ライフサイエンスコーパス: gastrointestinal stromal tumor

1 of acute lymphoblastic leukemia), and c-Kit (gastrointestinal stromal tumor).

2 aganglioma (PPGL), renal cell carcinoma, and gastrointestinal stromal tumor.

3 ests performed to confirm the diagnosis of a gastrointestinal stromal tumor.

4 utcomes in Ewing's, soft tissue sarcomas and gastrointestinal stromal tumor.

5 with an advanced unresectable or metastatic gastrointestinal stromal tumor.

6 tivity of imatinib in patients with advanced gastrointestinal stromal tumor.

7 and the association of c-kit mutations with gastrointestinal stromal tumor.

8 d clinical course of pediatric patients with gastrointestinal stromal tumor.

9 homas, sarcoma, hepatomas, mesothelioma, and gastrointestinal stromal tumor.

10 se inhibitors with activity against advanced gastrointestinal stromal tumors.

11 ic mutations in mast-cell proliferations and gastrointestinal stromal tumors.

12 noted in the understanding and management of gastrointestinal stromal tumors.

13 for treatment monitoring for lung cancer and gastrointestinal stromal tumors.

14 provided insight into the true incidence of gastrointestinal stromal tumors.

15 o reevaluate the role of surgery in advanced gastrointestinal stromal tumors.

16 b for either chronic myelogenous leukemia or gastrointestinal stromal tumors.

17 subsequently found to treat c-Kit-expressing gastrointestinal stromal tumors.

18 st cell disease, acute myeloid leukemia, and gastrointestinal stromal tumors.

19 enous leukemia, human mast cell disease, and gastrointestinal stromal tumors.

20 ult human mastocytosis (SAHM) and with human gastrointestinal stromal tumors.

21 ne kinase is critical in the pathogenesis of gastrointestinal stromal tumors.

22 terine and ovarian cancer, colon cancer, and gastrointestinal stromal tumors.

23 ucosal tumors such as lipoma, leiomyoma, and gastrointestinal stromal tumors.

24 s a clinically validated target for treating gastrointestinal stromal tumors.

25 yeloid leukemia and in 2002 for treatment of gastrointestinal stromal tumors.

26 y activated and oncogenic in the majority of gastrointestinal stromal tumors.

27 iladelphia chromosome-positive leukemias and gastrointestinal stromal tumors.

28 43.8% vs 5.5%; difference, 38.2%), imatinib (gastrointestinal stromal tumor, 37.4% vs 6.1%; differenc

29 een implicated in many human cancers such as gastrointestinal stromal tumors, acute myeloid leukemia,

30 mutations play an important "driver" role in gastrointestinal stromal tumors, acute myeloid leukemias

31 oved for the treatment of imatinib-resistant gastrointestinal stromal tumors after recent encouraging

32 cancers, 40% of melanomas, and most cases of gastrointestinal stromal tumor and Ewing's sarcoma.

33 cent work in two selected soft tissue tumors-gastrointestinal stromal tumor and inflammatory myofibro

34 differences between children and adults with gastrointestinal stromal tumor and some new potential th

35 sine kinase KIT function as major drivers of gastrointestinal stromal tumors and a subset of acute my

36 he JMD of c-Kit and Flt3 are associated with gastrointestinal stromal tumors and acute myeloid leukem

37 Activating mutations in KIT are common in gastrointestinal stromal tumors and mastocytosis.

38 bitor recently approved for the treatment of gastrointestinal stromal tumors and renal cell carcinoma

39 man cancers, such as acute myeloid leukemia, gastrointestinal stromal tumor, and mast cell leukemia,

40 stance in other solid tumors (colon cancers, gastrointestinal stromal tumors, and melanomas) responsi

41 eoplasms, especially gastric adenocarcinoma, gastrointestinal stromal tumors, and primary gastric lym

42 copic and endosonographic features common to gastrointestinal stromal tumors, and the optimal tests p

43 Gastrointestinal stromal tumors are the most common sarc

44 Endosonographic features of gastrointestinal stromal tumors associated with high-ris

45 ligand or by RT activating mutations such as gastrointestinal stromal tumors but that neither compoun

46 g, medullary thyroid, pancreatic, colon, and gastrointestinal stromal tumors) but displays limited ex

47 a human mast cell line and in situ in human gastrointestinal stromal tumors, but have not been demon

48 an tumors, including leukemia, lymphoma, and gastrointestinal stromal tumors, but it is not constitut

49 With the exception of gastrointestinal stromal tumors, CD34 protein expression

50 ase 1A was shown to enhance imatinib-induced gastrointestinal stromal tumor cell death.

51 plied DESIDE to deduce signaling activity in gastrointestinal stromal tumor cell lines treated with t

52 nt paradigms changed with the discovery that gastrointestinal stromal tumor cells express KIT, a tyro

53 gh imatinib induces apoptosis in a subset of gastrointestinal stromal tumor cells, it leads to a reve

54 myxoid liposarcomas, clear-cell sarcomas and gastrointestinal stromal tumors displayed remarkably dis

55 bility of surgical enucleation of esophageal gastrointestinal stromal tumors (E-GISTs).

56 Treatment for gastrointestinal stromal tumors, formerly limited to sur

57 aired gene analysis was shown to distinguish gastrointestinal stromal tumor from leiomyosarcoma with

58 is performed on the tissue to differentiate gastrointestinal stromal tumors from other spindle cell

59 laparoscopic versus open surgery for gastric gastrointestinal stromal tumors (gGISTs).

60 chronous gastric tumors that consist of both gastrointestinal stromal tumor (GIST) and adenocarcinoma

61 ndition predisposing affected individuals to gastrointestinal stromal tumor (GIST) and paraganglioma,

62 mesylate targets mutated KIT oncoproteins in gastrointestinal stromal tumor (GIST) and produces a cli

63 Certain cancers, including gastrointestinal stromal tumor (GIST) and subsets of mel

64 outcome of patients diagnosed with advanced gastrointestinal stromal tumor (GIST) and treated long-t

65 Targeted therapies for gastrointestinal stromal tumor (GIST) are modestly effec

66 the pathologic and epidemiologic features of gastrointestinal stromal tumor (GIST) as well as the con

67 We report evidence that gastrointestinal stromal tumor (GIST) cells invade the i

68 A fraction of gastrointestinal stromal tumor (GIST) cells overexpress

69 ree survival (RFS) of patients with operable gastrointestinal stromal tumor (GIST) compared with plac

70 nt paradigm of imatinib-resistant metastatic gastrointestinal stromal tumor (GIST) does not incorpora

71 inib has exceptional activity in controlling gastrointestinal stromal tumor (GIST) due to inhibition

72 Gastrointestinal stromal tumor (GIST) follow-up is recom

73 Gastrointestinal stromal tumor (GIST) has become a model

74 A mouse model of gastrointestinal stromal tumor (GIST) has been developed

75 Gastrointestinal stromal tumor (GIST) has emerged as a c

76 defined pathologic oddity, in recent years, gastrointestinal stromal tumor (GIST) has emerged as a d

77 Knowledge related to gastrointestinal stromal tumor (GIST) in the setting of

78 Gastrointestinal stromal tumor (GIST) is a mesenchymal n

79 Gastrointestinal stromal tumor (GIST) is a rare cancer t

80 Gastrointestinal stromal tumor (GIST) is driven by an ac

81 Gastrointestinal stromal tumor (GIST) is the most common

82 Gastrointestinal stromal tumor (GIST) is the most common

83 Gastrointestinal stromal tumor (GIST) is the most common

84 Gastrointestinal stromal tumor (GIST) is the most common

85 Gastrointestinal stromal tumor (GIST) is the most common

86 Gastrointestinal stromal tumor (GIST) is the most common

87 Gastrointestinal stromal tumor (GIST) is the most common

88 Dual targeting of the gastrointestinal stromal tumor (GIST) lineage-specific m

89 rogressive disease (PD) status in metastatic gastrointestinal stromal tumor (GIST) patients receiving

90 Most gastrointestinal stromal tumor (GIST) patients respond t

91 a (PDGFRA) have been reported in a subset of gastrointestinal stromal tumor (GIST) patients who do no

92 imatinib induces clinical responses in most gastrointestinal stromal tumor (GIST) patients.

93 b mesylate in the treatment of patients with gastrointestinal stromal tumor (GIST) were compared.

94 ard treatment for patients who have advanced gastrointestinal stromal tumor (GIST), but not all patie

95 To review the contemporary management of gastrointestinal stromal tumor (GIST), including endosco

96 y common human mesenchymal tumors, including gastrointestinal stromal tumor (GIST), rhabdomyosarcoma

97 in a number of human malignancies, including gastrointestinal stromal tumor (GIST), seminoma, acute m

98 In advanced gastrointestinal stromal tumor (GIST), there is an unmet

99 n of activating mutations of the KIT gene in gastrointestinal stromal tumor (GIST)-the most common sa

100 ced chordoma, soft tissue sarcoma (STS), and gastrointestinal stromal tumor (GIST).

101 itinib on pancreatic volume in patients with gastrointestinal stromal tumor (GIST).

102 65-year-old man with PLE caused by invasive gastrointestinal stromal tumor (GIST).

103 Gastrointestinal stromal tumors (GIST) are caused by act

104 Gastrointestinal stromal tumors (GIST) are characterized

105 Gastrointestinal stromal tumors (GIST) are characterized

106 Wild-type KIT and PDGFRA gastrointestinal stromal tumors (GIST) are rare tumors w

107 Gastrointestinal stromal tumors (GIST) are related to in

108 Gastrointestinal stromal tumors (GIST) are stromal or me

109 Gastrointestinal stromal tumors (GIST) are the most comm

110 Gastrointestinal stromal tumors (GIST) are uncommon but

111 kedly prolongs the survival of patients with gastrointestinal stromal tumors (GIST) by direct effects

112 Gastrointestinal stromal tumors (GIST) can be successful

113 Fewer than 15% of gastrointestinal stromal tumors (GIST) in pediatric pati

114 surgery in localized, high/intermediate-risk gastrointestinal stromal tumors (GIST) patients.

115 The targeting and therapy of gastrointestinal stromal tumors (GIST) using nonsticky a

116 receptor occur somatically in many sporadic Gastrointestinal Stromal Tumors (GIST), and similar muta

117 Gastrointestinal stromal tumors (GIST), driven by KIT an

118 low mutational testing rate in patients with Gastrointestinal Stromal Tumors (GIST), The Life Raft Gr

119 aling is the central oncogenic event in most gastrointestinal stromal tumors (GIST), which are human

120 carrying activating mutations identified in gastrointestinal stromal tumors (GIST).

121 the pathogenic mechanisms that characterize gastrointestinal stromal tumors (GIST).

122 utations are critical in the pathogenesis of gastrointestinal stromal tumors (GIST).

123 to treat chronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GIST).

124 602306) in patients with oligometastatic gastrointestinal stromal tumors (GIST).

125 Members of a family with hereditary gastrointestinal stromal tumors (GISTs) and a germline K

126 KIT is targeted for cancer therapy in gastrointestinal stromal tumors (GISTs) and chronic myel

127 Abl-T315I variants, as essential targets in gastrointestinal stromal tumors (GISTs) and chronic myel

128 Gastrointestinal stromal tumors (GISTs) are caused by ga

129 The majority of gastrointestinal stromal tumors (GISTs) are driven by on

130 Gastrointestinal stromal tumors (GISTs) are frequently d

131 Gastrointestinal stromal tumors (GISTs) are gaining the

132 Menetrier disease and gastrointestinal stromal tumors (GISTs) are hyperprolife

133 Gastrointestinal stromal tumors (GISTs) are mesenchymal

134 Gastrointestinal stromal tumors (GISTs) are prototypes o

135 Gastrointestinal stromal tumors (GISTs) are rare but tre

136 Gastric gastrointestinal stromal tumors (GISTs) are rare neoplas

137 Gastrointestinal stromal tumors (GISTs) are the most com

138 Gastrointestinal stromal tumors (GISTs) are the most com

139 Gastrointestinal stromal tumors (GISTs) are the most com

140 Gastrointestinal stromal tumors (GISTs) are the most com

141 Gastrointestinal stromal tumors (GISTs) are the most com

142 ous leukemia (CML) but excluded treatment of gastrointestinal stromal tumors (GISTs) because of remai

143 Gastrointestinal stromal tumors (GISTs) commonly harbor

144 Gastrointestinal stromal tumors (GISTs) commonly harbor

145 Gastrointestinal stromal tumors (GISTs) comprise the lar

146 Most gastrointestinal stromal tumors (GISTs) contain KIT or P

147 The treatment of gastrointestinal stromal tumors (GISTs) driven by activa

148 Most gastrointestinal stromal tumors (GISTs) exhibit aberrant

149 Most gastrointestinal stromal tumors (GISTs) express constitu

150 Most gastrointestinal stromal tumors (GISTs) express constitu

151 Most gastrointestinal stromal tumors (GISTs) express oncogeni

152 Gastrointestinal stromal tumors (GISTs) express the rece

153 Gastrointestinal stromal tumors (GISTs) form an interest

154 Most gastrointestinal stromal tumors (GISTs) harbor a gain-of

155 Most gastrointestinal stromal tumors (GISTs) harbor mutant KI

156 Although gastrointestinal stromal tumors (GISTs) harboring activa

157 Most gastrointestinal stromal tumors (GISTs) have activating

158 Gastrointestinal stromal tumors (GISTs) have recently be

159 The incidence of gastrointestinal stromal tumors (GISTs) increased after

160 A subset of gastrointestinal stromal tumors (GISTs) lack gain-of-fun

161 Patients with resectable gastrointestinal stromal tumors (GISTs) might not receiv

162 Most gastrointestinal stromal tumors (GISTs) possess a gain-o

163 Gastrointestinal stromal tumors (GISTs) predominantly ha

164 w treatment targets need to be identified in gastrointestinal stromal tumors (GISTs) to extend the tr

165 as an early way to evaluate the response of gastrointestinal stromal tumors (GISTs) to imatinib trea

166 umors (RECIST) are insensitive in evaluating gastrointestinal stromal tumors (GISTs) treated with ima

167 urrence-free survival (RFS) in patients with gastrointestinal stromal tumors (GISTs) treated with sur

168 ow that inhibition of c-KIT with imatinib in gastrointestinal stromal tumors (GISTs) triggered the up

169 ly characterized gene expression patterns in gastrointestinal stromal tumors (GISTs) using cDNA micro

170 phenotypes in mast cells and intestines, and gastrointestinal stromal tumors (GISTs) when heterozygou

171 PURPOSE OF REVIEW: The treatment of gastrointestinal stromal tumors (GISTs) with tyrosine ki

172 which is expressed in the majority of human gastrointestinal stromal tumors (GISTs), a subtype of ga

173 pathogenesis of systemic mastocytosis (SM), gastrointestinal stromal tumors (GISTs), and some cases

174 s are compelling therapeutic targets in most gastrointestinal stromal tumors (GISTs), and the KIT inh

175 ations are compelling therapeutic targets in gastrointestinal stromal tumors (GISTs), and the KIT/PDG

176 IT expression is a key diagnostic feature of gastrointestinal stromal tumors (GISTs), and virtually a

177 Many cancer subtypes, including KIT-mutant gastrointestinal stromal tumors (GISTs), are driven by a

178 cy in the majority of patients with advanced gastrointestinal stromal tumors (GISTs), cure remains el

179 the features of Carney's syndrome, including gastrointestinal stromal tumors (GISTs), extra-adrenal p

180 yeloproliferative neoplasms, particularly in gastrointestinal stromal tumors (GISTs), in which the he

181 mutation identifies a molecular subgroup of gastrointestinal stromal tumors (GISTs), primarily resis

182 TK) inhibitor approved for the management of gastrointestinal stromal tumors (GISTs), renal cell carc

183 of the receptor tyrosine kinase KIT occur in gastrointestinal stromal tumors (GISTs), some cases of a

184 Gastrointestinal stromal tumors (GISTs), the most common

185 Gastrointestinal stromal tumors (GISTs), the most common

186 e Bcr-Abl kinase, as well as a proportion of gastrointestinal stromal tumors (GISTs), where its targe

187 Wild-type (WT) gastrointestinal stromal tumors (GISTs), which lack KIT

188 e insensitive in evaluating imatinib-treated gastrointestinal stromal tumors (GISTs).

189 inoma, acute myelogenous leukemia (AML), and gastrointestinal stromal tumors (GISTs).

190 lay an important role in the pathogenesis of gastrointestinal stromal tumors (GISTs).

191 d are associated with human mastocytosis and gastrointestinal stromal tumors (GISTs).

192 challenge in the treatment of patients with gastrointestinal stromal tumors (GISTs).

193 escent and young adult (AYA) population with gastrointestinal stromal tumors (GISTs).

194 but is disrupted by DNA hypermethylation in gastrointestinal stromal tumors (GISTs).

195 GLUT4 may play a role in (18)F-FDG uptake in gastrointestinal stromal tumor, GLUT4 levels decrease af

196 imatinib in patients with imatinib resistant gastrointestinal stromal tumor has shown promise.

197 tent and specific gene expression profile of gastrointestinal stromal tumors has been published.

198 n the protooncogene c-kit which is unique to gastrointestinal stromal tumors has led to their reclass

199 The validation of inhibitors developed in gastrointestinal stromal tumors has taken several years,

200 ogy, radiographic imaging and the biology of gastrointestinal stromal tumor have become apparent.

201 survival rates; in patients with metastatic gastrointestinal stromal tumors, imatinib can provide ef

202 ch is associated with the Bcr-Abl kinase; in gastrointestinal stromal tumors, imatinib is known to ac

203 called WBZ_4, was instead preserved against gastrointestinal stromal tumors in both in vitro and in

204 ced oncoprotein (KIT) leading to malignancy (gastrointestinal stromal tumor) in contrast to loss of f

205 cancer (paraganglioma, renal cell carcinoma, gastrointestinal stromal tumor) in others.

206 aberrant tyrosine kinase pathway signaling: gastrointestinal stromal tumor, inflammatory myofibrobla

207 Pediatric gastrointestinal stromal tumor is an uncommon tumor, the

208 The clinical behavior of gastrointestinal stromal tumors is variable.

209 me of the critical biological role of Kit in gastrointestinal stromal tumor led to the development of

210 other mesenchymal tumors (leiomyoma, lipoma, gastrointestinal stromal tumor, leiomyosarcoma, granular

211 ating mutations in c-KIT are associated with gastrointestinal stromal tumors, mastocytosis, and acute

212 Continued intense study of gastrointestinal stromal tumor may lead to new paradigms

213 vasive Treatment of Patients with Metastatic Gastrointestinal Stromal Tumors ('MITIGATE') (grant agre

214 oma (n = 36), biliary tract cancer (n = 43), gastrointestinal stromal tumor (n = 1), adenocarcinoma o

215 astases (n = 6), cholangiocarcinoma (n = 5), gastrointestinal stromal tumor (n = 2), hepatoblastoma (

216 sia (n = 6), recalcitrant stricture (n = 8), gastrointestinal stromal tumor (n = 3), and gastric card

217 reatment of chronic myelogenous leukemia and gastrointestinal stromal tumors or anti-HER2/neu (Hercep

218 o underwent complete resection, 34 (61%) had gastrointestinal stromal tumors or gastrointestinal leio

219 ion of PDGFR signaling has been described in gastrointestinal stromal tumors (PDGFRA mutations) as we

220 These findings suggest that, in addition to gastrointestinal stromal tumors, rare tumors that show P

221 Although most gastrointestinal stromal tumors respond well to treatmen

222 diated proliferation of tumors such as SCLC, gastrointestinal stromal tumors, seminomas, and leukemia

223 The multidisciplinary management of gastrointestinal stromal tumors serves as a model of how

224 araffin-embedded (FFPE) samples of 121 human gastrointestinal stromal tumors, set up stringent parame

225 KIT/PDGFRA mutation status in patients with gastrointestinal stromal tumor undergoing neoadjuvant im

226 A decade ago, the only therapy for gastrointestinal stromal tumors was surgery.

227 ked to malignant peripheral nerve sheath and gastrointestinal stromal tumors, whereas heritable defec

228 Juxtamembrane domain mutations are common in gastrointestinal stromal tumors, whereas mutations in th

229 ive responses, with little host toxicity, in gastrointestinal stromal tumors, which harbor activating

230 athway is a promising treatment for advanced gastrointestinal stromal tumors, which resist convention

231 hase 3 study in adult patients with advanced gastrointestinal stromal tumor who had disease progressi

232 with either chronic myelogenous leukemia or gastrointestinal stromal tumors who were receiving imati

233 ll provide an update of important studies in gastrointestinal stromal tumor with an emphasis on those

234 For example, the success of the treatment of gastrointestinal stromal tumor with Imatinib has led to

235 ists and clinical investigators have studied gastrointestinal stromal tumor with no major advances in

236 Purpose Wild-type gastrointestinal stromal tumors (WT-GISTs) that lack KIT