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-TACC fusions could potentially identify a subset of

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

4 These findings demonstrate that FGF-2/FGFR signaling is sufficient and necessary for the behav

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

6 ur suppressor in cartilage, acting through a FGFR/MEK/ERK-dependent pathway in a novel progenitor cel

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

8 Activated FGFR/FRS2 signaling may play a functional role in the de

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

10 Although FGFR tyrosine phosphorylation and the recruitment of Src

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

12 he aneuploidy, and oral administration of an FGFR inhibitor prolongs survival of mice harboring intra

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

14 We observed high expression of SOX-9 and FGFR-3, as well as aberrant cellular localization of hep

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

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

17 overexpressed in bladder cancers (BCs), and FGFR inhibitors are currently being evaluated in clinica

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

19 a model in which Zpr1 mediates both EGFR and FGFR signal transduction cascades required for lumen for

20 a potential interaction between ERalpha and FGFR signalling.

21 g those that are dependent on Src family and FGFR kinase activity.

22 te endocrine FGF ligand (FGF19 or FGF21) and FGFR independently through two distinct binding sites.

23 Basal phosphorylated FGFR and FGFR-dependent downstream signalling were constitutively

24 The significance of FRS2 and FGFR signaling in high-grade liposarcomas is unknown.

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

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

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

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

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

30 Moreover, we found that FRS2 and FGFRs proteins are highly expressed and functional in th

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

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

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

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

35 to heparin in a trans-dimeric manner before FGFR recruitment.

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

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

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

39 nstrate that STAT3 inhibition decreases both FGFR-driven tumor growth and hyaluronan levels within th

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

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

42 f the ones observed in mice characterized by FGFR gain-of-function mutations.

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

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

45 These findings suggest N-cadherin/FGFR has a pivotal role in promoting metastasis through

46 act as a decoy receptor to inhibit canonical FGFR ligand-induced signaling.

47 Unlike canonical FGFRs that initiate signaling via tyrosine kinase domain

48 king comparisons with the well-characterized FGFR inhibitor PD173074.

49 llular domains of FGFR2 lead to constitutive FGFR dimerization.

50 rongly linked to the presence of deregulated FGFR signalling, indicating that addiction to deregulate

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

52 ng, indicating that addiction to deregulated FGFRs provides a therapeutic opportunity for selective i

53 on were uniformly resistant to the different FGFR inhibitors.

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

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

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

57 Overexpression of Fn14 with either FGFR-1 long [FGFR-1(L)] or FGFR-1 short [FGFR-1(S)] isof

58 ouse mammary epithelial cells and endogenous FGFR in the triple negative breast cancer cell line, HS5

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

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

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

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

63 r, the molecular interactions leading to FGF-FGFR-Klotho ternary complex formation remain incompletel

64 a novel mechanism by which Mks underwent FGF-FGFR signaling dependent expansion to accelerate rapid F

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

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

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

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

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

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

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

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

73 the clinic but has not yet been explored for FGFR inhibitors.

74 on gene may aid in selection of patients for FGFR-targeted therapy.

75 Our findings indicate a dual role for FGFR signaling in cerebellar morphogenesis.

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

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

78 alternate receptors provided protection from FGFR inhibition, including receptor tyrosine kinases (RT

79 Furthermore, FGFR-mediated hyaluronan accumulation requires activatio

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

81 To assess how FGFR-dependent tumour cells adapt to long-term FGFR inhi

82 ng impair motor learning and coordination in FGFR DKO mice.

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

84 d FGF, EGFR, and HGFR, with no difference in FGFR; differences between groups were not seen in normal

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

86 how first that neurofibromin is expressed in FGFR-positive prehypertrophic and hypertrophic chondrocy

87 ion of Fgf receptors, were also misplaced in FGFR DKO mice, possibly as a consequence of altered Berg

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

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

90 daptor protein that plays a critical role in FGFR signaling.

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

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

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

94 hus, we demonstrate that miR-200c influences FGFR-mediated epithelial proliferation during branching

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

96 FGFR), and does so most likely by inhibiting FGFR's role in epidermal-glia adhesion rather than signa

97 show that Fgfr1 and Fgfr2 double knockouts (FGFR DKO) generated by Cre-mediated recombination driven

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

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

100 derivative of the KMS-11 myeloma cell line (FGFR(Y373C)) with acquired resistance to AZ12908010 (KMS

101 rexpression of Fn14 with either FGFR-1 long [FGFR-1(L)] or FGFR-1 short [FGFR-1(S)] isoforms resulted

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

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

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

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

106 sformation can be reversed by small-molecule FGFR inhibitors currently being developed for clinical u

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

108 tive FGFR inhibitor BGJ398 and multitargeted FGFR inhibitor ponatinib.

109 al precursors in late embryonic and neonatal FGFR DKO mice.

110 fine the selectivity and efficacy of two new FGFR inhibitors and identify a secondary gatekeeper muta

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

112 Thus, ErbB-2, but not FGFR-1, shows a similar trafficking pathway to EGFR for

113 criptional regulation may involve the NOTCH, FGFR, or other signaling pathways in which SPEN particip

114 terogeneous subpopulations and activation of FGFR-3.

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

116 otho coreceptors enhance binding affinity of FGFR for endocrine FGFs, they actively suppress binding

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

118 Moreover, the triple combination of FGFR, MET, and ERBB family inhibitors showed the largest

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

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

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

122 ant determinant of the biological effects of FGFR inhibitors in patients.

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

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

125 Inhibition of FGFR kinase corrects the aneuploidy, and oral administra

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

127 ocess of identifying selective inhibitors of FGFR provide a step-by-step illustration of the process.

128 domain III (D3) of the "c" splice isoform of FGFR.

129 directly interacted with various isoforms of FGFR.

130 reast cancers associated with high levels of FGFR activity.

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

132 laminar architecture resulting from loss of FGFR signaling impair motor learning and coordination in

133 Using a novel in vivo model of FGFR-dependent tumor growth, we demonstrate that STAT3 i

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

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

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

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

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

139 ERK1/2 signaling, is a negative regulator of FGFR signaling in differentiating chondrocytes.

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

141 l signaling in HNSCC cells in the setting of FGFR inhibition.

142 Sa-2 cells with a concomitant suppression of FGFR signal transduction.

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

144 ansport of EGFR family proteins with that of FGFR-1.

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

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

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

148 FRS2 and FRS3 in mediating the functions of FGFRs.

149 Here we used a novel inhibitor of FGFRs 1-3 and RNAi to determine the effects of inhibitin

150 ns, most commonly by activating mutations of FGFRs 1-3, and inactivating mutations of TWIST1.

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

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

153 Fn14 with either FGFR-1 long [FGFR-1(L)] or FGFR-1 short [FGFR-1(S)] isoforms resulted after FGF1/TW

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

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

156 activation of Ras and ERK but not for other FGFR phosphotyrosine pathways.

157 different from the known structures of other FGFR kinases.

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

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

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

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

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

163 Tumors were acutely sensitive to pan-FGFR inhibition.

164 Basal phosphorylated FGFR and FGFR-dependent downstream signalling were const

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

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

167 ith activating FGFR3 mutations and potential FGFR inhibitor sensitivity.

168 sistent with N-cadherin's ability to promote FGFR signaling.

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

170 ed Erk phosphorylation was preceded by rapid FGFR and EGFR transactivation; however, only EGFR inhibi

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

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

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

174 er of the fibroblast growth factor receptor (FGFR) family expressed in adult pancreas.

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

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

177 es is the fibroblast growth factor receptor (FGFR) family, with amplification or mutation observed in

178 omains of fibroblast growth factor receptor (FGFR) genes (FGFR1 or FGFR3) to the transforming acidic

179 on of the fibroblast growth factor receptor (FGFR) heartless and its ligands, pyramus (pyr) and thisb

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

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

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

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

184 , whereas fibroblast growth factor receptor (FGFR) or mitogen-activated protein kinase kinase (MEK) i

185 Fibroblast growth factor receptor (FGFR) signaling determines the size of the cerebral cort

186 dependent fibroblast growth factor receptor (FGFR) signaling in chondrocytes.

187 1) FGF-2/fibroblast growth factor receptor (FGFR) signaling is sufficient and required for mediating

188 autocrine fibroblast growth factor receptor (FGFR) signaling.

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

190 ed in the fibroblast growth factor receptor (FGFR) signalling pathway: the receptor itself and Src.

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

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

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

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

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

196 domain of Fibroblast Growth Factor Receptor (FGFR).

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

198 ) 1 and FGF2 signaling through FGF receptor (FGFR) 1c.

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

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

201 pressing the dominant-negative FGF receptor (FGFR) identified orphan nuclear receptor Nurr1 and FGFR1

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

203 disorders caused by activating FGF receptor (FGFR) mutations.

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

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

206 te that CIMA-1 antagonizes the FGF receptor (FGFR), and does so most likely by inhibiting FGFR's role

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

208 Fibroblast growth factor (FGF) receptor (FGFR) substrate 2 (FRS2) is an adaptor protein that play

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

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

211 oreceptors along with classic FGF receptors (FGFR) to mediate potent biologic activity.

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

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

214 Fibroblast growth factor receptors (FGFRs) are activated by mutation and overexpressed in bl

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

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

217 Fibroblast growth factor receptors (FGFRs) can act as driving oncoproteins in certain cancer

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

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

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

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

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

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

224 The FGF receptors (FGFRs) control a multitude of cellular processes both du

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

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

227 ms heteromeric complexes with FGF receptors (FGFRs) to initiate intracellular signaling.

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

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

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

231 t growth factors (FGFs) and their receptors (FGFRs) regulate cell proliferation and differentiation i

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

233 s ligand reelin, which unexpectedly regulate FGFR-dependent epithelial proliferation.

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

235 her FGFR-1 long [FGFR-1(L)] or FGFR-1 short [FGFR-1(S)] isoforms resulted after FGF1/TWEAK stimulatio

236 Furthermore, addition of a specific FGFR inhibitor readily reversed this Nanog repression st

237 analysis of Eps8 aimed to identify specific FGFR and Src family kinase dependent phosphosites and co

238 Suppressing FGFR or its downstream signal transduction pathways dimi

239 GBM patients who would benefit from targeted FGFR kinase inhibition.

240 support the concept that therapies targeting FGFR signaling may have efficacy in prostate cancer and

241 ally designed combinations of TKIs targeting FGFR, ERBB family members, and MET.

242 FR-dependent tumour cells adapt to long-term FGFR inhibition, we generated a derivative of the KMS-11

243 environment, these studies demonstrate that FGFR activation also leads to induction of CX3CL1 in a t

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

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

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

247 At the molecular level, we showed that FGFR-1 expressed in lymphatic endothelial cells is a cru

248 ely described, we have previously shown that FGFR is also phosphorylated on Ser(779) in response to l

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

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

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

252 The FGFR immediate early genes that were identified include

253 The FGFR-TACC fusion protein displays oncogenic activity whe

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

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

256 Importantly, the FGFR selective inhibitor NVP-BGJ-398 significantly inhib

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

258 own potentiated the inhibitory effect of the FGFR inhibitor, AZ8010, in HNSCC cell lines.

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

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

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

262 find that the three mutations stabilize the FGFR dimers.

263 d underscore the potential for targeting the FGFR in advanced ErbB2-amplified breast tumors.

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

265 osphorylated FRS2 protein indicated that the FGFR/FRS2 signaling axis was generally activated in abou

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 rylation in these tumors correlates with the FGFR-2 splicing pattern and with Akt phosphorylation and

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

271 d with those produced by expression of these FGFR isoforms in fibroblasts, in which they both stimula

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

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

274 Our findings show that in addition to FGFR tyrosine phosphorylation, the phosphorylation of a

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

276 uppress binding of FGF8 subfamily ligands to FGFR.

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

278 o increased inhibition of growth relative to FGFR tyrosine kinase inhibitor (TKI) treatment alone.

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

280 ion as a mechanism of acquired resistance to FGFR inhibitors that should be anticipated as clinical e

281 y marked heterogeneity in their responses to FGFR inhibitors, and the biological mechanisms underlyin

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

283 ith FGFR3 fusions are extremely sensitive to FGFR-selective agents, the presence of a fusion gene may

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

285 xpressing cancers further sensitized them to FGFR inhibitor.

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

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

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

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

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

291 FGF1 is termed the "universal FGFR ligand" because it overrides this specificity barri

292 , by employing in silico modeling of various FGFR ligand-binding sites.

293 specific for interactions with FGF23 and was FGFR dependent.

294 structure in human thyroid cancer, in which FGFR expression is commonly dysregulated.

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

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

297 n of either ERBB2 or MET in combination with FGFR inhibition led to increased inhibition of growth re

298 , and recommend future clinical studies with FGFR inhibitors in patients with lung and head and neck

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

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