ライフサイエンスコーパス: RET

1 RET can be activated in cis or trans by its co-receptors

2 RET can only generate ROS when mitochondria are well pol

3 RET encodes a transmembrane receptor that is 20 exons lo

4 RET from the EuNPs to the QDs was confirmed and characte

5 RET is dynamically expressed during myogenic progression

6 RET is regulated by a distal and a proximal enhancer at

7 RET knockdown also increased sensitivity to cisplatin-in

8 RET mutations were associated with differentiation and m

9 RET protein expression by IHC had an association with OS

10 RET rearrangements are found in 1-2% of non-small-cell l

11 RET rs2435357 also showed significant frequency differen

12 RET(DeltaE345), in contrast, displays higher baseline au

13 Mean NET expression in hereditary cluster 2 (RET, NF1, MAX) and apparently sporadic tumors was signif

14 ydrogenase); von Hippel-Lindau (VHL; n = 2); RET (n = 12); neurofibromin 1 (NF1; n = 2); and MYC-asso

15 ary mutations in SDHB (n = 2), SDHD (n = 3), RET (n = 5), neurofibromatosis 1 (n = 1), and myc-associ

16 tic or unresectable lung cancer harbouring a RET rearrangement, Karnofsky performance status higher t

17 ) and from 2 patients with S-HSCR (without a RET mutation), as well as RET(+/-) and RET(-/-) iPSCs.

18 ation of the cells with 100 pM ART activated RET at the rate of approximately 10 molecules/cell/min,

19 roduced by neighboring DRG neurons activates RET in RA mechanoreceptors.

20 ined by both genetic alterations (activating RET oncoprotein) and physiological stresses, namely hypo

21 a1, the co-receptor implicated in activating RET in trans, causes no significant central projection o

22 After RET, 1-RM increased in Y (+35 +/- 4%) and O (+25 +/- 3%;

23 kbp5 mRNA expression following EXT and after RET.

24 th RPT and RMT, and >50% gene knockout after RET.

25 ained ROS production by this mechanism after RET-driven ROS production has ceased.

26 multikinase inhibitor with activity against RET that produced a 10% overall response in unselected p

27 n protected the dopaminergic systems of aged RET-deficient mice.

28 and ERBB2, and translocations involving ALK, RET and ROS1.

29 atelet-derived growth factor receptor alpha, RET, and KIT, showed clinical activity in a phase 2 stud

30 (17%), NTRK1 (16%), ALK (10%), BRAF (5%) and RET (3%) in a mutually exclusive pattern.

31 These results suggest that ASCL1 and RET expression defines a clinically relevant subgroup of

32 with high endogenous expression of ASCL1 and RET implicated ASCL1 as a potential upstream regulator o

33 BRAFV600E and RET/PTC-positive PTCs were histologically similar.

34 d single cases of CDKN1B, CDKN2C, CTNNB1 and RET mutations.

35 that, like full-length RET, RET(DeltaE3) and RET(DeltaE345) are trafficked to the cell surface, inter

36 5 and are referred to as RET(Delta) (E3) and RET(Delta) (E345), respectively.

37 fectiveness of dual inhibition of the ER and RET pathways in regulating cell growth.

38 ER and RET primarily function through distinct pathways regulat

39 ing the luminal phenotype including ESR1 and RET, but pathway cross talk and potential for distinct e

40 d dose-dependent enhancement of both EXT and RET.

41 stance regeneration by binding GFRalpha3 and RET.

42 thelial growth factor receptor 2, c-MET, and RET multitargeted tyrosine kinase inhibitor that has ant

43 in-deficient animals, which showed none, and RET-deficient mice, in which we found moderate degenerat

44 Novel configurations of BRAF, NTRK3, and RET gene fusions resulting from chromosomal translocatio

45 Mice lacking both parkin and RET exhibited accelerated dopaminergic cell and axonal l

46 emonstration of crosstalk between parkin and RET highlights the interplay in the protein network that

47 biopsy MT for BRAF, RAS, PAX8-PPARgamma, and RET-PTC expedites optimal initial surgery for differenti

48 lean mass and leg strength gains when PS and RET were used than with RET alone, with the standard mea

49 ns, DDR2 mutations, ROS1 rearrangements, and RET rearrangements.

50 ich controls both ER (estrogen receptor) and RET, demonstrated a greater effect on cell growth than e

51 ular endothelial growth factor receptors and RET (rearranged during transfection) have been used when

52 out a RET mutation), as well as RET(+/-) and RET(-/-) iPSCs.

53 panel) to those obtained from ALK, ROS1 and RET FISH on 51 clinical specimens.

54 ALK, ROS1 and RET gene fusions are important predictive biomarkers for

55 s including by age, prior TKI treatment, and RET mutation status (hereditary or sporadic).

56 neurotrophin receptors TrkA, TrkB, TrkC, and RET and the sensory neurofilament peripherin.

57 BRAF(V600E)- and RET/PTC3-expressing PcCL3 cells were used as cellular mo

58 file against the target proteins, VEGFR2 and RET, and their antiproliferative efficacy against the me

59 d receptor tyrosine kinases, like VEGFR2 and RET, as viable and promising targets.

60 immunostaining of CCH and MTC using an anti-RET antibody demonstrated increased RET expression.

61 mbination therapy with antiestrogen and anti-RET in luminal breast cancer.

62 tion, as measured by Ki-67 and S-phase, anti-RET primarily increased apoptosis, as demonstrated by cl

63 ing of 49 frozen MTC specimens classified as RET mutation, we identified PROM1, LOXL2, GFRA1, and DKK

64 or exons 3, 4, and 5 and are referred to as RET(Delta) (E3) and RET(Delta) (E345), respectively.

65 S-HSCR (without a RET mutation), as well as RET(+/-) and RET(-/-) iPSCs.

66 ndardized Reference Evapotranspiration (ASCE RET) equation, and an energy balance model, both paramet

67 lar to ASCE RET estimates; however, the ASCE RET equation overestimated bottommost ET values during t

68 shown to underestimate ET compared the ASCE RET equation.

69 amic chamber ET results were similar to ASCE RET estimates; however, the ASCE RET equation overestima

70 ificant genetic risk can only be detected at RET (rs2435357 and rs2506030) and at SEMA3 (rs11766001),

71 e donor-acceptor distance is around 15 nm at RET efficiencies, equal to 15% for QD655 and 13% for QD7

72 Because RET can only generate ROS when mitochondria are fully po

73 this explanation may be incomplete, because RET on reperfusion is self-limiting and therefore transi

74 erimental evidence for the crosstalk between RET and HIF-1 that can explain the increased expression

75 tion, whereas a physical interaction between RET/PTC3 and STAT1, followed by a direct tyrosine phosph

76 In comparison to Y, O displayed blunted RET-induced increases in muscle thickness (at 3 and 6 we

77 asts and blocked the phosphorylation of both RET and VEGFR2 in tumor tissue.

78 abrogated the formation of tumors induced by RET-mutant fibroblasts and blocked the phosphorylation o

79 val NF-kappaB pathway, which was mediated by RET through the phosphoinositide-3-kinase (PI3K) pathway

80 ther, our results suggest that trans and cis RET signaling could function in the same developmental p

81 Conversely, RET/PTC3-expressing cells were characterized by a high I

82 the interaction of GFRAL with the coreceptor RET.

83 nts with RET-rearranged lung cancers defines RET rearrangements as actionable drivers in patients wit

84 In detail, RET/PTC3 induced STAT1 overexpression and phosphorylatio

85 /CCH predisposition do not have a detectable RET mutation.

86 Moreover, mortalin depletion downregulated RET expression independently of MEK/ERK and TP53.

87 Finally, specific ablation of early RET+ dDH neurons increases basal and chronic pain, where

88 nd pain pathways and suggest that some early RET+ dDH neurons could function as pain "gating" neurons

89 These early RET+ dDH neurons receive excitatory as well as polysynap

90 iluminescence resonance energy transfer (ECL-RET) approach, Fe3O4@SiO2/dendrimers/QDs exhibited ampli

91 a greater effect on cell growth than either RET or ER alone.

92 fic, low-frequency missense variant encoding RET p.Asp489Asn (rs9282834, conditional OR = 20.3, condi

93 is compound significantly reduced endogenous RET protein levels and increased apoptosis in these cell

94 find that haematopoietic stem cells express RET and that its neurotrophic factor partners are produc

95 tivity in transfected tumor cells expressing RET and/or the HIF-alpha subunit.

96 olymer pluronic F-127-folic acid (F-127-FA), RET-BDP molecules can form uniform and small organic nan

97 To decipher the molecular basis for RET kinase activation and oncogenic deregulation, we def

98 hich can block the blood supply required for RET-stimulated growth.

99 istance dependence characteristic of Forster RET.

100 kinase pathways, which transmit signals from RET and regulate HIF-1, abrogated their cooperative effe

101 Together, our results establish GDNF-RET signaling as a rational therapeutic target to combat

102 Furthermore, GDNF-RET signaling promoted the survival of aromatase inhibit

103 sion restored mitochondrial function in GDNF/RET-deficient cells, while GDNF stimulation rescued mito

104 phenotype correlation with specific germline RET mutations, knowledge of pathways specifically associ

105 perplasia (CCH), is associated with germline RET mutations causing multiple endocrine neoplasia type

106 ndicate that topical application of GFRalpha/RET receptor signaling modulators may be a unique therap

107 dergic IB4+ neurons expressing the GFRalpha1-RET GDNF receptor complex.

108 rformed in the MZ-CRC-1 cell line, harboring RET(M918T), caused an increase in apoptotic nuclei, sugg

109 ar profile, includingKRAS,EGFR,ALK,BRAF,HER2,RET,MET, andROS, did not reveal an actionable abnormalit

110 hly expressed genes included HOXA11, HOXA10, RET, PERP, and GGA2.

111 ene, complementing four known drivers (HRAS, RET, EPAS1, and NF1).

112 in the proximal promoter region of the human RET gene (-51 to -33 relative to transcription start sit

113 ntaneous melanoma [mice expressing the human RET oncogene under the control of the metallothionein pr

114 redisposition to MTC/CCH and no identifiable RET mutation.

115 lar states of ENS progenitors and identified RET as a regulator of neurogenic commitment.

116 the ATF4 inducer eeyarestatin as well as in RET-depleted TT cells.

117 hway was instrumental for IDO1 expression in RET/PTC3 expressing cells.

118 for a physiologic role of these isoforms in RET pathway function.

119 aganglionosis (with the G731del mutation in RET) and from 2 patients with S-HSCR (without a RET muta

120 Eight of the DNMs we identified occur in RET, the main HSCR gene, and the remaining 20 DNMs resid

121 lopment, such SRY repression could result in RET protein haploinsufficiency and promotion of HSCR dev

122 eration, activation of the ERE and increased RET expression.

123 hts into a novel mechanism causing increased RET expression in tumourigenesis.

124 an anti-RET antibody demonstrated increased RET expression.

125 alidated these findings by showing increased RET protein expression levels in an independent cohort o

126 Indeed, RET kinase activity was required to inhibit the ATF4-dep

127 KIF5B-RET was the predominant fusion type identified in 16 (62

128 s well as 1 EML4-ALK gene fusion and 1 KIF5B-RET gene fusion.

129 anslocation event and the EML4-ALK and KIF5B-RET inversion events.

130 known fusions involving EZR- ROS1 and KIF5B-RET were identified by RNA-Seq as well as a third novel

131 ween parkin and the receptor tyrosine kinase RET in two different mouse models of PD.

132 The receptor tyrosine kinase, RET, and its coreceptor, GFRalpha1, are upregulated in a

133 yr) undertook 6 wk of unilateral (1-legged) RET [6 x 8 repetitions, 75% 1 repetition maximum (1-RM)

134 oforms, demonstrating that, like full-length RET, RET(DeltaE3) and RET(DeltaE345) are trafficked to t

135 horylated in a similar manner to full-length RET.

136 e ability to heterodimerize with full-length RET.

137 hat in addition to cytoplasmic localization, RET is localized in the nucleus and functions as a tyros

138 (3 patients) and de novo (41 patients) M918T RET mutations were examined for signs and symptoms promp

139 and three-dimensional culture, GDNF-mediated RET signaling is enhanced in a model of aromatase inhibi

140 do-distyryl-BODIPY) to form a dyad molecule (RET-BDP).

141 n vitro and in cell-based assays, but moving RET into intact animals has proven difficult.

142 overexpression of both wild-type and mutant RET can increase the CA9 promoter activity induced by HI

143 d to block the kinase activity of the mutant RET(V804L), which still lacks effective inhibitors.

144 d with transcriptional activation of mutated RET gene in human medullary thyroid carcinoma TT cells.

145 ALK(F1174L) induces NEFM, RET, and VACHT and results in decreased expression of pr

146 y associated with each mutation and with non-RET-mutated sporadic MTC remains lacking.

147 ce, PLP1 cells that co-express S100b but not RET also give rise to neurons following colitis.

148 screen led to the identification of a novel RET inhibitor, Pz-1.

149 1 expression and the oncogenic activation of RET in thyroid carcinoma and describe the involved signa

150 Activation of RET results in improved haematopoietic stem cell surviva

151 are known to induce oncogenic activation of RET tyrosine kinase, are associated with the development

152 GFRalpha1) and signals through activation of RET tyrosine kinase.

153 In short, further development of RET-based probes, optical microscopy techniques, and mou

154 accompanied by substantial downregulation of RET, induction of the tumor-suppressor TP53 and altered

155 We also demonstrate that the effects of RET and NRG1 are universal across European and Asian anc

156 We show that the efficiency of RET coupling to ERK and Akt depends strongly on ART conc

157 factors, opening the way for exploration of RET agonists in human haematopoietic stem cell transplan

158 Accordingly, enforced expression of RET downstream targets, Bcl2 or Bcl2l1, is sufficient to

159 Inhibition of RET either by gene knockdown or by treatment with suniti

160 by perineurial macrophages, or inhibition of RET with shRNA or a small-molecule inhibitor, reduced pe

161 ly, sunitinib, a small-molecule inhibitor of RET, blocked GDNF-mediated activation of ERK and AKT.

162 Knockdown of RET by shRNA in medullary thyroid cancer-derived cells s

163 High levels of RET expression in ASCL1(+) but not in ASCL1(-) tumors wa

164 cant association between the localization of RET mutations and the expression of three genes: NNAT (s

165 RY could be a Y-located negative modifier of RET expression; and if it is ectopically expressed durin

166 ely enhances but not diversifies outcomes of RET signaling.

167 present case, it is assumed that the rate of RET between RuDCBPY centers has an r(-6) separation dist

168 r placebo; responses were seen regardless of RET mutation status.

169 ulation, we defined the temporal sequence of RET autophosphorylation by label-free quantitative mass

170 ng is most active during the early stages of RET, reflecting longer-term MPS.

171 on profile of MTC with regard to the type of RET gene mutation and the cancer genetic background (her

172 We report here that 20 weeks of RET also restores muscle MBF in older individuals.

173 and represses their regulatory functions on RET.

174 frequent variants in the ret proto-oncogene (RET).

175 give rise to constitutively active oncogenic RET, were found to cause multiple endocrine neoplasia ty

176 reveals an unappreciated role for oncogenic RET kinase mutations in promoting intermolecular autopho

177 Comparison with oncogenic RET kinase revealed that late autophosphorylation sites

178 RAS or PAX8/PPARG-positive TCs, BRAFV600E or RET/PTC-positive TCs were more often associated with sta

179 Downregulation of either parkin or RET in neuronal cells impaired mitochondrial function an

180 Knockdown of TFAP2C or RET inhibited GDNF (glial cell line-derived neurotrophic

181 gathered clinical information about patients'RET genotype, type of treatment for phaeochromocytoma (i

182 and exercise strategies, especially PS plus RET, to effectively improve the physical activity and he

183 IT, KRAS, MAP2K1, MET, NF1, NF2, NRAS, RAF1, RET, and ROS1 were found in 90 (72%) ACUPs but in only 2

184 y for TC with routine testing for BRAF, RAS, RET/PTC, and PAX8/PPARG alterations.

185 utic targets, including ROS1 rearrangements, RET fusions, MET amplification, and activating mutations

186 e show that the neurotrophic factor receptor RET (rearranged during transfection) drives haematopoiet

187 -derived neurotrophic factor (GDNF) receptor RET have both been independently linked to the dopaminer

188 he SRY targets, the tyrosine kinase receptor RET represents the most important disease gene, whose mu

189 and cell lines, we demonstrate that reduced RET expression propagates throughout its gene regulatory

190 eatment with sunitinib or vandetanib reduced RET-dependent growth of luminal breast cancer cells.

191 tion of CRE variants synergistically reduces RET expression and its effects throughout the GRN.

192 The resulting RET-BDP shows significantly enhanced absorption and sing

193 s, demonstrating that, like full-length RET, RET(DeltaE3) and RET(DeltaE345) are trafficked to the ce

194 XT training and then examined EXT retention (RET) 24 h later to determine whether dexamethasone suppr

195 Together these findings reveal RET as a novel dual kinase with nuclear localization and

196 N 2A syndrome demonstrated the moderate risk RET p.Val804Met (protein valine at residue 804 replaced

197 druggable kinase fusions involving ALK, ROS, RET, NTRK and FGFR gene families were detected in bladde

198 Oncogenic kinase fusions of ALK, ROS1, RET, and NTRK1 act as drivers in human lung and other ca

199 u hybridization and negative for EGFR, ROS1, RET, BRAF, KRAS, and other oncogenes.

200 TRIM4-BRAF, VAMP2-NRG1, TPM3-NTRK1 and RUFY2-RET in lung cancer, FGFR2-CREB5 in cholangiocarcinoma an

201 from these neuron-derived iPSCs called STEM-RET.

202 andardized quantitative protocol called STEM-RET.

203 Strikingly, RET signals provide haematopoietic stem cells with criti

204 r to Ret(-/-) cells, and that YAP suppresses RET signalling and tip identity.

205 Suppressing RET activity using Sunitinib, a clinically-approved tyro

206 ib, the tyrosine kinase inhibitors targeting RET, vascular endothelial growth factor receptor, epider

207 ngly inhibited phosphorylation of all tested RET oncoproteins.

208 We conclude that RET enhances fed-state LBF and MBV and restores nutrient

209 ent and Ret mutant mice, we demonstrate that RET-mediated GDNF signaling in UGS increases proliferati

210 Signaling experiments indicate that RET(DeltaE3) is phosphorylated in a similar manner to fu

211 It is well known that RET mutations affecting the cysteine-rich region of the

212 We observed that RET physically interacted with and phosphorylated ATF4 a

213 ysis of human cancer specimens revealed that RET expression is upregulated during PDAC tumorigenesis.

214 Taken together, our findings show that RET is upregulated during pancreas tumorigenesis and its

215 The RET (rearranged during transfection) proto-oncogene enco

216 The RET proto-oncogene, a tyrosine kinase receptor, is widel

217 in a subset of ER(+) breast cancers, and the RET ligand, glial-derived neurotrophic factor (GDNF) is

218 alpha-mediated activation of the ERE and the RET promoter contains three EREs.

219 of the QDs to the EuNPs is prevented and the RET signal decreases.

220 se observations indicate that parkin and the RET signaling cascade converge to control mitochondrial

221 SC using CRISPR/Cas9 editing, as well as the RET G731del mutation that causes Hirschsprung disease wi

222 tic screening for a germline mutation at the RET gene was performed in 11 family members.

223 ommon disease-susceptibility variants at the RET, SEMA3 and NRG1 loci have been detected through geno

224 f seven common susceptibility alleles at the RET, SEMA3 and NRG1 loci.

225 ese effects were selectively reverted by the RET kinase inhibitor, NVP-BBT594.

226 of TNFalpha or IL-1beta were blocked by the RET-receptor blocker vandetanib.

227 d that BM-derived macrophages expressing the RET ligand GDNF are highly abundant around nerves invade

228 disorder caused by germline mutations in the RET (formerly MEN2A, MEN2B) proto-oncogene located on ch

229 entified an intronic enhancer variant in the RET gene disrupting SOX10 binding and increasing Hirschs

230 cing to phase two variants 9 kb apart in the RET gene.

231 ecific G-quadruplex structures formed in the RET promoter region act to repress the transcription of

232 eoplasia type 2 (MEN2) have mutations in the RET protooncogene and virtually all of them will develop

233 e activating germline point mutations in the RET, which are known to induce oncogenic activation of R

234 hibit fed-state increases in LBF or MBV, the RET group exhibited increases in both LBF and MBV.

235 Oncogenic conversion of the RET (rearranged during transfection) tyrosine kinase is

236 CRISPR/Cas9 correction of the RET G731del and VCL M209L mutations in iPSCs restored th

237 zygous mutations in the coding region of the RET gene cause a severe form of Hirschsprung disease (to

238 al role in transcriptional regulation of the RET gene in vivo, providing insight into a novel strateg

239 We also noticed that the site of the RET gene mutation slightly influenced the gene expressio

240 For the detection of C533G mutation of the RET gene, biotinylated oligonucleotide probes were used.

241 iers of germline pathogenic mutations of the RET gene, or were first-degree relatives with histologic

242 ignificantly higher expression levels of the RET oncogene in ASCL1-positive tumors (ASCL1(+)) compare

243 CL1 as a potential upstream regulator of the RET oncogene.

244 ) can be caused by germline mutations of the RET proto-oncogene or occurs as a sporadic form.

245 Here, we measure how activation of the RET receptor tyrosine kinase on mouse neuroblastoma cell

246 respective transactivation activities on the RET promoter.

247 Finally, whereas only the RET group exhibited fed-state suppression of MPB ( appro

248 ARTN signals primarily through the RET tyrosine kinase, an interaction that requires the no

249 When in trans with the RET intron 1 enhancer risk allele, rs9282834 increases t

250 reveal a second non-coding variant distal to RET and a non-coding allele on chromosome 7 within the c

251 lockade, our results extended this effect to RET and NTRK1 blockade and uncovered the other additiona

252 (-/-) phenotype resemble hypersensitivity to RET signaling, including excess budding of the ND, incre

253 ind nonspecifically to the EuNPs, leading to RET.

254 related to RET(M918T) and GAL as related to RET(634) mutation.

255 PROM1, LOXL2, GFRA1, and DKK4 as related to RET(M918T) and GAL as related to RET(634) mutation.

256 g effectors in different pathways respond to RET activation with different lag times, such that the b

257 0.1% day(-1) ), MPS increased in response to RET only in Y (3 weeks, Y: 1.61 +/- 0.1% day(-1) ; O: 1.

258 Hypertrophic responses to RET with age are diminished compared to younger individu

259 f rapamycin complex 1 signaling responses to RET, beyond 3 wk.

260 ynthesis (MPS) and hypertrophic responses to RET.

261 ed, whole-body resistance exercise training (RET) (72.8 +/- 1.4 years; BMI 26.3 +/- 1.2 kg m(2) ).

262 Resistance exercise training (RET) can rejuvenate limb blood flow responses to nutriti

263 Resistance exercise training (RET) has a beneficial effect on muscle protein synthesis

264 Resistance exercise training (RET) is one of the most effective strategies for prevent

265 Resistance exercise training (RET) is widely used to increase muscle mass in athletes

266 c responses to resistance exercise training (RET).

267 tions in the rearranged during transfection (RET) proto-oncogene.

268 Rearranged during transfection (RET), a receptor tyrosine kinase that is activated by th

269 ptor (EGFR), rearranged during transfection (RET), anaplastic lymphoma kinase (ALK), and MAPK1/3 and

270 Met), EphA2, rearranged during transfection (RET), and insulin-like growth factor I receptor.

271 eptor 2, and rearranged during transfection (RET), demonstrated clinical activity in patients with me

272 assay is based on resonance energy transfer (RET) between two luminescent nanosized particles.

273 nted to utilize a resonance energy transfer (RET) mechanism to construct a novel dyad photosensitizer

274 and the design of resonance energy transfer (RET) networks are demonstrated.

275 Resonance energy transfer (RET)-based biosensors allow for all of these possibiliti

276 ), and retrovirus-mediated episome transfer (RET) represent powerful methodologies for transient prot

277 ipole homogeneous resonance energy transfer, RET.

278 succinate-driven reverse electron transport (RET) through complex I as a major source of damaging rea

279 Succinate-driven reverse electron transport (RET) through complex I is hypothesized to be a major sou

280 al analysis of oncogenic M918T and wild-type RET kinase domains reveal a cis-inhibitory mechanism inv

281 e phosphorylated much earlier than wild-type RET, which is due to a combination of an enhanced enzyma

282 in response to PS in older people undergoing RET remains unclear.This study was conducted to identify

283 lity improvements in older people undergoing RET.We included 17 RCTs; the overall mean +/- SD age and

284 physical function of older people undergoing RET.We performed a comprehensive search of online databa

285 9 +/- 3 years), performed 6 weeks unilateral RET (6 x 8 repetitions, 75% of one repetition maximum (1

286 rosine kinase inhibitor, targets MET, VEGFR, RET, ROS1, and AXL, which are implicated in lung cancer

287 a novel tyrosine kinase inhibitor of VEGFR2, RET, and EGFR, all of which are in involved in the patho

288 In response to 6 weeks RET, we found blunted hypertrophic responses with age ar

289 However, the mechanisms by which RET promotes cell survival and prevents cell death remai

290 localization and provide mechanisms by which RET represses the proapoptotic genes through direct inte

291 ults suggest (1) the dimensionality in which RET occurs is dependent on the RuDCBPY concentration ran

292 PS.Compared with RET alone, PS combined with RET may have a stronger effect in preventing aging-relat

293 levant gains in response to PS.Compared with RET alone, PS combined with RET may have a stronger effe

294 ches will be needed to improve outcomes with RET-directed targeted treatment.

295 , 2012, and April 30, 2016, 26 patients with RET-rearranged lung adenocarcinomas were enrolled and gi

296 The accrual of patients with RET-rearranged lung cancer to this protocol has been com

297 ed activity of cabozantinib in patients with RET-rearranged lung cancers defines RET rearrangements a

298 he activity of cabozantinib in patients with RET-rearranged lung cancers, we did a prospective phase

299 tant metastasis was highest in patients with RET/PTC-positive TC (10.8%, P = 0.02).

300 th gains when PS and RET were used than with RET alone, with the standard mean differences (SMDs) bei