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

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

4 with an advanced unresectable or metastatic gastrointestinal stromal tumor.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

21 iladelphia chromosome-positive leukemias and gastrointestinal stromal tumors.

22 se inhibitors with activity against advanced gastrointestinal stromal tumors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

38 Gastrointestinal stromal tumors are the most common sarc

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

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

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

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

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

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

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

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

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

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

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

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

51 Treatment for gastrointestinal stromal tumors, formerly limited to sur

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

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

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

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

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

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

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

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

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

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

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

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

64 Gastrointestinal stromal tumor (GIST) has become a model

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

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

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

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

69 Gastrointestinal stromal tumor (GIST) is the most common

70 Gastrointestinal stromal tumor (GIST) is the most common

71 Gastrointestinal stromal tumor (GIST) is the most common

72 Gastrointestinal stromal tumor (GIST) is the most common

73 Gastrointestinal stromal tumor (GIST) is the most common

74 Most gastrointestinal stromal tumor (GIST) patients respond t

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

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

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

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

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

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

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

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

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

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

85 65-year-old man with PLE caused by invasive gastrointestinal stromal tumor (GIST).

86 Gastrointestinal stromal tumors (GIST) are caused by act

87 Gastrointestinal stromal tumors (GIST) are characterized

88 Gastrointestinal stromal tumors (GIST) are characterized

89 Gastrointestinal stromal tumors (GIST) are related to in

90 Gastrointestinal stromal tumors (GIST) are stromal or me

91 Gastrointestinal stromal tumors (GIST) are the most comm

92 Gastrointestinal stromal tumors (GIST) are uncommon but

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

94 Gastrointestinal stromal tumors (GIST) can be successful

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

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

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

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

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

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

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

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

103 Gastrointestinal stromal tumors (GISTs) are caused by ga

104 Gastrointestinal stromal tumors (GISTs) are gaining the

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

106 Gastrointestinal stromal tumors (GISTs) are mesenchymal

107 Gastrointestinal stromal tumors (GISTs) are rare but tre

108 Gastric gastrointestinal stromal tumors (GISTs) are rare neoplas

109 Gastrointestinal stromal tumors (GISTs) are the most com

110 Gastrointestinal stromal tumors (GISTs) are the most com

111 Gastrointestinal stromal tumors (GISTs) are the most com

112 Gastrointestinal stromal tumors (GISTs) are the most com

113 Gastrointestinal stromal tumors (GISTs) commonly harbor

114 Gastrointestinal stromal tumors (GISTs) commonly harbor

115 Gastrointestinal stromal tumors (GISTs) comprise the lar

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

117 Most gastrointestinal stromal tumors (GISTs) exhibit aberrant

118 Most gastrointestinal stromal tumors (GISTs) express constitu

119 Most gastrointestinal stromal tumors (GISTs) express constitu

120 Most gastrointestinal stromal tumors (GISTs) express oncogeni

121 Gastrointestinal stromal tumors (GISTs) express the rece

122 Gastrointestinal stromal tumors (GISTs) form an interest

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

124 Most gastrointestinal stromal tumors (GISTs) harbor mutant KI

125 Although gastrointestinal stromal tumors (GISTs) harboring activa

126 Most gastrointestinal stromal tumors (GISTs) have activating

127 Gastrointestinal stromal tumors (GISTs) have recently be

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

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

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

131 Gastrointestinal stromal tumors (GISTs) predominantly ha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 Gastrointestinal stromal tumors (GISTs), the most common

148 Gastrointestinal stromal tumors (GISTs), the most common

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 Pediatric gastrointestinal stromal tumor is an uncommon tumor, the

168 The clinical behavior of gastrointestinal stromal tumors is variable.

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

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

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

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

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

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

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

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

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

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

179 Although most gastrointestinal stromal tumors respond well to treatmen

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

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

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

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

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

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

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

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

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

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

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

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

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