ライフサイエンスコーパス: FGFR

1 FGFR activation of YAP appears to be driven largely by F

2 FGFR inhibition (or gene silencing) interrupts stromal a

3 FGFR) entails formation of an allosteric 2:1 FGFR-PLCgamma complex.

4 other three cohorts), and in ten (67%) of 15 FGFR mRNA-overexpressing tumours without apparent FGFR g

5 ssion, of whom 126 patients were treated (23 FGFR mRNA-unselected patients in the dose-escalation pha

6 hway-independent growth, driven instead by a FGFR/MAPK/ID1 signaling cascade.

7 ion on glutamatergic neurons, we generated a FGFR gain-of-function (GOF) transgenic mouse, which expr

8 TIMP3 may promote angiogenesis and CNV via a FGFR-1-dependent pathway by increasing bFGF release and

9 e approach to examine the impact of aberrant FGFR function on glutamatergic neurons, we generated a F

10 e specific mechanisms through which aberrant FGFR activity contributes to breast cancer are not compl

11 Accordingly, FGFR targeted tyrosine kinase inhibitors (TKIs) are curr

12 Accordingly, FGFRs accumulate and stimulate prolonged Erk1/2 phosphor

13 FGFR-amplified breast cancer cells-activated FGFR siganalling in osteoblasts, including increased exp

14 AMA1 (PI3K-Akt signaling pathway) and ADCY3 (FGFR signaling pathway) for CRC evolution.

15 to phosphate intake and binds to alphaKlotho-FGFR complexes, which are expressed most abundantly in r

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

17 S-1 transcription factors, as well as for an FGFR-like molecule, in the specification and maintenance

18 of PLCgamma by the phosphorylated tail of an FGFR kinase induces a conformational change at the regio

19 Increased expression levels of FGFR-2 and FGFR-3 through gene amplification correlate with treatme

20 trials using combinations of ER, CDK4/6 and FGFR antagonists.

21 profiles accumulating in GPCR, PI3K-Akt and FGFR signaling pathways.

22 mutations specifically in GPCR, PI3K-Akt and FGFR signaling pathways.

23 thin the domains involved in FGF binding and FGFR activation.

24 sitive feed-back loop between N-cadherin and FGFR at adhesion sites limiting N-cadherin-based single-

25 These results suggest that dual EGFR and FGFR blockade may be a promising clinical strategy for b

26 for the clinical study of combined EGFR and FGFR inhibition in EGFR-mutated NSCLCs.

27 this study, we find that combining EGFR and FGFR inhibitors inhibited the survival and expansion of

28 o can exert effects independent of FGF23 and FGFR.

29 performed using anti-ESRP1, FGFR-2 IIIb and FGFR-2 IIIc antibodies in 123 PDAC cases.

30 be achieved by combining MTOR inhibitors and FGFR-specific TKIs.

31 ical inhibition of MEK together with JAK and FGFR enhanced tumor regression.

32 se fusions involving ALK, ROS, RET, NTRK and FGFR gene families were detected in bladder carcinoma (3

33 tiation and morphogenesis, whereby Prox1 and FGFR signaling interact to mediate LF differentiation in

34 er expression of luminal genes in tumors and FGFR inhibition increased transcription of these same ge

35 hosphorylation of these tyrosines by another FGFR kinase in trans.

36 Our findings support the development of anti-FGFR inhibitors as potential antimetastatic therapy.

37 A number of anti-FGFR therapies are currently under investigation in clin

38 ical trials are testing the efficacy of anti-FGFR therapies.

39 mRNA-overexpressing tumours without apparent FGFR genetic aberration.

40 clib (cell cycle gene alterations), AZD4547 (FGFR alteration), rilotumumab plus erlotinib (MET), tala

41 mproves the overall survival of mice bearing FGFR-driven HCCs.

42 cells depends on an optimum balance between FGFR-regulated N-cadherin adhesion and actin dynamics.

43 its N-terminal Src homology 2 domain to bind FGFR once stimulated by FGF1, and this was necessary for

44 N-Cadherin cell-autonomously binds FGFRs and inhibits FGFR K27- and K29-linked polyubiquiti

45 l cycle activation was inhibited by blocking FGFR-1 signaling.

46 Conversely, inhibiting SGK1, blocking FGFR dimerization, or knocking down Klotho expression di

47 that combinatorial therapies inhibiting both FGFR activity and hyaluronan synthesis is more effective

48 23 as an upstream negative regulator of both FGFR and canonical Hh-GLI1 signaling, and additionally i

49 ibroblast growth factor receptor/breathless (FGFR, Btl) signaling to maintain the proper size of unic

50 oth oncogenic and sensitive to inhibition by FGFR kinase inhibitors.

51 es whose expression is directly regulated by FGFR activity during the transition from endoderm to hep

52 Selection by FGFR mRNA expression could be a useful additional biomar

53 technology allowed us to interrogate central FGFR/beta klotho (Klb) system at the cellular level in t

54 d this subtype is susceptible to combination FGFR and mTOR inhibition, with implications for targeted

55 r (FGFR) inhibition, and more so to combined FGFR and KIT inhibition, validating the functional signi

56 Thus deregulated FGFR signalling has an important role in osteoblast tran

57 Different FGFR somatic alterations may confer different levels of

58 on were uniformly resistant to the different FGFR inhibitors.

59 hat, within lung epithelial cells, different FGFRs function independently; they bind receptor-specifi

60 eal a key requirement for cell-autonomous EC FGFR signaling in injury-induced angiogenesis, but not f

61 for vascular homeostasis, identifying the EC FGFR signaling pathway as a target for diseases associat

62 In addition, ectopic FGFR activation in mesenchyme was sufficient to increase

63 ails of multivalent interactions among eFGF, FGFR, and Klotho.

64 ty ligation assays indicated that endogenous FGFR-1 and Fn14 interact with each other in cardiomyocyt

65 annels expressed in cells lacking endogenous FGFRs.

66 link between loss of protective endothelial FGFR signaling, development of EndMT, and progression of

67 cal analysis was performed using anti-ESRP1, FGFR-2 IIIb and FGFR-2 IIIc antibodies in 123 PDAC cases

68 We examined FGFR expression in CCA tumor specimens obtained from pat

69 ometry analysis, we show that RPTECs express FGFR-beta1C.

70 The potent impact of FGF-FGFR in multiple embryonic developmental processes makes

71 Here, we demonstrate that the autocrine FGF/FGFR axis is essential for multiple myeloma cell surviva

72 h other FGF/FGFR alterations, 18 with no FGF/FGFR alterations, and one with an undetermined FGF/FGFR

73 GF/FGFR alterations, or patients with no FGF/FGFR alterations.

74 fusions or rearrangements, 20 with other FGF/FGFR alterations, 18 with no FGF/FGFR alterations, and o

75 s or rearrangements, patients with other FGF/FGFR alterations, or patients with no FGF/FGFR alteratio

76 Because of the complex nature of the FGF/FGFR axis, and the numerous effects of FGFR activation o

77 Aberrant signaling of the FGF/FGFR pathway occurs frequently in cancers and is an onco

78 dings dissect the mechanism by which the FGF/FGFR system plays a nonredundant role in multiple myelom

79 atus can be a target for cancer therapy, FGF/FGFR blockade by FGF trapping or tyrosine kinase inhibit

80 lterations, and one with an undetermined FGF/FGFR alteration.

81 available pan-FGF trap able to inhibit FGF2/FGFR interaction and endowed with promising antitumor ac

82 esistance to radiotherapy, so targeting FGF2/FGFR pathways might offer a rational strategy for tumor

83 Perturbing the expression levels of FGFs/FGFRs by excessive glutamatergic neurotransmission could

84 little is known regarding the roles of FGFs/FGFRs in cortical circuit formation.

85 Together, our data suggest that FGFs/FGFRs can be regulated by glutamate transmission to modu

86 These data suggest that FGFs/FGFRs have a role in stabilizing dendritic patterning.

87 patient population who could be eligible for FGFR inhibitor treatment.

88 migration, suggest a physiological role for FGFR and N-Cadherin interaction in vivo and identify Ree

89 July 5, 2017, 866 patients were screened for FGFR mRNA expression, of whom 126 patients were treated

90 combined with MD simulations, shows that for FGFR kinase, there are populations of inactive and activ

91 These findings reveal novel functions for FGFRs in cortical projection neuron migration, suggest a

92 Finally, we document an essential role for FGFRs in embryonic stem cell (ESC) differentiation, with

93 Furthermore, FGFR-mediated hyaluronan accumulation requires activatio

94 appeared to be limited to cancers harboring FGFR activating mutations and fusions, although AZD4547

95 For patients with tumors harboring FGFR fusions, the response rate was 22% (90% CI, 4.1% to

96 y differentiated cancers also exhibited high FGFR-2 IIIb and low FGFR-2 IIIc expression, whereas this

97 itor, potently suppresses the growth of high-FGFR-expressing and sorafenib-resistant HCCs.

98 growth in soft of agar in cells deficient in FGFR-1 (FGF2 receptor).

99 P expression may be a biomarker to employ in FGFR-directed therapy.

100 Amplification and mutations in FGFR genes have been identified in patients with NSCLCs,

101 sults highlight the role played by RasGAP in FGFR signaling and how graded stress intensities, by gen

102 l changes in the FGFR dimers, which increase FGFR phosphorylation.

103 ineered to express ESRP1 exhibited increased FGFR-2 IIIb expression and decreased migration and invas

104 -transfected KLM-1 cells exhibited increased FGFR-2 IIIc expression and increased cell growth, migrat

105 ned to deplete VAT stores of FGF2 or inhibit FGFR-1 in abdominally obese individuals may be important

106 e use of NRP1-blocking antibodies, inhibited FGFR signaling and reduced tumor cell growth in vitro an

107 n cell-autonomously binds FGFRs and inhibits FGFR K27- and K29-linked polyubiquitination and lysosoma

108 Infigratinib inhibits FGFR signaling and its downstream targets, cell prolifer

109 tion of the crystal structures of FGF-Klotho-FGFR complexes is paving the way for the development of

110 ontrolled by Hedgehog signaling in a largely FGFR-dependent manner.

111 the assembly and dynamics of the full-length FGFRs on the cell surface.

112 cers also exhibited high FGFR-2 IIIb and low FGFR-2 IIIc expression, whereas this ratio was reversed

113 FGF-2 activation of both membrane FGFRs and INFS-dependent FGFR1 pathways may provide a me

114 ar FGFR1, to determine the roles of membrane FGFRs and integrative nuclear FGFR1 signaling (INFS) in

115 outer hair cells and SCs, while mesenchymal FGFRs regulate the size of the sensory progenitor popula

116 er (HNSCC) cells to ponatinib, a multikinase FGFR-active inhibitor.

117 tive FGFR inhibitor BGJ398 and multitargeted FGFR inhibitor ponatinib.

118 et small-molecule inhibitors of these nodes (FGFR/PTENi) show only modest activity in preclinical mod

119 and then determined the effects of the novel FGFR inhibitor, derazantinib (DZB; formally, ARQ 087), w

120 and Fgfr2 in development and uncouple novel FGFR kinase-dependent cell adhesion properties from cano

121 trategy results in the optical activation of FGFR with low background activity and high sensitivity,

122 terogeneous subpopulations and activation of FGFR-3.

123 ntiation were mediated through activation of FGFR/MEK/Erk1/2 signaling and downregulation of bone mor

124 oncogenic drivers because administration of FGFR tyrosine kinase inhibitors (F-TKIs) can elicit mean

125 lications for the therapeutic application of FGFR inhibitors as they identify both common and diverge

126 The combination of FGFR inhibitors and MTOR or AKT inhibitors resulted in s

127 duration, intensity and cellular context of FGFR signaling during growth plate chondrocyte maturatio

128 Deregulation of FGFR-mediated signaling involving the Ras/PI3K/Akt and t

129 in of KLA fused to the cytoplasmic domain of FGFR and employ total internal reflection fluorescence m

130 e FGF/FGFR axis, and the numerous effects of FGFR activation on tumor cells and the surrounding micro

131 ts and osteoclasts), and also the effects of FGFR inhibition in bone metastasis.

132 However, the efficacy of FGFR TKIs in the bone microenvironment where breast canc

133 associated mouse model of CCA, expression of FGFR 1, 2, and 4 was also significantly increased.

134 Inhibition of FGFR as well as MAPK pathway reduces the proliferative a

135 Thus, inhibition of FGFR can modulate stromal function, reduce exosome secre

136 Similarly, inhibition of FGFR signalling in vivo with the small-molecule inhibito

137 reast cancers associated with high levels of FGFR activity.

138 shows that cancer cells with high levels of FGFR and integrin beta3 are resistant to crizotinib trea

139 Increased expression levels of FGFR-2 and FGFR-3 through gene amplification correlate w

140 ung adenocarcinoma, although mouse models of FGFR-driven lung cancers have not been reported.

141 ESRP1 regulates the expression pattern of FGFR-2 isoforms, attenuates cell growth, migration, inva

142 experimentally validated KAR predictions of FGFR and MTOR dependence in lung cancer cell line H1581,

143 nd MEK/ERK signaling even in the presence of FGFR inhibitor.

144 Currently, the anti-tumor properties of FGFR inhibitors are being tested in preclinical and clin

145 Although numerous previous reports of FGFR signaling contributing to EGFR TKI resistance in vi

146 testing this hypothesis, nor has the role of FGFR in promoting the survival of persister cells been e

147 orm, suggesting that the biological roles of FGFR heterodimers may be as significant as the homodimer

148 , inhibition of stemness, and suppression of FGFR/RTK signaling in ErbB2-overexpressing human breast

149 fitinib has been tested for the treatment of FGFR-rearranged bladder cancer.

150 Clinical validation of FGFR as a therapeutic target has been demonstrated in bl

151 prehypertrophic chondrocytes, downstream of FGFRs and via an indirect mechanism, is required for nor

152 non-FRS intracellular adapters downstream of FGFRs could therefore in principle explain how FGFs play

153 ulator and Erk1/2 as downstream effectors of FGFRs during neuron migration.

154 vitro data correlated with the expression of FGFRs in human CCA specimens by immunohistochemistry (FG

155 FRS2 and FRS3 in mediating the functions of FGFRs.

156 Nevertheless, reports on FGFR inhibitor-mediated breast cancer prevention are spa

157 tors of mitogen-activated kinase kinase 1 or FGFR ablated these responses.

158 Pharmacological inhibitors of MAPK or FGFR repressed the growth of double-negative PCs in vitr

159 FGFR2 and other FGFR kinase family gene alterations have been found in b

160 different from the known structures of other FGFR kinases.

161 FGFR3 dependency but not dependency on other FGFR family members.

162 we demonstrate significant activity of a pan FGFR inhibitor against organoids derived from the FGFR1-

163 Infigratinib, a pan-FGFR inhibitor, potently suppresses the growth of high-F

164 P-positive CCA cell lines with BGJ398, a pan-FGFR inhibitor, resulted in a decrease in YAP activation

165 While a number of pan-FGFR inhibitors are being clinically evaluated, their ap

166 To evade the potential limitations of pan-FGFR inhibitors, we generated H3B-6527, a highly selecti

167 edicted response to rogaratinib, an oral pan-FGFR inhibitor.

168 Here, we have reported that the pan-FGFR TKI, NVP-BGJ398, reduces FGFR3 phosphorylation and

169 Tumors were acutely sensitive to pan-FGFR inhibition.

170 ines show increased levels of phosphorylated FGFRs and phosphorylated FRS2, a direct substrate of FGF

171 Our results show that all possible FGFR heterodimers form, suggesting that the biological r

172 by next-generation sequencing for predefined FGFR amplification, activating mutations, or fusions.

173 in regulating neuronal positioning, prevents FGFR degradation through N-Cadherin, causing Erk1/2 phos

174 n exon IIIb and IIIc, and primarily promotes FGFR-2 IIIb expression.

175 seems restricted to cancers harbouring rare FGFR genetic aberrations.

176 ion(s) in fibroblast growth factor receptor (FGFR) 1-3 were treated with AZD4547, an oral FGFR1-3 inh

177 Fibroblast growth factor receptor (FGFR) 2 gene alterations are involved in the pathogenesi

178 ctions of fibroblast growth factor receptor (FGFR) 2 in urothelium after cyclophosphamide exposure.

179 activate fibroblast growth factor receptor (FGFR) 4 independently of alpha-klotho, the canonical co-

180 level of fibroblast growth factor receptor (FGFR) activation and ERK1/2 phosphorylation, both at bas

181 plex with fibroblast growth factor receptor (FGFR) and fibroblast growth factor 23 (FGF23) indicates

182 mplicated fibroblast growth factor receptor (FGFR) as a key regulator for antiproliferative effects o

183 e type of fibroblast growth factor receptor (FGFR) but produces neither HS nor fibroblast growth fact

184 The fibroblast growth factor receptor (FGFR) family of receptor tyrosine kinases (RTKs) regulat

185 mily, the fibroblast growth factor receptor (FGFR) family, the platelet-derived growth factor recepto

186 -directed fibroblast growth factor receptor (FGFR) inhibitor therapy in SCC, which contrasts to the r

187 tivity of fibroblast growth factor receptor (FGFR) inhibitors seems restricted to cancers harbouring

188 EGFR and fibroblast growth factor receptor (FGFR) inhibitors was active in an EGFR mutant resistant

189 ll-length fibroblast growth factor receptor (FGFR) mutants harboring pathogenic cysteine substitution

190 Hippo and fibroblast growth factor receptor (FGFR) oncogenic signaling pathways in cholangiocarcinoma

191 on of the fibroblast growth factor receptor (FGFR) pathway and this subtype is susceptible to combina

192 low-level fibroblast growth factor receptor (FGFR) signaling.

193 vation of fibroblast growth factor receptor (FGFR) signalling contributes to progression and metastas

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

195 in caused fibroblast growth factor receptor (FGFR) upmodulation, resulting in epithelial-to-mesenchym

196 (IGF2R), fibroblast growth factor receptor (FGFR), etc.

197 including fibroblast growth factor receptor (FGFR), platelet-derived growth factor receptor (PDGFR) a

198 required fibroblast growth factor receptor (FGFR)-1 signaling to maintain viability and were sensiti

199 nitiating fibroblast growth factor receptor (FGFR)-dependent biochemical signalling.

200 n for the fibroblast growth factor receptor (FGFR).

201 domain of Fibroblast Growth Factor Receptor (FGFR).

202 d KL secretion and upregulated FGF receptor (FGFR) 1.

203 ) 1 and FGF2 signaling through FGF receptor (FGFR) 1c.

204 y targets cardiac myocytes via FGF receptor (FGFR) 4 thereby inducing hypertrophic myocyte growth and

205 inary complexes composed of an FGF receptor (FGFR) bound to either alpha-Klotho or beta-Klotho recept

206 y disease-causing mutations in FGF receptor (FGFR) during embryogenesis.

207 We report high FGF receptor (FGFR) expression in 17.7% (11 of 62) of hepatocellular c

208 X model is highly sensitive to FGF receptor (FGFR) inhibition, and more so to combined FGFR and KIT i

209 e examined anxiety behavior in FGF receptor (FGFR) KO mice; however, FGFR1, FGFR2, and FGFR3 KO mice

210 osed of alpha-Klotho (KLA) and FGF receptor (FGFR) resulting in kinase activation, regulation of phos

211 heir requirement for mediating FGF receptor (FGFR) signaling and activating downstream mediators that

212 Here we identify FGF receptor (FGFR) signalling as a critical regulator of vascular dev

213 st growth factor 2 (FGF2b) and FGF receptor (FGFR)1 in LMC formation.

214 ation of fibroblast growth factor receptors (FGFR) contributes to breast cancer growth, progression,

215 SH2 containing substrate, by FGF receptors (FGFR) entails formation of an allosteric 2:1 FGFR-PLCgam

216 express fibroblast growth factor receptors (FGFRs) and are exquisitely sensitive to FGF signals.

217 ssion of fibroblast growth factor receptors (FGFRs) and can bind to their promoters, correlating with

218 Fibroblast growth factor receptors (FGFRs) are frequently up-regulated in subsets of hepatoc

219 Fibroblast growth factor receptors (FGFRs) are involved in proliferative and differentiation

220 tions of fibroblast growth factor receptors (FGFRs) have been described in a wide range of malignanci

221 amily of fibroblast growth factor receptors (FGFRs) plays an important and well-characterized role in

222 ontrast, fibroblast growth factor receptors (FGFRs) recruit Fibroblast Growth Factor Receptor Substra

223 tions in fibroblast growth factor receptors (FGFRs) to determine the maximum tolerated dose (MTD), th

224 Fibroblast growth factors receptors (FGFRs) are thought to initiate intracellular signaling c

225 Of the four FGF receptors (FGFRs 1-4), FGFR1 and FGFR3 are strongly implicated in o

226 Whether FGF receptors (FGFRs) accomplish such varied tasks in part by activatin

227 ast growth factors (FGFs) and FGF receptors (FGFRs) are known for their potent effects on cell prolif

228 ast growth factors (FGFs) and FGF receptors (FGFRs) have been detected in various neurological disord

229 The functions of FGF receptors (FGFRs) in early development of the cerebral cortex are w

230 ast growth factors (FGFs) and FGF receptors (FGFRs) in establishing and maintaining cortical circuits

231 factors (FGFs) signal through FGF receptors (FGFRs) mediating a broad range of cellular functions dur

232 distinct sets of overlapping FGF receptors (FGFRs), FGFR2b and FGFR1b, mediate excitatory or inhibit

233 tivates complexes composed of FGF receptors (FGFRs), including FGFR1, and alpha-Klotho in the kidney

234 9 and FGF10 activate distinct FGF receptors (FGFRs), we hypothesized that they would control distinct

235 erm through activation of the FGF receptors (FGFRs).

236 21 and FGF23 to their cognate FGF receptors (FGFRs).

237 H3K36me3-bound MRG15 and PTB regulate FGFR-2 splicing, which controls tumor growth and invasiv

238 ffected, though these activities did require FGFR kinase activity.

239 ification and translocation to the selective FGFR inhibitor BGJ398 and multitargeted FGFR inhibitor p

240 We show here that FGFR activation induces accumulation of hyaluronan withi

241 Collectively, this study indicates that FGFR signaling provides an important input into the Ras-

242 Our findings support the notion that FGFR inhibitors, like DZB, should be further evaluated a

243 Here, we show that FGFR-1 can interact with the TNF receptor superfamily me

244 ese correlated in vitro studies suggest that FGFR may play an important role in the pathogenesis and

245 Taken together, our data suggest that FGFR-1/Fn14 interaction may represent a novel endogenous

246 These results suggest that FGFR-mediated pY240-PTEN is a key mechanism of radiation

247 ant to crizotinib treatment, suggesting that FGFR and integrin beta3 could be used as predictive mark

248 Collectively, our results support that FGFR inhibitors inhibit the bone microenvironment stroma

249 We further find that FGFRs are required in the presynaptic neuron to respond

250 We have found that FGFRs regulate multipolar neuron orientation and the mor

251 Mechanistically, our results suggest that FGFRs are activated by N-Cadherin.

252 The FGFR immediate early genes that were identified include

253 icing regulatory protein 1 (ESRP1) binds the FGFR-2 auxiliary cis-element ISE/ISS-3, located in the i

254 In contrast, fragment N2 bound the FGFR, and this inhibited mTORC2-dependent Akt Ser-473 ph

255 d binding triggers structural changes in the FGFR dimers, which increase FGFR phosphorylation.

256 We investigated the FGFR-mediated interactions among cancer and the bone mic

257 epithelium by modulating the response of the FGFR signalling pathway to FGF stimulation.

258 N-cadherin potentiation of the FGFR stimulated extracellular signal regulated kinase (E

259 Addition of the FGFR TKI erdafitinib to palbociclib/fulvestrant induced

260 the mutations alter the configuration of the FGFR transmembrane dimers.

261 ignaling via lipid rafts, independent of the FGFR-FGF23 pathway.

262 a provide the most robust central map of the FGFR/Klb system to date and highlight central regions th

263 stabilisation of cell adhesions require the FGFR activity stimulated by N-cadherin engagement.

264 find that the three mutations stabilize the FGFR dimers.

265 These results suggest that targeting the FGFR-mitochondrial metabolism-Notch1 axis prevents resis

266 necessary for the recruitment of Akt to the FGFR complex.

267 Fragment N, which did not associate with the FGFR complex, favored FGF1-induced ERK stimulation, lead

268 Treatment of cells with the FGFR inhibitors substantially restored the efficacy of S

269 sistance was abrogated by treatment with the FGFR tyrosine kinase inhibitor (TKI) lucitanib.

270 y modest sensitivity to monotherapy with the FGFR-specific TKI, AZD4547, but when combined with the M

271 c precursor cells, in which any one of three FGFRs (FGFR1, FGFR2, or FGFR3) is sufficient for surviva

272 oblast differentiation were mediated through FGFR/MEK/Erk1/2 signaling, increases in Bmp2, and activa

273 nse rates of FGFR1-amplified lung cancers to FGFR inhibitors, relationships between gene copy number,

274 ion does not sensitise bladder cell lines to FGFR/PTENi, but newly identify an autophagy-independent

275 p cell line models of acquired resistance to FGFR inhibition by exposure of cell lines harboring FGFR

276 e basal SG lack the competence to respond to FGFR signaling, preventing its differentiation into WG.

277 ein-expressing lung cancers are sensitive to FGFR inhibitor monotherapy by downregulating ERK signali

278 ance of these factors for the sensitivity to FGFR inhibitors was determined by analyzing drug screen

279 xpressing cancers further sensitized them to FGFR inhibitor.

280 ng 23 response-evaluable patients with tumor FGFR pathway alterations, four confirmed responses and o

281 In preclinical studies, high tumour FGFR mRNA expression predicted response to rogaratinib,

282 However, the machinery fine-tuning FGFR signaling in chondrocytes is incompletely defined.

283 In turn, FGFR signaling in a cell line with minimal basal YAP exp

284 examined the requirement of Frs genes in two FGFR-dependent processes.

285 ophagy is proposed to promote survival under FGFR/PTENi, we have investigated this relationship in a

286 ast cancer bone metastasis mouse model using FGFR non-amplified MDA-MB-231 cells.

287 f culture supernatant from the MDA-MB-134-VI FGFR-amplified breast cancer cells-activated FGFR sigana

288 e for KLA binding and for cell signaling via FGFRs.

289 s most frequently metastasize and also where FGFR is biologically active, has not been clearly invest

290 sm-to-membrane translocation approach, where FGFR ICD is recruited from the cytoplasm to the plasma m

291 e a novel targetable mechanism through which FGFR activation in breast cancer cells induces a protumo

292 rs a novel molecular mechanism through which FGFR-linked pathologies can arise.

293 ion as primary high-affinity receptors while FGFRs function as the catalytic subunits that mediate in

294 Thus, we propose breast cancers with FGFR pathway alterations should be considered for trials

295 ally, inhibition of SHP2 in combination with FGFR-targeted kinase inhibitors synergistically blocked

296 that sKlotho only functions in complex with FGFR and FGF23 and that sKlotho's pleiotropic effects al

297 ective in a subset of patients with HCC with FGFR-driven tumors.

298 al combination of epigenetic modulators with FGFR-targeted kinase inhibitors may provide improved out

299 dose-escalation phase and 103 patients with FGFR mRNA-overexpressing tumours [52 patients with uroth

300 igation in clinical trials for subjects with FGFR gene amplifications, mutations and translocations.

301 (sqNSCLC; arm 1) or other solid tumors with FGFR genetic alterations (mutations/amplifications/fusio

302 ho proteins and regulatory interactions with FGFRs that control their pleiotropic cellular responses.