ライフサイエンスコーパス: KIT

1 KIT and KITLG are expressed by a subset of human colon t

2 KIT and KITLG were expressed heterogeneously by a subset

3 KIT and PDGFRA mutations account for 85-90% of GISTs; su

4 KIT and/or KITLG was stably knocked down by expression o

5 KIT D816V is present in a majority of patients with syst

6 KIT D816V was detected in 92/105 patients (88%).

7 KIT D816V-mutated MSCs were detected in 22 of 83 cases.

8 KIT exon 11 deletion mutations, deletions that involved

9 KIT exon 11 mutations were further grouped as deletion o

10 KIT is targeted for cancer therapy in gastrointestinal s

11 KIT K509I biopsied mast cells were round, CD25(-), and w

12 KIT K509I progenitors cultured in stem cell factor (SCF)

13 KIT knockdown also increased RAS/MAPK pathway activation

14 KIT knockdown cells had increased expression of enterocy

15 KIT mutations were detected in only 10 (30%) of 33 patie

16 KIT signaling promotes growth of colon cancer cells and

17 KIT, PDGFRA, NF1 and SDH mutations are alternate initiat

18 ing of the regenerated donor Lin(-) SCA-1(+) KIT(+) (LSK) cells shows dysregulated expression of ZEB1

19 aring mast cells (MCs) often lacking exon 17 KIT mutations.

20 P53 (13%), NRAS (13%), SNX31 (9%), NF1 (9%), KIT (7%) and APC (7%).

21 in patients with metastatic GIST harboring a KIT exon 11 mutation.

22 trial to evaluate the effect of imatinib, a KIT inhibitor, on airway hyperresponsiveness, a physiolo

23 KIT exon 11 deletion of any type, but not a KIT exon 11 insertion or point mutation, KIT exon 9 muta

24 rcomas and the oncogenic driver is usually a KIT or PDGFRA mutation.

25 ssociated with higher RFS in patients with a KIT exon 11 deletion of any type, but not a KIT exon 11

26 3-year group), 274 (80.4%) had GISTs with a KIT mutation, 43 (12.6%) had GISTs that harbored a PDGFR

27 , whereas targeted DNMT1 depletion abrogates KIT signaling cascade through Sp1/miR-29b network.

28 e treatments for cancers driven by activated KIT and other RTKs may rely on clear understanding of th

29 The discovery of activated KIT mutations in gastrointestinal (GI) stromal tumors (G

30 Interestingly, activating KIT mutations also promoted sensitivity to TRAIL-mediate

31 oplastic mast cells harboring the activating KIT mutation D816V in the bone marrow and other internal

32 reatment concepts use drugs directed against KIT and other relevant targets in neoplastic mast cells

33 and multikinase inhibitors directed against KIT D816V and other key signaling molecules.

34 PDGFRA-mutant GIST, similar progress against KIT/PDGFRA wild-type GIST, including mutant BRAF-driven

35 AS (21%), TP53 (16%), BRAFNon-V600 (6%), and KIT (4%).

36 yrosine kinase activity of ABL1/BCR-ABL1 and KIT, platelet-derived growth factor receptors (PDGFRs),

37 on of the receptor tyrosine kinases, ALK and KIT.

38 transcripts POU5F1, TFAP2C, LIN28A, ALPP and KIT were also reduced by ibuprofen.

39 The prevalence of BRAFV600 and KIT mutations were significantly associated with melanom

40 Xenograft tumors were grown from control and KIT-knockdown DLD1 and UM-COLON#8 cells in immunocomprom

41 We demonstrated that DNMT1 and KIT form a positive regulatory loop, in which ectopic DN

42 Overexpression of DNMT1 and KIT is prevalent in lung cancer, yet the underlying mole

43 ncer pathogenesis, whether and how DNMT1 and KIT orchestrate lung tumorigenesis are unclear.

44 ing from simultaneous inhibition of FLT3 and KIT.

45 ly druggable, mutations in the EGFR, MET and KIT oncogenes.

46 Finally, cabozantinib, a dual MET and KIT small-molecule inhibitor, was markedly more effectiv

47 targets IKBKB, WEE1, FGF2, RAD50, MSH2, and KIT.

48 PDGFRA mutations and KIT exon 11 insertion or duplication mutations were asso

49 rived growth factor receptor alpha, RET, and KIT, showed clinical activity in a phase 2 study involvi

50 ing consensus, our results show that SCF and KIT signaling are dispensable for early mast cell develo

51 ive, mature, and proliferate without SCF and KIT signaling in vitro.

52 n that mast cell progenitors require SCF and KIT signaling throughout differentiation.

53 ssumed to require stem cell factor (SCF) and KIT signaling during differentiation for the formation o

54 udy describes the role of mTOR signaling and KIT ligand in granulosa cells of primordial follicles fo

55 ), size of the largest lesion (smaller), and KIT mutation (exon 11) were significant prognostic facto

56 did not show mediator-related symptoms, and KIT D816V-positive MCs obtained from patients with SM di

57 S-tryptase and KIT D816V allele burden were monitored.

58 class of KIT mutants responded well to anti-KIT antibody treatment alone or in combination with a lo

59 n of TKI with anti-KIT antibodies or to anti-KIT toxin conjugates, respectively.

60 onded well to a combination of TKI with anti-KIT antibodies or to anti-KIT toxin conjugates, respecti

61 EAB) at month 6, patients were classified as KIT responders (>/=25%, n = 17) or KIT nonresponders (<2

62 studies of 20 cases originally classified as KIT/PDGFRA wild-type GIST revealed that 17 (85.0%) harbo

63 Only, the siliceous material labelled as KIT-6 was not suitable for wine fining.

64 y be possible to define anti-targets such as KIT in the case of AML to allow improved kinase inhibito

65 for selective FLT3 inhibition while avoiding KIT inhibition with the staurosporine analog, Star 27.

66 dings identify functional cross-talk between KIT and DNMT1 in the development of drug resistance, imp

67 In addition, CCL2 secreted by KIT D816V(+) mast cells was found to promote the migrati

68 activation of compensatory MET signaling by KIT inhibition may contribute to tumor resistance.

69 SM), disease evolution is often triggered by KIT mutations (D816V in >80% of cases) and by additional

70 Capsaicin did not alter c-KIT expression or nasal epithelial morphology in patient

71 receptors, VEGF receptors, PDGFR-beta, and c-KIT, as second-line therapy both in patients with FGFR2-

72 me B and CD107A), resistance to apoptosis (c-KIT and Bcl2), and enhanced stemness (beta-catenin and L

73 seq) in SSEA4(+) hSSCs and differentiating c-KIT(+) spermatogonia, and performed validation studies v

74 L LSCs, including receptor tyrosine kinase c-KIT and FMS-related tyrosine kinase 3 (FLT3).

75 by targeting the receptor tyrosine kinase c-KIT.

76 ce the distribution of melanocyte markers (C-KIT, DCT, PAX3, and TYR) coupled with markers of prolife

77 Inhibition of c-KIT and FLT3 expression significantly inhibited JAK/STAT

78 k for relapse, together with the impact of c-KIT mutations.

79 ible secondary melanocyte germ composed of C-KIT+ melanocytes was found in the infundibulum and inter

80 use basal cells selected for expression of c-KIT.

81 d was more predictive of relapse risk than c-KIT mutations.

82 We show that c-KIT signaling regulates self-renewal capacity and preven

83 x sequence from the promoter region of the c-KIT gene forms a stable quadruplex, as characterized by

84 Treatment of mice with the c-KIT inhibitor imatinib mesylate limited effusion precipi

85 or of a G-rich sequence located within the c-KIT proximal promoter (kit2) in the presence of monovale

86 existing structures, demonstrate that the c-KIT quadruplex fold does not change with differing envir

87 hereas the P/-8-kb enhancer targeted TIE2+/c-KIT+/CD41- endothelial cells that were enriched for hema

88 0% (P 5 .12) for patients with and without c-KIT mutations, respectively.

89 management of GIST harboring the most common KIT and PDGFRA mutations, optimal management of other ge

90 em cell factor (SCF)-induced or constitutive KIT activation.

91 trointestinal stromal tumors (GISTs) contain KIT or PDGFRA kinase gain-of-function mutations, and the

92 signal transduction by directly controlling KIT receptor expression, suggesting its potential as a t

93 tized PKC412(R) cells to PKC412; conversely, KIT depletion synergized with decitabine in eliminating

94 diated inflammatory diseases and deregulated KIT disorders.

95 FLT3, NRAS, PTPN11, WT1, TET2, DHX15, DHX30, KIT, ETV6, KRAS), with variable persistence at relapse.

96 perties and responds distinctly to different KIT inhibitors.

97 or binimetinib further decreased downstream KIT signaling.

98 ion is not unspecific, because ligand-driven KIT internalization is not accompanied by CD13 internali

99 most harbor an activating mutation in either KIT or platelet-derived growth factor A ( PDGFRA).

100 Cancer cells with endogenous KIT expression were more tumorigenic in mice.

101 Accordingly MITF reconstitution enhances KIT expression levels in 3BP2-silenced cells.

102 genesis, reduced proliferation of epithelial KIT(+) progenitors, and increased expression of a target

103 by mesenchymal cells can regulate epithelial KIT(+) progenitor cell expansion during murine salivary

104 elanocytes during development, and excessive KIT activity hyperactivates the RAS/MAPK pathway and can

105 3-O-HS may expand KIT+ progenitors in vitro for regenerative therapy.

106 ions in ALK, ARAF, BRAF, EGFR, FGFR1, FGFR2, KIT, KRAS, MAP2K1, MET, NF1, NF2, NRAS, RAF1, RET, and R

107 hms, and discovered additional ITDs in FLT3, KIT, CEBPA, WT1 and other genes.

108 , localized GISTs with mutation analysis for KIT and PDGFRA performed centrally using conventional se

109 ients with this mutation may be eligible for KIT kinase inhibitor-based therapy.

110 oward stem cell factor (SCF), the ligand for KIT receptor.

111 To identify novel targets responsible for KIT oncoprotein function, we performed parallel genome-s

112 pigenetic regulator of genes responsible for KIT(+) progenitor expansion during organogenesis.

113 g1-null mice, there was loss of staining for KIT in DMP and SMP regions, as well as for 2 additional

114 tations or amplifications; and sunitinib for KIT or PDGFRA mutations or amplification.

115 of the myenteric plexus (ICC-MY) arise from KIT-positive progenitor cells during mouse embryogenesis

116 KIT-expressing colon tumors can benefit from KIT RTK inhibitors.

117 signal transduction pathways emanating from KIT for tumorigenesis, the oncogenic Kit(V558Delta) muta

118 Functionally, KIT and DNMT1 co-expression promotes, whereas dual inact

119 Furthermore, KIT tyrosine activity inhibition reduced 3BP2 and MITF e

120 ht to investigate the effect of the germline KIT K509I mutation on human mast cell development and fu

121 Mastocytosis associated with germline KIT activating mutations is exceedingly rare.

122 been reported, including those with germline KIT and PDGFRalpha mutations.

123 High KIT mutant allele ratios defined a group of t(8;21) AML

124 rmatogonia committing to gametogenesis (high KIT(+)).

125 man 4 feline sarcoma viral oncogene homolog (KIT) receptor tyrosine kinase.

126 Rapid autocrine feedback increases 3-O-HS, KIT, and progenitor expansion.

127 ified a panel of 6 genes, ALDH1A1, HSP90AB1, KIT, KRT16, SPRR3 and TMEM45B whose expression values di

128 hylation; in turn, DNMT1 dysfunction impairs KIT kinase signaling.

129 t work, we found that 3BP2 silencing impairs KIT signaling pathways, thus affecting phosphoinositide

130 ive therapy showed a significant decrease in KIT D816V (P < 0.05).

131 pression, a transcription factor involved in KIT expression.

132 rpin RNA (shRNA)-mediated gene knockdowns in KIT-mutant GIST-T1 and GIST882.

133 Activating mutations in KIT have been associated with several diseases including

134 Activating mutations in KIT have been identified in melanomas of acral and mucos

135 or older with known WT GIST (no mutations in KIT or PDGFRA) were recruited; 116 patients with WT GIST

136 Gain-of-function mutations in KIT or PDGFRalpha are key drivers in most gastrointestin

137 No activating mutations in KIT were detected in DLD1, POP77, or UM-COLON#8 cells.

138 cluding novel recurrent somatic mutations in KIT, its downstream mediators KRAS and NRAS, and its neg

139 quently mutated, with recurrent mutations in KIT, TSC2, and MAPK pathway genes (BRAF, KRAS, and NRAS)

140 se inhibitors to overcome these mutations in KIT.

141 regulates huMC survival and participates in KIT-mediated signal transduction by directly controlling

142 onic and adult cardiac stem cells, including KIT(+), PDGFRalpha(+), ISL1(+)and SCA1(+)cells, side pop

143 ions in receptor tyrosine kinases, including KIT.

144 ivating tyrosine kinase signaling (including KIT, N/KRAS, and FLT3) were frequent in both subtypes of

145 4 in human mast cells altered ligand-induced KIT endocytosis pathways and reduced receptor recycling

146 Masitinib inhibits KIT and LYN kinases that are involved in indolent system

147 e multikinase inhibitor midostaurin inhibits KIT D816V, a primary driver of disease pathogenesis.

148 Imatinib treatment, which inhibits KIT signaling, depletes mast cells in vivo.

149 We isolated KIT+ progenitors from fetal salivary glands during a sta

150 ransferase DNMT1 and tyrosine-protein kinase KIT, the enhanced phosphorylation of KIT and its downstr

151 The receptor tyrosine kinase KIT plays an important role in development of germ cells

152 The receptor tyrosine kinase KIT promotes survival and migration of melanocytes durin

153 trafficking of the receptor tyrosine kinase KIT through endocytic recycling rather than degradation

154 ng mutations in the receptor tyrosine kinase KIT.

155 KIT proto-oncogene receptor tyrosine kinase (KIT) and platelet-derived growth factor receptor alpha (

156 se of the oncogenic protein tyrosine kinase (KIT)-containing exosomes, which triggers the phenotypic

157 d dimers of intact receptor tyrosine kinase, KIT.

158 Also, KITLG-KIT signaling and MITF are suggested to mutually interac

159 testinal stromal tumors (WT-GISTs) that lack KIT or PDGFRA mutations represent a unique subtype of GI

160 ntestinal stromal tumors (GISTs), which lack KIT and PDGFRA gene mutations, are the primary form of G

161 D842V mutation or patients with GIST lacking KIT and PDGFRA mutations.

162 Here, we show that each of the six major KIT oncogenic mutants exhibits different enzymatic, cell

163 e subtype of advanced systemic mastocytosis, KIT mutation status, or exposure to previous therapy.

164 ed phase 2 study, midostaurin, a multikinase/KIT inhibitor, demonstrated an overall response rate (OR

165 All MSC-mutated patients had multilineage KIT mutation (100% vs 30%, P = .0001) and they more freq

166 sing molecules for the inhibition of mutated KIT.

167 t a KIT exon 11 insertion or point mutation, KIT exon 9 mutation, PDGFRA mutation, or wild-type tumor

168 ck of metabolic response (P < 0.001) and non-KIT exon 11-mutated GISTs (P < 0.001).

169 anagement in GIST patients harboring the non-KIT exon 11 mutation and should be considered the standa

170 summary, we have identified CCL2 as a novel KIT D816V-dependent key regulator of vascular cell migra

171 We report a novel KIT gain-of-function mutation with S628N substitution (e

172 y described.OBSERVATIONS We describe a novel KIT mutation in a patient with metastatic melanoma.

173 Until now, KIT has been considered an oncogenic driver and a potent

174 melanomas and lack mutations in BRAF, NRAS, KIT, and NF1.

175 terns lacked common mutations in BRAF, NRAS, KIT, GNAQ, and HRAS.

176 ed a MEGS with five genes (FLT3, IDH2, NRAS, KIT, and TP53) and a MEGS (NPM1, TP53, and RUNX1) whose

177 In the absence of KIT D816V and other signs or symptoms of mastocytosis or

178 Activation of KIT regulates the function of TRAIL-Rs in MCs.

179 ured murine and human MCs upon activation of KIT.

180 lls and supported the clonogenic capacity of KIT(+) colonosphere cells.

181 ttern of inactivation of the X-chromosome of KIT-mutated BM mast cells (64% vs 0%; P = .01) vs other

182 One class of KIT mutants responded well to anti-KIT antibody treatmen

183 A second class of KIT mutants, including a mutant resistant to imatinib tr

184 Moreover, downregulation of KIT expression by miRNA-221 overexpression or the protea

185 uggest that signaling pathways downstream of KIT may have distinct and opposing roles in the pathogen

186 tion of intracellular pathways downstream of KIT, expression of Interstitial Cell of Cajal-like marke

187 ve microtubule assembly and dysregulation of KIT-MAPK signaling also feature as recurrently disrupted

188 To investigate the effect of KIT and PDGFRA mutations on recurrence-free survival (RF

189 Hypoxia induced expression of KIT in cultured cells and in human colon tumor xenograft

190 Expression of KIT in human tumors was analyzed with gene expression ar

191 tween a morphogen (RA) and the expression of KIT protein, which together direct the differentiation o

192 ed a requirement for RA in the expression of KIT, a receptor tyrosine kinase essential for spermatogo

193 of ets variant 1 and increased expression of KIT, causing rapid GE.

194 revealed a correlation between expression of KIT- and hypoxia-related genes in colon tumors, which wa

195 Imatinib inhibited growth of KIT(+) colon cancer organoids in culture and growth of x

196 active DNMT1 or KIT, because inactivation of KIT or DNMT1 reciprocally blocked decitabine(R) or PKC41

197 Conversely, an increase of KIT levels augments, but a reduction of KIT expression a

198 osperes; this was prevented by inhibition of KIT or SCF.

199 Knockdown of KIT decreased proliferation of colon cancer cell lines a

200 n and RNA interference-mediated knockdown of KIT reduced expression of CCL2.

201 lele ratios were associated with the lack of KIT or FLT3 mutations and a favorable outcome.

202 by immunohistochemistry to measure levels of KIT and its ligand KITLG.

203 these melanomas exhibit a surprising loss of KIT expression, which raises the question of whether los

204 which raises the question of whether loss of KIT in these tumors facilitates tumorigenesis.

205 umber gain of chromosome 12p and mutation of KIT, we identify recurrent mutations in the tumour suppr

206 MCs) associated with activating mutations of KIT.

207 kinase KIT, the enhanced phosphorylation of KIT and its downstream effectors, and the increased glob

208 Moreover, presence of KIT-mutated MSCs was associated with more advanced disea

209 Moreover, suppressing production of KIT-ligand in Sca1(+) progenitors inhibits their ability

210 by a mechanism that involves recruitment of KIT to caveolin-1-enriched microdomains.

211 univariate analyses at month 6, reduction of KIT D816V EAB >/=25%, tryptase >/=50%, and alkaline phos

212 e of KIT levels augments, but a reduction of KIT expression ablates DNMT1 transcription by STAT3 path

213 3BP2 in knockdown cells leads to reversal of KIT expression as well as survival phenotype.

214 ib influences the prognostic significance of KIT proto-oncogene receptor tyrosine kinase (KIT) and pl

215 osine in the prophase nucleus of a subset of KIT(+) progenitors during mitosis.

216 The altered endocytic trafficking of KIT also resulted in an increase in SCF-induced mast cel

217 espite clinical advances in the treatment of KIT/PDGFRA-mutant GIST, similar progress against KIT/PDG

218 sitively correlated with the upregulation of KIT in tumor tissues.

219 l have important implications for the use of KIT inhibitors in treating melanomas.

220 acking the SRC family kinase-binding site on KIT (pY567) exhibited attenuated MAPK signaling and tumo

221 abrogating specific phosphorylation sites on KIT.

222 Oncogenic KIT mutations play an important "driver" role in gastroi

223 eating cancers driven by all known oncogenic KIT mutants.

224 of the activities of a variety of oncogenic KIT mutations, reveals that the strength of homotypic co

225 In multivariate analysis, only KIT D816V EAB reduction >/=25% remained an independent o

226 sified as KIT responders (>/=25%, n = 17) or KIT nonresponders (<25%, n = 11).

227 While the deregulated activation of DNMT1 or KIT has been implicated in lung cancer pathogenesis, whe

228 were attributed to the hyperactive DNMT1 or KIT, because inactivation of KIT or DNMT1 reciprocally b

229 Suppression of SCF or KIT signaling greatly reduced the expression of genes th

230 ecycling to the cell surface, thus promoting KIT signaling in the endosomes while reducing that in th

231 igenicity that was caused by the reactivated KIT kinase signaling and further CDH1 silencing.

232 kinase mast/stem cell growth factor receptor KIT is an example of a clinically relevant RTK.

233 Stem cell factor and its receptor, KIT, are central to mast-cell homeostasis.

234 Some recurrent KIT mutations are well characterized; others are poorly

235 Unexpectedly, silencing of 3BP2 reduces KIT expression in normal huMCs as well as in HMC-1 cells

236 3BP2 silencing reduces KIT transcription expression levels.

237 ase (encoded by Ptpn11) positively regulates KIT (CD117) signaling in mast cells and is required for

238 h prior observations for the closely related KIT receptor.

239 ike domain (D5) of the ectodomain, rendering KIT tyrosine kinase activity constitutively activated.

240 and they systematically showed MC-restricted KIT mutation.

241 eral signaling pathways were activated, ROSA(KIT D816V) did not exhibit an increased, but did exhibit

242 Moreover, NSG mice bearing ROSA(KIT D816V)-derived tumors did not show mediator-related

243 T) cells into an SCF-independent clone, ROSA(KIT D816V), which produced a mastocytosis-like disease i

244 Transfection with KIT D816V converted ROSA(KIT WT) cells into an SCF-independent clone, ROSA(KIT D8

245 We investigated the role of the RTK KIT in development of human colon cancer.

246 , SHP2 inhibitors may be useful to limit SCF/KIT-induced mast cell recruitment to inflamed tissues or

247 Sensitive KIT D816V mutation analysis of blood has been proposed t

248 tional investigations, including a sensitive KIT mutation analysis of blood leucocytes or measurement

249 The outcome of sensitive KIT D816V analysis of blood was compared to the result o

250 one marrow (BM) hematopoiesis by the somatic KIT D816V mutation is present in a subset of adult indol

251 risk of GIST recurrence associated with some KIT mutations, including deletions that affect exon 11 c

252 prognostic factors, only performance status, KIT mutation, and size of largest lesion predicted long-

253 We provided evidence that KIT inactivation induces global DNA hypomethylation, res

254 lysis of single CD44(+) cells indicated that KIT can promote growth via KITLG autocrine and/or paracr

255 We observe that KIT protomers form close contacts throughout the entire

256 Our data show that KIT D816V is a disease-propagating oncoprotein, but it d

257 Here we show that KIT D816V promotes expression of the proangiogenic cytok

258 Together, these results suggest that KIT can activate signaling through wild-type RAF protein

259 These results suggest that KIT-dependent processes and mast cells contribute to the

260 The KIT D816V burden also correlated with serum tryptase (R

261 The KIT receptor whose ligand is the stem cell factor is nec

262 ents with mutated MSCs may have acquired the KIT mutation in a common pluripotent progenitor cell, pr

263 Finally, brentuximab-vedotin and the KIT D816V-targeting drug PKC412 produced synergistic gro

264 l stem cells (MSCs) from ISM patients by the KIT D816V mutation and its potential impact on disease p

265 To conclude, the KIT D816V burden correlates with the variant of mastocyt

266 Correspondingly, the KIT-targeting drug midostaurin and RNA interference-medi

267 We determined the KIT D816V allele burden by quantitative real-time PCR in

268 We find the KIT/RAS signalling pathway frequently mutated in more th

269 ASqPCR for the KIT D816V mutation was a useful adjunct in helping ident

270 e-specific quantitative PCR (ASqPCR) for the KIT D816V mutation, and a bone marrow examination.

271 KITLG encodes a ligand for the KIT receptor.

272 rs, and identified frequent mutations in the KIT gene.

273 ically containing secondary mutations in the KIT kinase domain, which can be heterogeneous between an

274 on 13, resulted in S628N substitution in the KIT receptor.

275 only 10 (30%) of 33 patients, including the KIT D816V (n = 5), K509I (n = 3), N819Y (n = 1), and I81

276 et al. show that in cutaneous melanomas the KIT promoter is a target for hypermethylation, leading t

277 Depending on the relative reduction of the KIT D816V expressed allele burden (EAB) at month 6, pati

278 dentification of activating mutations of the KIT gene in gastrointestinal stromal tumor (GIST)-the mo

279 ed a 42-base pair deletion in exon 11 of the KIT gene that would delete all or part of codons 558 to

280 a clinical point of view, acquisition of the KIT mutation in an earlier BM precursor cell confers a s

281 f, or highly suspected SM, regardless of the KIT mutation status.

282 rom PAG-knockout mice were activated via the KIT receptor, enhanced degranulation and tyrosine phosph

283 lso expressed cell surface CD30, whereas the KIT-transformed MC line HMC-1.2 expressed no detectable

284 tions enriched for particular markers (THY1, KIT, OCT4, ID4, or GFRa1).

285 nd that nuclear factor kappaB contributes to KIT-dependent upregulation of CCL2 in mast cells.

286 Paracrine signaling from SCF to KIT, between differentiated tumor cells and undifferenti

287 LC-associated IL7R (CD127), TNFSF10 (TRAIL), KIT (CD117), IL2RA (CD25), CD27, CXCR3, DPP4 (CD26), GPR

288 No significant changes in s-tryptase/KIT D816V allele burden were observed.

289 normal huMCs as well as in HMC-1 cells where KIT is mutated, thus increasing cellular apoptosis and c

290 were associated with favorable RFS, whereas KIT exon 9 mutations were associated with unfavorable ou

291 he action of D4D5 regions determines whether KIT is normally regulated or constitutively activated in

292 erapeutic target in diseases associated with KIT mutations, such as mastocytosis.

293 says of FLT3-transformed cells compared with KIT-transformed cells, shows no toxicity towards normal

294 unrecognized clonal mast cell disorders with KIT mutations may present as Hymenoptera-induced or idio

295 Patients with KIT exon 11 deletion mutations benefit most from the lon

296 Patients with KIT exon 11 deletion or insertion-deletion mutation had

297 Patients with KIT exon 11 deletions assigned to 1 year of adjuvant ima

298 Patients with KIT-expressing colon tumors can benefit from KIT RTK inh

299 Similarly, in the subset with KIT exon 11 deletion mutations, higher-than-the-median m

300 Transfection with KIT D816V converted ROSA(KIT WT) cells into an SCF-indep