhibitor lestaurtinib was highest ranke

114 Finally, bosutinib, a tyrosine kinase inhibitor, markedly reduced the level of

115 ta are available, second-line therapy with a tyrosine kinase inhibitor may be recommended for appropr

116 exed and carboplatin chemotherapy to an oral tyrosine kinase inhibitor may improve outcomes.

117 that treatment with a VEGF receptor (VEGFR) tyrosine kinase inhibitor might be effective in patients

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

119 Tyrosine kinase inhibitors might still have potential in

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

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

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

123 The tyrosine kinase inhibitor neratinib is a human epidermal

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

125 overexpression counteracts the effects of a tyrosine kinase inhibitor, Nilotinib, while USP13 knockd

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

127 mTOR inhibitor, sirolimus, and the receptor tyrosine kinase inhibitor, nintedanib, could synergistic

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

129 le in vitro data of treatment with different tyrosine kinase inhibitors of BT-20 triple-negative brea

130 Although the use of ATP-competitive tyrosine kinase inhibitors of oncoprotein BCR-ABL1 has e

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

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

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

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

135 combination immune checkpoint inhibitor and tyrosine-kinase inhibitors or VEGF inhibitors for increa

136 ither progressed on imatinib and one or more tyrosine kinase inhibitor, or only received imatinib pre

137 hat differ in their mechanism of action (the tyrosine kinase inhibitor pazopanib in MKN45 gastric car

138 Finally, combining FLT3 tyrosine kinase inhibitor PKC412 with MS023 treatment en

139 Although tyrosine kinase inhibitors provide an effective treatmen

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

141 Fostamatinib is a spleen tyrosine kinase inhibitor recently approved for the trea

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

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

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

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

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

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

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

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

150 emia burden in mice injected with de novo or tyrosine kinase inhibitor-resistant primary Ph+ ALL cell

151 Importantly, we showed that tyrosine kinase inhibitor-resistant tumors, with EGFRT79

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

153 Small-molecule tyrosine kinase inhibitors seem well suited to be tailor

154 nts without mutation and six patients with a tyrosine kinase inhibitor-sensitive mutation, p=0.0031).

155 1 year of neratinib, an irreversible pan-HER tyrosine kinase inhibitor, significantly improves 2-year

156 Although the multi-tyrosine kinase inhibitor sorafenib is useful in the tre

157 g FLT3 inhibitors, such as the multitargeted tyrosine kinase inhibitor sorafenib, improves outcome af

158 y approved first-line treatment is the multi-tyrosine kinase inhibitor sorafenib, which shows low res

159 ications to atezolizumab and/or bevacizumab, tyrosine kinase inhibitors sorafenib or lenvatinib may b

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

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

162 Tyrosine kinase inhibitors such as gefitinib, erlotinib,

163 The long-term effectiveness of tyrosine kinase inhibitors such as the EGFR inhibitor (E

164 man BC models to Erlotinib, a selective EGFR tyrosine kinase inhibitor, suggesting a promising combin

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

166 r endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor sunitinib have shown positive

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

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

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

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

171 Here, we tested the effect of tyrosine kinase inhibitors targeting the ErbB receptors

172 was significantly better with crizotinib (a tyrosine kinase inhibitor) than with the combination of

173 Here we report incorporation of sunitinib, a tyrosine kinase inhibitor that blocks VEGF receptors, in

174 h-dose (10 uM) crizotinib as an ICD-inducing tyrosine kinase inhibitor that has exceptional antineopl

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

176 We identified several tyrosine kinase inhibitors that inhibit CAR T-cell cytot

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

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

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

180 ell lymphoma following prior failed Bruton's tyrosine kinase inhibitor therapy, with an overall respo

181 ing NGS, irrespective of patient response to tyrosine kinase inhibitor therapy.

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

183 f 2 or less, and received no previous Bruton tyrosine-kinase inhibitor therapy.

184 ntually develop drug resistance against EGFR tyrosine-kinase inhibitors; therefore, better understand

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

186 The irreversible ErbB family tyrosine kinase inhibitor (TKI) afatinib plus the EGFR m

187 The development of the tyrosine kinase inhibitor (TKI) imatinib allows patients

188 an therefore be effectively treated with the tyrosine kinase inhibitor (TKI) imatinib mesylate.

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

190 nce was abrogated by treatment with the FGFR tyrosine kinase inhibitor (TKI) lucitanib.

191 The third-generation tyrosine kinase inhibitor (TKI) ponatinib has been assoc

192 RELAY assessed erlotinib, an EGFR tyrosine kinase inhibitor (TKI) standard of care, plus r

193 a potent, brain-penetrant, third-generation tyrosine kinase inhibitor (TKI) that targets ALK and ROS

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

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

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

197 R-ABL1 point mutation-mediated resistance to tyrosine kinase inhibitor (TKI) therapy in Philadelphia

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

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

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

201 ponse leading to discontinuation of BCR-ABL1 tyrosine kinase inhibitor (TKI) therapy-has become a pot

202 chronic myeloid leukaemia have discontinued tyrosine kinase inhibitor (TKI) treatment abruptly and h

203 Tyrosine kinase inhibitor (TKI) treatment of chronic mye

204 wing epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment of EGFR-mutant

205 risk of molecular recurrence after stopping tyrosine kinase inhibitor (TKI) treatment substantially

206 vivo deletion of alpha6 in combination with tyrosine kinase inhibitor (TKI) treatment was more effec

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

208 t role in disease control and maintenance of tyrosine kinase inhibitor (TKI)-free remission in chroni

209 activity in various cancer models, including tyrosine kinase inhibitor (TKI)-resistant EGFR-mutant no

210 identified that exhibited potent activity in tyrosine kinase inhibitor (TKI)-sensitive and TKI-resist

211 Evolved resistance to tyrosine kinase inhibitor (TKI)-targeted therapies remai

212 also seen with direct KIT inhibition using a tyrosine kinase inhibitor (TKI).

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

214 measures of ctDNA with clinical responses to tyrosine kinase inhibitors (TKI) and immune checkpoint i

215 KIT tyrosine kinase inhibitors (TKI) are superior to convent

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

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

218 Tyrosine kinase inhibitors (TKI) have significantly incr

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

220 s in EGFR are proven therapeutic targets for tyrosine kinase inhibitors (TKI) in lung adenocarcinoma,

221 ents with cancer treated with small-molecule tyrosine kinase inhibitors (TKI) remains controversial.

222 Consequently, tyrosine kinase inhibitors (TKI) targeting the EGFR are

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

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

225 astatic melanoma using immune checkpoint and tyrosine kinase inhibitors (TKI), the majority of stage

226 n of molecularly targeted therapies, such as tyrosine kinase inhibitors (TKI), with concurrent chemot

227 ate primary and secondary resistance to EGFR tyrosine kinase inhibitors (TKI).

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

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

230 ey obstacle to the clinical efficacy of EGFR tyrosine kinase inhibitors (TKI).

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

232 FLT3 receptor, including small-molecule FLT3 tyrosine kinase inhibitors (TKIs) and anti-FLT3 antibodi

233 s have investigated the benefit of combining tyrosine kinase inhibitors (TKIs) and cytoreductive neph

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

235 t with the highly effective CML therapeutics tyrosine kinase inhibitors (TKIs) and interferon-alpha (

236 While tumor responses to tyrosine kinase inhibitors (TKIs) are accompanied by mar

237 Accordingly, FGFR targeted tyrosine kinase inhibitors (TKIs) are currently under de

238 low response rate of those patients to EGFR tyrosine kinase inhibitors (TKIs) are not well understoo

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

240 ROS1-directed tyrosine kinase inhibitors (TKIs) are therapeutically ac

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

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

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

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

245 Multiple clinically relevant RET protein-tyrosine kinase inhibitors (TKIs) have been identified,

246 The development of resistance to EGFR Tyrosine kinase inhibitors (TKIs) in NSCLC with activati

247 fferential sensitivities to eleven EGFR/HER2 tyrosine kinase inhibitors (TKIs) in vitro, and molecula

248 Tyrosine kinase inhibitors (TKIs) induce molecular remis

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

250 In chronic myeloid leukemia (CML) patients, tyrosine kinase inhibitors (TKIs) may select for drug-re

251 Tumor resistance to EGFR tyrosine kinase inhibitors (TKIs) occurs invariably, and

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

253 Preclinical data suggest that EGFR tyrosine kinase inhibitors (TKIs) plus MET TKIs are a po

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

255 vestigating the potential of the addition of tyrosine kinase inhibitors (TKIs) to chemotherapy to imp

256 tcome of most patients with CML treated with tyrosine kinase inhibitors (TKIs), a greater number of c

257 yeloid leukemia (CML) in adults treated with tyrosine kinase inhibitors (TKIs), but the rarity of thi

258 owever, enable them to develop resistance to tyrosine kinase inhibitors (TKIs), even when these are m

259 tor (EGFR) mutations spurred the use of EGFR tyrosine kinase inhibitors (TKIs), such as erlotinib, as

260 Tyrosine kinase inhibitors (TKIs), the treatment of choi

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

262 kemia cells, and protect leukemia cells from tyrosine kinase inhibitors (TKIs).

263 BL) oncogene and is effectively treated with tyrosine kinase inhibitors (TKIs).

264 r endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs).

265 GFR-mutant NSCLCs frequently respond to EGFR tyrosine kinase inhibitors (TKIs).

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

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

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

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

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

271 velop drug resistance when treated with EGFR tyrosine kinase inhibitors (TKIs).

272 -185 levels anticipate their response to ABL tyrosine kinase inhibitors (TKIs).

273 ll lymphoma (ALCL) resistant to ALK-specific tyrosine kinase inhibitors (TKIs).

274 significantly benefited from the use of EGFR tyrosine kinase inhibitors (TKIs).

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

276 ed in non-small cell lung cancer, NSCLC, are tyrosine kinase inhibitors, TKIs, and immune checkpoint

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 vations demonstrate a potential for the ErbB tyrosine kinase inhibitors to induce neuromuscular toxic

280 ained release platform for local delivery of tyrosine kinase inhibitors to treat corneal NV.

281 of (68)Ga-NeoBOMB1 in patients with advanced tyrosine-kinase inhibitors-treated GIST using PET/CT.

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

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

284 ilable at 3 months after starting first-line tyrosine kinase inhibitor treatment; all four subsequent

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

286 aluating the potential benefit of first-line tyrosine-kinase inhibitor treatment in patients with ABL

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

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

289 Tyrosine kinase inhibitors (TyKIs) approach disease gene

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

291 The activity of MET tyrosine kinase inhibitors varies by MET alteration cate

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

293 Lenvatinib, another tyrosine-kinase inhibitor, was found to be non-inferior

294 Bruton tyrosine kinase inhibitors were active in progressive CL

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

296 e compound osimertinib is a third-generation tyrosine kinase inhibitor, which was granted full FDA ap

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

298 Ibrutinib is a Bruton tyrosine kinase inhibitor with remarkable efficacy again

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

300 calabrutinib is a selective, covalent Bruton tyrosine-kinase inhibitor with activity in chronic lymph