ライフサイエンスコーパス: GIST

1 GIST cells were infected with a lentiviral shRNA pooled

2 GIST is highly responsive to several selective tyrosine

3 GIST patients treated with the tyrosine kinase inhibitor

4 GIST-specific survival and OS.

5 GISTs occur throughout the intestinal tract, and most ha

6 nty (18)F-FDG PET scans were obtained for 63 GIST patients to evaluate for an early response to neoad

7 s of the chromosome 14q MAX gene in 16 of 76 GISTs (21%).

8 Among 1413 patients treated for a GIST in 61 European centers between 2001 and 2013, patie

9 lth starting in 2008 and were evaluated in a GIST clinic held once or twice yearly.

10 01), patients were required to have advanced GIST that was not surgically curable.

11 ial of regorafenib in patients with advanced GIST after failure of at least imatinib and sunitinib.

12 gnificant activity in patients with advanced GIST after failure of both imatinib and sunitinib.

13 nefit the majority of patients with advanced GIST but have no or limited efficacy in patients with th

14 ement in prognosis of patients with advanced GIST, we changed the primary end point to imatinib failu

15 a large population of patients with advanced GIST.

16 prognostic factor in patients with advanced GIST.

17 irst-line therapy for patients with advanced GISTs.

18 e status of GIST management before and after GIST's "Big Bang" and new steps being taken to further i

19 y means of immunohistochemical analysis, all GIST cells expressed CD117, CD34 and Dog1 in all six syn

20 Nearly all GISTs have somatic mutations in either the KIT or PDGFRA

21 Although GIST is highly responsive to several selective tyrosine

22 Although GISTs are often initially sensitive to imatinib or other

23 s containing both gastric adenocarcinoma and GIST.

24 ding breast cancer, head and neck cancer and GIST.

25 hronous gastric adenocarcinoma with GIST and GIST alone.

26 matinib for chronic myelogenous leukemia and GIST has become a desired route to regulatory approval o

27 ailed to inhibit oncogenic Kit signaling and GIST growth.

28 )) and in a meta-analysis of both the US and GIST datasets (1.3 x 10(-6), OR 2.17 (1.58-2.98 for the

29 ow known that neurofibromatosis-1-associated GISTs are SDHB-positive, whereas Carney-Stratakis syndro

30 whereas Carney-Stratakis syndrome-associated GISTs are SDHB-deficient with underlying germline mutati

31 AG patients and 178 controls from Australia (GIST).

32 is is the first reported association between GIST and PLE.

33 or potential therapeutic strategies to block GIST progression and metastatic spread.

34 d geometry corresponded to that predicted by GIST, for one of these the pose without the GIST term wa

35 perimentally, 13/14 molecules prioritized by GIST did bind, whereas none of the molecules that it dep

36 l cell of Cajal hyperplasia as well as cecal GIST.

37 eria, Memorial Sloan Kettering Cancer Center GIST nomogram, and American Joint Committee on Cancer ga

38 etic, and epigenetic studies, which classify GISTs into two distinct clusters: an SDH-competent group

39 onger in the subset with centrally confirmed GIST and without macroscopic metastases at study entry (

40 , 19-94 years) with pathologically confirmed GIST who were identified with a natural language process

41 of SDHB by IHC; and 2 types of SDH-deficient GIST (n = 84).

42 used as a diagnostic marker to differentiate GIST from other sarcomas.

43 tinib therapy in inoperable and disseminated GIST patients, specific CT images, not seen during conve

44 between tumor and stromal cells that drives GIST development and offers unique insights for potentia

45 se by (18)F-FDG PET in patients in the Dutch GIST registry treated with neoadjuvant imatinib.

46 E-GIST enucleation seems safe for tumors of less than 65 m

47 retherapeutic biopsy on the feasibility of E-GIST enucleation, and (iii) the impact of mucosal ulcera

48 E-GISTs are very rare tumors and esophageal resection has

49 sophageal gastrointestinal stromal tumors (E-GISTs).

50 nter retrospective study, 19 patients with E-GISTs were identified between 2001 and 2010.

51 Of over 19 patients identified with E-GISTs, curative treatment was surgical for 16 patients,

52 three of eight micro-GISTs, which are early GISTs.

53 sion, fostering cell cycle activity in early GISTs.

54 the receiver operating curve) of established GIST recurrence risk prognostic scoring systems.

55 Several new familial GIST kindreds have been reported, including those with g

56 o of six synchronous tumors and four of five GISTs.

57 alysis of inherited genetic risk factors for GIST offers some clues about the disease's genetic origi

58 new drugs targeting these gene mutations for GIST therapy.

59 by cabozantinib as an effective strategy for GIST treatment.

60 , 400 patients who had undergone surgery for GISTs with a high risk of recurrence were randomized to

61 Exosomes derived from GIST patients but not healthy donors show enhanced MMP1

62 ore than 2-fold increased risk of death from GISTs (subdistribution hazard ratio, 2.27; 95% CI, 1.21-

63 mpleted December 31, 2013), 142 patients had GIST recurrence.

64 arbored a PDGFRA mutation, and 24 (7.0%) had GISTs that were wild type for these genes.

65 years in the 3-year group), 274 (80.4%) had GISTs with a KIT mutation, 43 (12.6%) had GISTs that har

66 ad GISTs with a KIT mutation, 43 (12.6%) had GISTs that harbored a PDGFRA mutation, and 24 (7.0%) had

67 tributions to our knowledge about hereditary GIST multiple tumor syndromes.

68 (SDH) deficiency and mutations in hereditary GIST syndromes has expanded.

69 standing of the molecular basis of heritable GIST syndromes has improved.

70 cture, an ordered water molecule with a high GIST displacement penalty was observed to stay in place.

71 al responses to RAF inhibition seen in human GIST.

72 In freshly obtained human GIST specimens, the T cell profile correlated with imati

73 study, we determined that a subset of human GIST specimens that acquired imatinib resistance acquire

74 was cytotoxic to an imatinib-resistant human GIST cell population.

75 on also occurred in imatinib-sensitive human GIST cell lines after imatinib treatment in vitro.

76 1, is able to slow the growth of three human GIST cell lines in vitro.

77 In human GISTs that eventually developed resistance to imatinib,

78 model of GIST and 57 freshly procured human GISTs, we discovered that TAMs displayed an M1-like phen

79 ression profile as TAMs from untreated human GISTs.

80 und that CD3(+) TIL were highly activated in GIST and were especially enriched in areas of the tumor

81 us gastric adenocarcinomas with GIST, and in GIST alone.

82 P90 inhibitors, but clinical applications in GIST patients are constrained by the toxicity resulting

83 s a crucial regulator of chloride balance in GIST cells, we found that RNAi-mediated silencing or pha

84 should be considered the standard of care in GIST patients treated with neoadjuvant intent.

85 e of response assessment by Choi criteria in GIST patients.

86 ishes prolonged KIT inhibition (>20 days) in GIST.

87 n of response affects treatment decisions in GIST patients treated with neoadjuvant intent.

88 establish the oncogenic activity of DOG1 in GIST involving modulation of IGF/IGF receptor signaling

89 Hence, MAX inactivation is a common event in GIST progression, fostering cell cycle activity in early

90 ch is strongly and specifically expressed in GIST, is used as a diagnostic marker to differentiate GI

91 tic mutations in the KIT and PDGFRA genes in GIST tumors may similarly be mutational signatures that

92 The mutation rate was higher in GIST alone than in synchronous adenocarcinoma with GIST.

93 cial to the antitumor effects of imatinib in GIST, and concomitant immunotherapy may further improve

94 IT and downstream signaling intermediates in GIST; and (3) unlike direct HSP90 inhibition, CDC37 knoc

95 e often results in a change of management in GIST patients harboring the non-KIT exon 11 mutation and

96 d growth factor receptor alpha is mutated in GIST; the gene products of both are inhibited by imatini

97 to screen and identify genetic mutations in GIST for targeted therapy using the new Ion Torrent next

98 Given the high toxicity rate in GIST patients, there is variability in the post-marketin

99 designed to overcome imatinib resistance in GIST and to investigate the consequences of oncogenic KI

100 ction behavior in PGCs distinct from that in GIST development.

101 rocessed pro-IGF-II, called 'big'-IGF-II, in GISTs.

102 Examination of downstream signaling in GISTs from cKit(V558Delta/+) mice confirmed hyperphospho

103 pathway and potential therapeutic target in GISTs.

104 have previously shown that imatinib induces GIST cell quiescence in vitro through the APC(CDH1)-SKP2

105 e, we provide evidence that imatinib induces GIST cell quiescence in vivo and that this process also

106 duction restores p16 expression and inhibits GIST proliferation.

107 ion may be a mechanism by which SR1 inhibits GIST growth.

108 ients, more AYA patients had small-intestine GISTs (139 [35.5%] vs 1465 [27.3%], P = .008) and were m

109 ve docking of large libraries to investigate GIST's impact on ligand discovery, geometry, and water s

110 ecommended for broad use to treat first-line GIST.

111 n survival, both for patients with localized GIST and those with advanced disease.

112 NCR1) in a cohort of patients with localized GIST.

113 1 (85.9%) had centrally confirmed, localized GISTs with mutation analysis for KIT and PDGFRA performe

114 al tumours (GIST), but almost all metastatic GIST eventually develop resistance to these agents, resu

115 was found in 96%, 100% and 62% of metastatic GIST, embryonal RMS and LMS samples, respectively.

116 red with placebo in patients with metastatic GIST after progression on standard treatments.

117 red with placebo in patients with metastatic GIST after progression on standard treatments.

118 A subset of patients with metastatic GIST experiences durable, long-term overall survival wit

119 matinib mesylate in patients with metastatic GIST harboring a KIT exon 11 mutation.

120 rned to a grid-based version of this method, GIST, readily implemented in molecular docking.

121 s, respectively, and in three of eight micro-GISTs, which are early GISTs.

122 Moreover, GIST were infiltrated by a homogeneous subset of cytokin

123 ICC hyperplasia and formation of multifocal GIST-like tumors in the mouse gastrointestinal tract wit

124 -derived growth factor receptor alpha-mutant GIST specimens.

125 model of human sporadic forms of BRAF-mutant GIST to help unravel its pathogenesis and therapeutic re

126 hRNA)-mediated gene knockdowns in KIT-mutant GIST-T1 and GIST882.

127 vances in the treatment of KIT/PDGFRA-mutant GIST, similar progress against KIT/PDGFRA wild-type GIST

128 onse (P < 0.001) and non-KIT exon 11-mutated GISTs (P < 0.001).

129 Validations in treatment-naive (GIST-T1, GIST882) vs imatinib-resistant GISTs (GIST48, G

130 derwent surgery for a primary, nonmetastatic GIST between January 1, 1998, and December 31, 2012, at

131 sufficient to drive ICC hyperplasia but not GIST tumorigenesis.

132 curative primary treatment and cures >50% of GIST patients who present with localized disease.

133 In 70-80% of GIST cases, oncogenic mutations in KIT are present, lead

134 bility of imatinib, led to the "Big Bang" of GIST therapy (ie, the successful treatment of the first

135 the natural history and molecular biology of GIST, risk stratification, and drug resistance.

136 8Delta) mutation found in a familial case of GIST and the Kit(T669I) (human KIT(T670I)) "gatekeeper"

137 ) , a mutation observed in clinical cases of GIST, we observed that Braf(V600E) activation was suffic

138 he non-neoplastic and benign counterparts of GIST, RMS and LMS tumors, and DMD deletions inactivate l

139 Detection of GIST recurrence may be enhanced by adjusting the timing

140 Recognition and early diagnosis of GIST syndromes allows for improved comprehensive medical

141 Diagnosis of GIST was confirmed in 382 of 397 patients (96%) in the i

142 ecause KIT and PDGFR-alpha remain drivers of GIST after resistance to imatinib and sunitinib, we perf

143 GFRA gene mutations, are the primary form of GIST in children and occasionally occur in adults.

144 vation of Ptch in mice leads to formation of GIST-like tumors that express Pdgfralpha, but not Kit.

145 imatinib induces apoptosis in a fraction of GIST cells while, at the same time, a subset of cells un

146 ntrast, DOG1 silencing delayed the growth of GIST xenografts in vivo.

147 , are associated with the natural history of GIST.

148 is study provides guidance for management of GIST harboring the most common KIT and PDGFRA mutations,

149 he incidence, pathogenesis and management of GIST is also presented.

150 an attractive next step in the management of GIST.

151 d after imatinib therapy in a mouse model of GIST (KitV558del/+ mice), where it was associated with i

152 Using a spontaneous mouse model of GIST and 57 freshly procured human GISTs, we discovered

153 cells of Cajal (ICC), the cells of origin of GIST, were normal.

154 e of heterogeneity in the cellular origin of GIST.

155 (ICC), thought to be the cells of origin of GIST.

156 derstanding of the molecular pathogenesis of GIST multiple tumor syndromes, we can refine our screeni

157 e that accounts for the nonlinear pattern of GIST recurrence was applied to tumor site, mitotic count

158 that SR1 treatment enhances phagocytosis of GIST cells by macrophages, indicating that treatment wit

159 on of adjuvant imatinib modifies the risk of GIST recurrence associated with some KIT mutations, incl

160 The risk of GIST recurrence was estimated using the modified Nationa

161 urvival of GIST patients with a high risk of GIST recurrence.

162 In this review, the status of GIST management before and after GIST's "Big Bang" and n

163 r with loss of KIT expression in a subset of GIST resistant to KIT inhibitors, and we illustrate the

164 GFRA mutations represent a unique subtype of GIST that predominantly affects children.

165 matinib improved RFS and overall survival of GIST patients with a high risk of GIST recurrence.

166 the alterations in the neoplastic tissue of GIST following Imatinib treatment.

167 Treatment of GIST cell lines with SR1 reduces cell-surface KIT expres

168 Treatment of GIST with imatinib, a small-molecule tyrosine kinase inh

169 lls resulted in the development of tumors of GIST-like localization and histology; these were reduced

170 ration, demonstrated in approximately 70% of GISTs, is chromosome 14q deletion.

171 T and PDGFRA mutations account for 85-90% of GISTs; subsequent genetic studies have led to the identi

172 The vast majority of GISTs contain an activating mutation in either the KIT o

173 f recurrence following surgical resection of GISTs is typically reported from the date of surgery.

174 -year, and 5-year DFS following resection of GISTs was 95%, 83%, and 74%, respectively.

175 FS improves over time following resection of GISTs.

176 s strategies for optimizing the treatment of GISTs.

177 consequences of second-site Kit mutations on GIST development and imatinib sensitivity, we engineered

178 STs and investigate the effect of surgery on GIST-specific survival (GSS) and overall survival (OS).

179 igible patients with advanced CD117-positive GIST from 56 institutions in 13 countries were randomly

180 derived from parental DOG1 and KIT-positive GIST cells, where a 5,000-fold increase in IGFBP5 mRNA t

181 NG, AND PATIENTS: Patients with KIT-positive GIST removed at surgery were entered between February 20

182 trol in 70-85% of patients with KIT-positive GIST.

183 in Kit(V558Delta;Y719F/Y719F) mice prevented GIST development, although the interstitial cells of Caj

184 US patients with complete primary GIST resection after 2010 were grouped as underestimated

185 , we show that in cancer tissue from primary GIST patients as well as in cell lines, mutant Kit accum

186 e mainstay of therapy for localized, primary GIST, postoperative tumor recurrence is common.

187 Most primary GIST patients respond to the Kit inhibitor imatinib, but

188 Adjuvant imatinib in patients with primary GIST who are at high risk of recurrence prolongs OS comp

189 bridization was present in 91% of 60 primary GISTs.

190 keeper" mutation found in imatinib-resistant GIST patients.

191 In imatinib-resistant GIST with a secondary Kit mutation, Kit localizes predom

192 of imatinib-sensitive and imatinib-resistant GIST, we demonstrate that SR1 is able to strongly inhibi

193 of imatinib-sensitive and imatinib-resistant GIST.

194 th imatinib-sensitive and imatinib-resistant GIST.

195 iad KIT/PDGFRA oncoproteins in TKI-resistant GIST patients.

196 ive (GIST-T1, GIST882) vs imatinib-resistant GISTs (GIST48, GIST430) demonstrated that: (1) CDC37 int

197 new strategy for treating imatinib-resistant GISTs.

198 Among 528 patients with high-risk GIST by local pathologist, 5-year IFFS was 79% versus 73

199 evable in patient populations with high-risk GIST.

200 en imatinib-resistant and imatinib-sensitive GIST cell lines.

201 ve than imatinib alone in imatinib-sensitive GIST models.

202 eral models from computer vision (e.g. SIFT, GIST, self-similarity features, and a deep convolutional

203 HSP90 cofactor, CDC37, as one of the top six GIST-specific essential genes.

204 Most small GISTs are cured with surgery.

205 Hedgehog (HH) signaling is activated in some GIST.

206 Sporadic GIST patients have increased risk of developing synchron

207 view describes associations between sporadic GIST and second malignancies, as well as new contributio

208 This mouse model of sporadic GIST model was amenable to therapeutic intervention, and

209 re recombinase in ICC as a strategy to study GIST pathogenesis.

210 in 48% and 90% of sporadic and NF1-syndromic GISTs, respectively, and in three of eight micro-GISTs,

211 in 17% and 50% of sporadic and NF1-syndromic GISTs, respectively, and we find loss of MAX protein exp

212 iscontinued imatinib for a reason other than GIST recurrence.

213 We replicated this finding in the GIST cohort (p =7.3 x 10(-3), and in the pooled sample (

214 their relatives, fundamentally, based on the GIST genotype.

215 ranked docked molecules with and without the GIST term often overlapped, many ligands were meaningful

216 GIST, for one of these the pose without the GIST term was wrong, and three crystallographic poses di

217 ns and probably contributed independently to GIST immunosurveillance.

218 ive, or complementary, approach for treating GIST.

219 sist of both gastrointestinal stromal tumor (GIST) and adenocarcinoma are rare.

220 inently the recognition of GI stromal tumor (GIST) as a specific sarcoma subtype and the availability

221 vidence that gastrointestinal stromal tumor (GIST) cells invade the interstitial stroma through the r

222 fraction of gastrointestinal stromal tumor (GIST) cells overexpress the platelet-derived growth fact

223 ith operable gastrointestinal stromal tumor (GIST) compared with placebo.

224 Gastrointestinal stromal tumor (GIST) has become a model for targeted therapy in cancer.

225 e related to gastrointestinal stromal tumor (GIST) in the setting of nonhereditary and hereditary mul

226 Metastatic GI stromal tumor (GIST) is a life-threatening disease with no therapy of p

227 Gastrointestinal stromal tumor (GIST) is the most common human sarcoma and typically res

228 Gastrointestinal stromal tumor (GIST) is the most common sarcoma of the gastrointestinal

229 Gastrointestinal stromal tumor (GIST) is the most common subtype of sarcoma.

230 atients with gastrointestinal stromal tumor (GIST) were compared.

231 ommended for patients with GI stromal tumor (GIST) with high-risk features, according to survival fin

232 s, including gastrointestinal stromal tumor (GIST), rhabdomyosarcoma (RMS) and leiomyosarcoma (LMS),

233 KIT gene in gastrointestinal stromal tumor (GIST)-the most common sarcomaof the gastrointestinal tra

234 atients with gastrointestinal stromal tumor (GIST).

235 high- or intermediate-risk GI stromal tumor (GIST).

236 after resection of primary GI stromal tumor (GIST).

237 by invasive gastrointestinal stromal tumor (GIST).

238 Gastrointestinal stromal tumors (GIST) are characterized by activating mutations of KIT o

239 Gastrointestinal stromal tumors (GIST) are stromal or mesenchymal subepithelial neoplasms

240 Gastrointestinal stromal tumors (GIST) are the most common adult sarcomas and the oncogen

241 tients with gastrointestinal stromal tumors (GIST) by direct effects on tumor cells as well as by ind

242 Gastrointestinal stromal tumors (GIST) can be successfully treated with imatinib mesylate

243 targets in gastrointestinal stromal tumors (GISTs) and chronic myelogenous leukemia (CML).

244 therapy in gastrointestinal stromal tumors (GISTs) and chronic myelogenous leukemia (CML).

245 Gastrointestinal stromal tumors (GISTs) are caused by gain-of-function mutations in the K

246 GI stromal tumors (GISTs) are neoplasms with a varying malignancy potential

247 Gastrointestinal stromal tumors (GISTs) are rare but treatable soft tissue sarcomas.

248 Gastrointestinal stromal tumors (GISTs) are the most commonly diagnosed mesenchymal tumor

249 Most gastrointestinal stromal tumors (GISTs) contain KIT or PDGFRA kinase gain-of-function mut

250 Most gastrointestinal stromal tumors (GISTs) harbor a gain-of-function mutation in the Kit rec

251 ons in gastrointestinal (GI) stromal tumors (GISTs) in 1998 triggered a sea change in our understandi

252 resectable gastrointestinal stromal tumors (GISTs) might not receive the recommended duration of adj

253 Gastrointestinal stromal tumors (GISTs) predominantly harbor activating mutations in the

254 entified in gastrointestinal stromal tumors (GISTs) to extend the treatment options for patients expe

255 response of gastrointestinal stromal tumors (GISTs) to imatinib treatment.

256 tients with gastrointestinal stromal tumors (GISTs) treated with surgery and adjuvant imatinib.

257 stines, and gastrointestinal stromal tumors (GISTs) when heterozygous.

258 reatment of gastrointestinal stromal tumors (GISTs) with tyrosine kinase inhibitors (TKIs), such as i

259 d-type (WT) gastrointestinal stromal tumors (GISTs), which lack KIT and PDGFRA gene mutations, are th

260 lation with gastrointestinal stromal tumors (GISTs).

261 tatic or locally advanced GI stromal tumors (GISTs).

262 or advanced Gastrointestinal Stromal Tumour (GIST) at a starting dose of 160 mg daily 3 weeks on, 1 w

263 ients with gastrointestinal stromal tumours (GIST), but almost all metastatic GIST eventually develop

264 rplasia in gastrointestinal stromal tumours (GISTs), and additional genetic alterations are required

265 rs in most gastrointestinal stromal tumours (GISTs).

266 riginally classified as KIT/PDGFRA wild-type GIST revealed that 17 (85.0%) harbored a pathogenic muta

267 Wild-type GIST specimens from 95 patients (median age, 23 [range,

268 imilar progress against KIT/PDGFRA wild-type GIST, including mutant BRAF-driven tumors, has been limi

269 95% CI: 1.2-2.7 for rs1056836) and wild type GISTs (OR = 2.7, 95% CI: 1.5-4.8 for rs1800440 and OR =

270 in patients with metastatic or unresectable GIST progressing after failure of at least imatinib and

271 ically confirmed, metastatic or unresectable GIST, with failure of at least previous imatinib and sun

272 ically confirmed, metastatic or unresectable GISTs.

273 s of synchronous gastric adenocarcinoma with GIST and GIST alone.

274 lone than in synchronous adenocarcinoma with GIST.

275 six synchronous gastric adenocarcinomas with GIST, and in GIST alone.

276 ccessful treatment of the first patient with GIST with imatinib in 2000).

277 ts reported information on 506 patients with GIST after primary resection (65.8% were high-risk and 8

278 ses are relatively uncommon in patients with GIST and are significantly associated only with presence

279 h the PDGFRA D842V mutation or patients with GIST lacking KIT and PDGFRA mutations.

280 The authors evaluated 65 patients with GIST treated with oral sunitinib and a control group of

281 inib and a control group of 30 patients with GIST who did not receive any therapy (mean age: 56 years

282 sess the long-term survival of patients with GIST who were treated in SWOG study S0033 and to present

283 he risk of recurrence for many patients with GIST, especially for patients with tumors of intermediat

284 to further prolong survival in patients with GIST.

285 optimal risk stratification of patients with GIST.

286 referred patients younger than 19 years with GIST or 19 years or older with known WT GIST (no mutatio

287 utations in synchronous adenocarcinomas with GISTs was an uncommon mutation of CTT > CCA at amino aci

288 iology, and End Results (SEER) database with GISTs histologically diagnosed from January 1, 2001, thr

289 392 AYA and 5373 OA patients diagnosed with GISTs (207 [52.8%] male AYA patients, 2767 [51.5%] male

290 describe a large cohort of AYA patients with GISTs and investigate the effect of surgery on GIST-spec

291 hich can be heterogeneous between and within GIST metastases in a given patient.

292 with GIST or 19 years or older with known WT GIST (no mutations in KIT or PDGFRA) were recruited; 116

293 An observational study of WT GIST permitted the evaluation of a large number of patie

294 PDGFRA) were recruited; 116 patients with WT GIST were enrolled, and 95 had adequate tumor specimen a

295 Methods In 2008, a WT-GIST clinic was established at the National Cancer Insti

296 Conclusion WT-GIST is an indolent disease, and most patients survive w

297 d participants who underwent resection of WT-GIST.

298 These data suggest that resections for WT-GISTs be restricted to the initial procedure and that su

299 ild-type gastrointestinal stromal tumors (WT-GISTs) that lack KIT or PDGFRA mutations represent a uni

300 Results Among 76 participants with WT-GISTs, the median follow-up was 4.1 years.