ライフサイエンスコーパス: TKI

1 TKI treatment favored selection of lung cancer cells dis

2 TKI treatment was de-escalated to half the standard dose

3 TKI treatment was not associated with an increased posto

4 TKIs do not eliminate disease-propagating leukemic stem

5 achieved in seven (64%; 95% CI 31-89) of 11 TKI-naive patients and 12 (50%; 29-71) of 24 previous cr

6 13 (62%; 95% CI 38-82) of 21 TKI-naive patients and 14 (35%; 21-52) of 40 patients pr

7 ic to pediatric patients, the selection of a TKI continues to rely on clinical experience in adults.

8 ive in eradicating ALL than treatment with a TKI (nilotinib) alone.

9 population that is the precursor of acquired TKI resistance.

10 ies in patients with CML not only may affect TKI selection but also demands close monitoring of the o

11 n signaling emerge in lung cancers to affect TKI tolerance and lung cancer dissemination has yet to b

12 courses had been quantified before and after TKI cessation.

13 Here we reveal the mechanism of ALK-TKI addiction in ALCL.

14 1 overactivation is the key mechanism of ALK-TKI addiction in ALCL.

15 On unadjusted analysis, TKI use prior to CN was associated with higher overall c

16 Combination treatment with BBI and TKI led to superior cytotoxic effects in vitro and in vi

17 mal phenotype diminished SOX2 expression and TKI sensitivity, whereas SOX2 silencing induced vimentin

18 ling affects lung cancer cell plasticity and TKI tolerance.

19 yrosine kinase inhibitor (TKI)-sensitive and TKI-resistant NSCLC cells (IC(50) = 77 nM) and in xenogr

20 lly, PTN promoted CML stem cell survival and TKI resistance via induction of Jun and the unfolded pro

21 if the patients are not switched to another TKI or if they are switched to a inappropriate TKI or TK

22 responses, enabling more patients to attempt TKI discontinuation.

23 etion of Cxcl12 increases LSC elimination by TKI treatment.

24 t from intermittent compared with continuous TKI dosing.

25 Some patients develop TKI resistance without known resistance mutations, with

26 tic model to consider the value of different TKI approaches from the payer's perspective.

27 diators in GISTs that have converted, during TKI-therapy, to a KIT-independent state.

28 CIN significantly increased during TKI treatment in T790M-negative patients and is a candid

29 and persistent tumor cell population during TKI treatment can inform combination treatment strategie

30 mall-molecule inhibitor BGJ398 enhanced EGFR TKI sensitivity and promoted upregulation of BIM levels.

31 or G-alpha protein activation, enhanced EGFR TKI-induced cell death.

32 ockade of ERK1/2 reactivation following EGFR TKI treatment by combined EGFR/MEK inhibition uncovers c

33 viously treated with a third-generation EGFR TKI (B1) and those who had not been previously treated w

34 previously received a third-generation EGFR TKI and were Thr790Met negative; these patients received

35 viously treated with a third-generation EGFR TKI who were either Thr790Met negative (B2) or Thr790Met

36 I, plus osimertinib, a third-generation EGFR TKI, have provided recommended doses for study.

37 As the third generation EGFR TKI, osimertinib, has now been adopted in the first-line

38 pharmacological inhibition of TWIST1 in EGFR TKI-resistant EGFR-mutant cells increased sensitivity to

39 PK activators synergistically increases EGFR TKI sensitivity.

40 own of FGFR1 attenuated hypoxia-induced EGFR TKI resistance in each line.

41 itor treatment overcame TWIST1-mediated EGFR TKI resistance and were more effective in the setting of

42 TWIST1-mediated EGFR TKI resistance was due in part to TWIST1 suppression of

43 ng EGFR(WT) and that the combination of EGFR TKI and AMPK activator may be a potentially effective th

44 The combination of EGFR TKI and FGFR1 or MEK inhibitors may offer an attractive

45 ing to identify genetic determinants of EGFR TKI sensitivity and uncovered putative candidates.

46 f previously unidentified regulators of EGFR TKI sensitivity in EGFR-mutant human NSCLC, providing in

47 ding insights into the heterogeneity of EGFR TKI treatment responses.

48 Moreover, combined treatment of EGFR TKI with AMPK activators synergistically increases EGFR

49 ling, where a subsequent combination of EGFR TKI with FGFR1 inhibitors or MEK inhibitors reverses thi

50 biopsies of patients who progressed on EGFR TKI as surrogates for persister populations, we performe

51 vestigated a novel strategy to overcome EGFR TKI resistance through targeting the EMT-TF, TWIST1, in

52 t LKB1 may serve as a marker to predict EGFR TKI sensitivity in smokers with NSCLC carrying EGFR(WT)

53 udy, had shown resistance to a previous EGFR TKI, and had EGFR-activating mutations and acquired Thr7

54 o had disease progression on a previous EGFR TKI.

55 rate hypoxia promotes resistance to the EGFR TKI osimertinib (AZD9291) in the non-small cell lung can

56 naling, activation of which rescued the EGFR TKI sensitizing phenotype resulting from RIC8A knockout.

57 cells with wild-type EGFR (EGFR(WT)) to EGFR TKI by repressing expression of liver kinase B1 (LKB1),

58 dence for the reversal of resistance to EGFR TKI by the addition of small molecule S6K1/MDM2 antagoni

59 Time-to-treatment failure (TTF) to EGFR TKI in patients identified as MET-high and -low was esti

60 Hypoxia-induced resistance to EGFR TKI is driven by overexpression of FGFR1 to sustain ERK

61 ports of FGFR signaling contributing to EGFR TKI resistance in vitro exist, the data have not yet bee

62 a candidate mechanism for resistance to EGFR TKI therapy was investigated by interrogation of public

63 al response (TTF, 1.0 to 6.4 months) to EGFR TKI was observed in patients with coexisting MET amplifi

64 nger be inhibited by currently approved EGFR TKIs.

65 acquired resistance to first generation EGFR TKIs including EMT are now being observed at an increase

66 ll-cell lung cancer (NSCLC), failure of EGFR TKIs can result from both genetic and epigenetic mechani

67 lowed by large-scale clinical trials of EGFR TKIs demonstrating the emergence of RTK fusions in AR.

68 hese fusion events by the generation of EGFR TKIs, the specific RTK fusions and their fusion partners

69 cell lung cancer, who had progressed on EGFR TKIs.

70 ish TWIST1 as a driver of resistance to EGFR TKIs and provide rationale for use of TWIST1 inhibitors

71 riving force for acquired resistance to EGFR TKIs through increased expression of FGFR1.

72 s drivers of EMT-mediated resistance to EGFR TKIs, however, strategies to target EMT-TFs are lacking.

73 viously shown to overcome resistance to EGFR TKIs.

74 patients with MET-driven resistance to EGFR TKIs.

75 ide genetic mechanisms of resistance to EGFR TKIs.

76 to overcome EMT-mediated resistance to EGFR TKIs.

77 R-mutant cells increased sensitivity to EGFR TKIs.

78 in vivo models restores sensitivity to EGFR TKIs.

79 The FDA AERS database contained 27,123 EGFR-TKI-associated AERs within the reporting period from Jan

80 th advanced EGFR-TKI-naive NSCLC and 15 EGFR-TKI-resistant patients to identify somatic SNVs, small i

81 e a total of 119 patients with advanced EGFR-TKI-naive NSCLC and 15 EGFR-TKI-resistant patients to id

82 mulation and epigenetic control affects EGFR-TKI tolerance and cancer dissemination.

83 d by SOX2 and TGFbeta signaling affects EGFR-TKI tolerance and lung cancer dissemination.

84 e use of Apatinib Mesylate (AM) against EGFR-TKI resistance in lung adenocarcinoma (LA) patients.

85 EGFR revealed synergy when combining an EGFR-TKI with inhibitors of proximal signaling intermediates

86 potently and selectively inhibits both EGFR-TKI-sensitizing and T790M resistance mutations.

87 SRS followed by EGFR-TKI resulted in the longest OS and allowed patients to a

88 followed by EGFR-TKI, WBRT followed by EGFR-TKI, or EGFR-TKI followed by SRS or WBRT at intracranial

89 ients were treated with SRS followed by EGFR-TKI, WBRT followed by EGFR-TKI, or EGFR-TKI followed by

90 such as EGFR secondary mutation causing EGFR-TKI resistance, compensatory activation of signaling pat

91 vanced progressed LA patients to combat EGFR-TKI resistance.

92 LAURA (osimertinib, n = 279; comparator EGFR-TKI, n = 277) and AURA3 (osimertinib, n = 279; chemother

93 multiple parallel RTKs further enhances EGFR-TKI effectiveness.

94 addition to seeking for next-generation EGFR-TKI, developing novel EGFR-targeting strategies may hold

95 tor receptor tyrosine kinase inhibitor (EGFR-TKI) that potently and selectively inhibits both EGFR-TK

96 ons of EGFR-tyrosine kinase inhibitors (EGFR-TKI) have been developed for the treatment of patients w

97 or receptor tyrosine kinase inhibitors (EGFR-TKI) resistant LA patients.

98 might be an optional method to monitor EGFR-TKI resistance and to discover mechanisms of drug resist

99 The third-generation of EGFR-TKI osimertinib has been approved as a first-line therap

100 and serves as an alternative target of EGFR-TKI resistance in NSCLC.

101 bypass mechanism for the development of EGFR-TKI resistance.

102 EGFR-TKI, WBRT followed by EGFR-TKI, or EGFR-TKI followed by SRS or WBRT at intracranial progression.

103 Exclusion criteria included prior EGFR-TKI use, EGFR-TKI resistance mutation, failure to receiv

104 resistance mutation, failure to receive EGFR-TKI after WBRT/SRS, or insufficient follow-up.

105 to identify NSCLC patients sensitive to EGFR-TKI or ICI-treatments.

106 n criteria included prior EGFR-TKI use, EGFR-TKI resistance mutation, failure to receive EGFR-TKI aft

107 lysis, SRS versus EGFR-TKI, WBRT versus EGFR-TKI, age, performance status, EGFR exon 19 mutation, and

108 On multivariable analysis, SRS versus EGFR-TKI, WBRT versus EGFR-TKI, age, performance status, EGFR

109 OS1 inhibition strongly synergized with EGFR-TKI treatment only in 3D spheroid cultures.

110 nd in 46.7% (7/15) of the patients with EGFR-TKI-resistant NSCLC, suggesting that the NGS-based ctDNA

111 In EGFR-mutated lung adenocarcinoma, EGFR-TKIs show enhanced efficacy in spheroid cultures.

112 or receptor-tyrosine kinase inhibitors (EGFR-TKIs).

113 analysis of the adverse events (AEs) of EGFR-TKIs (gefitinib, erlotinib, afatinib, osimertinib) by da

114 associated with acquired resistance to EGFR-TKIs such as erlotinib remains an unmet need and a thera

115 g PFKFB3 inhibitors in combination with EGFR-TKIs to manage NSCLC.

116 survival (PFS) in patients treated with EGFR-TKIs, while EGFR-DLS is significantly and negatively ass

117 served in MMR and MR(4.5) is not an entirely TKI-mediated effect.

118 Combining catalytic suppression by the F-TKI BGJ398 with HSP90 blockade by ganetespib suppressed

119 ration of FGFR tyrosine kinase inhibitors (F-TKIs) can elicit meaningful objective clinical responses

120 vitro analyses showed that AZD4547, an FGFR TKI currently in clinical trials for breast cancer, decr

121 Addition of the FGFR TKI erdafitinib to palbociclib/fulvestrant induced compl

122 However, the efficacy of FGFR TKIs in the bone microenvironment where breast cancer ce

123 nges in the BCR-ABL1 dynamics resulting from TKI dose reduction convey information about the patient-

124 of the development of targeted therapy, from TKIs to targeted immunotherapy.

125 ntial benefit in favour of second-generation TKI (willingness to pay $200 000 per QALY, 66% of patien

126 resistance mechanism to the first-generation TKIs.

127 -1) and the annual cost of second-generation TKIs (base case US$152 814 [ie, the price of nilotinib i

128 ring the current prices of second-generation TKIs and of generic imatinib under different pricing sce

129 ric imatinib, the value of second-generation TKIs as frontline therapy for this particular treatment

130 $22 765 208, meaning that second-generation TKIs as frontline therapy to achieve sustained deep mole

131 hieving such response with second-generation TKIs at 66%, 88%, and a near-perfect response of 99%.

132 and developing countries, second-generation TKIs at current prices do not offer good value as frontl

133 treatment value for use of second-generation TKIs at the current prices in the USA or at the price of

134 the cost-effectiveness of second-generation TKIs compared with generic imatinib.

135 pediatric CML in 2003, the second-generation TKIs dasatinib and nilotinib were recently approved for

136 Highly priced second-generation TKIs might offer deep molecular response status more qui

137 ontline CML treatment with second-generation TKIs produces deeper molecular responses, driving diseas

138 QALY, the annual price of second-generation TKIs should not exceed $10 000 per year of therapy.

139 ess the potential value of second-generation TKIs used as frontline therapy in patients with chronic

140 scenario in the USA using second-generation TKIs versus imatinib (annual price $4400 per year) with

141 phase of 0.1), the cost of second-generation TKIs would need to be less than $25 000 per year to be a

142 with imatinib and 44% with second-generation TKIs.

143 resistance, and second- and third-generation TKIs largely mitigate this problem.

144 ibitors (TKIs) have been identified, but how TKIs bind to RET is unknown except for vandetanib.

145 However, TKI are not yet curative, because most patients retain l

146 rexpression increased EGFR levels, improving TKI tolerance, whereas SMURF2 knockdown decreased EGFR s

147 in vivo, with BBI preventing tumor growth in TKI-resistant xenografts.

148 The role of S6K1 in TKI resistance was determined in in vitro gain-and-loss

149 I or if they are switched to a inappropriate TKI or TKI dose.

150 enografts harboring EGFR mutations including TKI-resistant T790M.

151 ransdifferentiation accompanied by increased TKI tolerance, which can interfere with ectopic SOX2 exp

152 lls hinders cure and necessitates indefinite TKI therapy.

153 sible ErbB family tyrosine kinase inhibitor (TKI) afatinib plus the EGFR monoclonal antibody cetuxima

154 evelopment of the tyrosine kinase inhibitor (TKI) imatinib allows patients with CML to experience nea

155 treated with the tyrosine kinase inhibitor (TKI) imatinib mesylate.

156 ent with the FGFR tyrosine kinase inhibitor (TKI) lucitanib.

157 third-generation tyrosine kinase inhibitor (TKI) ponatinib has been associated with high rates of ac

158 rlotinib, an EGFR tyrosine kinase inhibitor (TKI) standard of care, plus ramucirumab, a human IgG1 VE

159 third-generation tyrosine kinase inhibitor (TKI) that targets ALK and ROS1 with preclinical activity

160 ted resistance to tyrosine kinase inhibitor (TKI) therapy in Philadelphia chromosome-positive (Ph(+))

161 ation of BCR-ABL1 tyrosine kinase inhibitor (TKI) therapy-has become a potential aim of therapy.

162 have discontinued tyrosine kinase inhibitor (TKI) treatment abruptly and have focussed on patients wi

163 r receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment of EGFR-mutant non-small cell lung cancer

164 ce after stopping tyrosine kinase inhibitor (TKI) treatment substantially depends on an individual's

165 combination with tyrosine kinase inhibitor (TKI) treatment was more effective in eradicating ALL tha

166 wing conventional tyrosine kinase inhibitor (TKI) treatment.

167 nd maintenance of tyrosine kinase inhibitor (TKI)-free remission in chronic myeloid leukemia (CML).

168 models, including tyrosine kinase inhibitor (TKI)-resistant EGFR-mutant non-small-cell lung cancers.

169 otent activity in tyrosine kinase inhibitor (TKI)-sensitive and TKI-resistant NSCLC cells (IC(50) = 7

170 ved resistance to tyrosine kinase inhibitor (TKI)-targeted therapies remains a major clinical challen

171 nhibition using a tyrosine kinase inhibitor (TKI).

172 cal responses to tyrosine kinase inhibitors (TKI) and immune checkpoint inhibitors, respectively, in

173 KIT tyrosine kinase inhibitors (TKI) are superior to conventional chemotherapy in their

174 Tyrosine kinase inhibitors (TKI) have significantly increased survival of patients w

175 utic targets for tyrosine kinase inhibitors (TKI) in lung adenocarcinoma, but acquired resistance to

176 h small-molecule tyrosine kinase inhibitors (TKI) remains controversial.

177 Consequently, tyrosine kinase inhibitors (TKI) targeting the EGFR are among the most effective the

178 t-selective EGFR tyrosine kinase inhibitors (TKI), such as osimertinib, are active agents for the tre

179 e checkpoint and tyrosine kinase inhibitors (TKI), the majority of stage IV melanoma patients eventua

180 erapies, such as tyrosine kinase inhibitors (TKI), with concurrent chemotherapy and radiation (CRT) t

181 sistance to EGFR tyrosine kinase inhibitors (TKI).

182 atment with EGFR tyrosine kinase inhibitors (TKI).

183 efficacy of EGFR tyrosine kinase inhibitors (TKI).

184 creasingly potent tyrosine kinas inhibitors (TKIs) has revolutionized therapy.

185 ll-molecule FLT3 tyrosine kinase inhibitors (TKIs) and anti-FLT3 antibodies, have demonstrated promis

186 fit of combining tyrosine kinase inhibitors (TKIs) and cytoreductive nephrectomy (CN) in patients wit

187 CML therapeutics tyrosine kinase inhibitors (TKIs) and interferon-alpha (IFNalpha).

188 mor responses to tyrosine kinase inhibitors (TKIs) are accompanied by marked tumor shrinkage, the res

189 y, FGFR targeted tyrosine kinase inhibitors (TKIs) are currently under development.

190 patients to EGFR tyrosine kinase inhibitors (TKIs) are not well understood.

191 ROS1-directed tyrosine kinase inhibitors (TKIs) are therapeutically active against these cancers,

192 vant RET protein-tyrosine kinase inhibitors (TKIs) have been identified, but how TKIs bind to RET is

193 sistance to EGFR Tyrosine kinase inhibitors (TKIs) in NSCLC with activating EGFR mutations is a criti

194 eleven EGFR/HER2 tyrosine kinase inhibitors (TKIs) in vitro, and molecular dynamics simulations revea

195 Tyrosine kinase inhibitors (TKIs) induce molecular remission in the majority of pati

196 (CML) patients, tyrosine kinase inhibitors (TKIs) may select for drug-resistant BCR-ABL1 kinase doma

197 sistance to EGFR tyrosine kinase inhibitors (TKIs) occurs invariably, and receptor tyrosine kinase (R

198 Tyrosine kinase inhibitors (TKIs) of the EGF receptor (EGFR) have provided a signifi

199 uggest that EGFR tyrosine kinase inhibitors (TKIs) plus MET TKIs are a possible treatment for EGFR mu

200 the addition of tyrosine kinase inhibitors (TKIs) to chemotherapy to improve clinical outcomes.

201 CML treated with tyrosine kinase inhibitors (TKIs), a greater number of comorbidities might be the mo

202 lts treated with tyrosine kinase inhibitors (TKIs), but the rarity of this leukemia in children and a

203 op resistance to tyrosine kinase inhibitors (TKIs), even when these are multitargeted or applied in c

204 the use of EGFR tyrosine kinase inhibitors (TKIs), such as erlotinib, as the first-line treatment of

205 Tyrosine kinase inhibitors (TKIs), the treatment of choice for chronic myeloid leuka

206 to ALK-specific tyrosine kinase inhibitors (TKIs).

207 the use of EGFR tyrosine kinase inhibitors (TKIs).

208 kemia cells from tyrosine kinase inhibitors (TKIs).

209 ely treated with tyrosine kinase inhibitors (TKIs).

210 respond to EGFR tyrosine kinase inhibitors (TKIs).

211 receptor (VEGFR) tyrosine kinase inhibitors (TKIs).

212 reated with EGFR tyrosine kinase inhibitors (TKIs).

213 response to ABL tyrosine kinase inhibitors (TKIs).

214 ncer, NSCLC, are tyrosine kinase inhibitors, TKIs, and immune checkpoint inhibitors, ICIs.

215 relation-driven topological Kondo insulator (TKI) with exotic ground states.

216 Interestingly, TKIs modulated the chemokine receptor repertoire of immu

217 arise (or that are selected for) during KIT TKI treatment.

218 To overcome the problem of KIT TKI resistance, we sought to identify novel therapeutic

219 nt cancer, particularly after failure of KIT TKIs.

220 ssociated with decreased affinity for larger TKIs.

221 s sensitivity to approved second-/third-line TKIs but shows high inter- and intratumoral heterogeneit

222 ovalent, wild-type EGFR sparing, macrocyclic TKI.

223 M2 is a downstream effector of S6K1-mediated TKI resistance.

224 MPL-504, volitinib), a potent, selective MET TKI, plus osimertinib, a third-generation EGFR TKI, have

225 R tyrosine kinase inhibitors (TKIs) plus MET TKIs are a possible treatment for EGFR mutation-positive

226 However, the scarcity of model TKI material families leaves difficulties in disentangli

227 The most TKI-insensitive cells of the LSC compartment can be capt

228 PI3K, and "BCR-like" signaling with multiple TKIs and/or dexamethasone prevented this signaling plast

229 Although up to 26% of TKI-naive EGFR-mutant-positive NSCLC harbor high MET CNG

230 old the key to overcome the vicious cycle of TKI resistance.

231 ly reported that differential degradation of TKI-sensitive (e.g. L858R) and resistant (T790M) EGFR mu

232 671 synergistically enhanced the efficacy of TKI without showing toxicity.

233 cl12 expression in maintaining quiescence of TKI-resistant LSC populations.

234 The withdrawal of TKI from addicted tumors in vitro and in vivo leads to o

235 ho stopped therapy after at least 3 years of TKI treatment and in molecular response 4.5 (MR4.5) with

236 ows clinicians to optimize administration of TKIs before chemoradiotherapy in oncogene-driven NSCLC.

237 tter interpreting the off-target efficacy of TKIs in tumors and to envisaging strategies aimed at fac

238 o determine whether the perioperative use of TKIs increases the postoperative morbidity following CN

239 T cells persisted in pre-MMR CML patients on TKI.

240 iously treated with crizotinib as their only TKI had an objective response.

241 previously received crizotinib as their only TKI, and eight (12%) had previously received one non-cri

242 they are switched to a inappropriate TKI or TKI dose.

243 who develop resistance to imatinib and other TKIs used to treat this disease.

244 inhibitors as promising strategy to overcome TKI resistance in GIST, while highlighting the complexit

245 plex may be an attractive target to overcome TKI resistance.

246 n to the formidable challenges of overcoming TKI resistance and treating the TKI-resistant BMs.

247 On multivariate analysis, perioperative TKI use was independently associated with higher risk fo

248 owever, with the introduction of more potent TKIs and other novel agents, as well as better methods f

249 is applicable for young patients and primary TKI-resistant, intolerant, or allograft candidate patien

250 t decrease drug binding affinity can produce TKI resistance, and second- and third-generation TKIs la

251 mmunotherapeutic approaches that may prolong TKI-free survival and even mediate cure of CML patients.

252 suppressed BCL2L11, expression and promoted TKI tolerance.

253 expression, whereas SOX2 expression promoted TKI sensitivity and inhibited the mesenchymal phenotype.

254 mia in first chronic phase, who had received TKI therapy for 3 years or more, with three or more BCR-

255 SCLC) population with mutated EGFR receiving TKIs and CRT.

256 ore than 50% of patients relapse and restart TKI, subsequently suffering unknown toxicity.

257 Nintedanib is a RET TKI that inhibits the vandetanib-resistant RET(G810A) mu

258 previously received one non-crizotinib ROS1 TKI or two or more ROS1 TKIs.

259 highlighting the utility of sequential ROS1 TKI therapy.

260 Higher-affinity next-generation ROS1 TKIs developed to have improved intracranial activity an

261 non-crizotinib ROS1 TKI or two or more ROS1 TKIs.

262 r extrinsic mechanisms of resistance to ROS1 TKIs can emerge in patients.

263 2-rearranged Ph-like ALL following selective TKI pressure, which occurs in the absence of genetic mut

264 ib was the most potent HER2 mutant-selective TKI tested.

265 trate that combining asciminib with ATP site TKIs enhances target inhibition and suppression of resis

266 Participants received half their standard TKI dose (imatinib 200 mg daily, dasatinib 50 mg daily,

267 Clinical responses to the EGFR-targeting TKIs are evaluated through 2-[(18)F]fluoro-2-deoxy-gluco

268 oring of mutation kinetics demonstrated that TKI-resistant low-level mutations are invariably selecte

269 n of the particular ROS1 oncoprotein and the TKI properties such as the preferential kinase conformat

270 veal a new form of vascular toxicity for the TKI ponatinib that involves VWF-mediated platelet adhesi

271 nd that prolonged NSCLC cell exposure to the TKI erlotinib drives PFKFB3 expression and that chemical

272 f overcoming TKI resistance and treating the TKI-resistant BMs.

273 mutant lung cancer patients treated with the TKI erlotinib.

274 L CD34(+) cells, and in combination with the TKI nilotinib (NIL) significantly enhanced inhibition of

275 s into resistance of RET mutants against the TKIs nintedanib and vandetanib.

276 Thus, TKI treatment was associated with an increased complicat

277 However, most patients develop resistance to TKI through BCR-ABL1-dependent and -independent mechanis

278 -secreting tumors, which normally respond to TKI treatment by secreting EDN1, promoting vasoconstrict

279 e (n = 124) or warning (n = 112) response to TKI therapy were analyzed in parallel by SS and NGS in 1

280 his did not significantly affect response to TKI, except in patients identified as MET-amplified.

281 important for EGFR stability and response to TKI.

282 In contrast, responses to TKI treatment are short lived in advanced phases of the

283 is correlated positively with sensitivity to TKI in patients with NSCLC.

284 vity, sensitizing therapy-resistant cells to TKIs.

285 r understand the drug-resistant mechanism to TKIs.

286 g adenocarcinoma, but acquired resistance to TKIs inevitably occurs.

287 therapeutic option to overcome resistance to TKIs.

288 GFR kinase domain that confers resistance to TKIs.

289 of drug-resistant cells, sensitized them to TKIs in vitro, and markedly eliminated long-term repopul

290 ies, in particular effective agents to treat TKI-refractory disease.

291 lung cancer (NSCLC) with EGFR-mutant tumors, TKI resistance often returns as a result of additional E

292 which ALK overactivity drives toxicity upon TKI withdrawal remained obscure.

293 Despite using TKIs, we have continued to remain reliant on cytotoxic c

294 21 (30%) of 69 patients were TKI-naive, 40 (58%) had previously received crizotinib a

295 ng CN in renal cell carcinoma patients, when TKI treatment is administered.

296 In this study, we have evaluated whether TKI-induced diarrhoea may be related to variation in the

297 ndocan-EGFR regulatory axis in patients with TKI-resistant NSCLC.

298 han their +/+ counterparts when treated with TKI.

299 t the risk of developing adverse events with TKIs.

300 Eighty-two patients treated with TKIs were matched (3:1) to 246 controls.