ライフサイエンスコーパス: GIST

1 GIST calculations reveal additional, but smaller, contri

2 GIST cells were infected with a lentiviral shRNA pooled

3 GIST relies on expression of these unamplified receptor

4 GIST-specific survival and OS.

5 GISTs driven by the V558Delta;V653A Kit double mutation

6 GISTs occur throughout the intestinal tract, and most ha

7 f 32 paraffin embedded tumours (including 15 GIST and 17 PPGL) was performed using a pyrosequencing t

8 off (August 31, 2019), 258 patients (n = 184 GIST) were enrolled, with 68 patients in the dose-escala

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

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

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

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

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

14 ctivity in patients with refractory advanced GIST.

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

16 igible patients included those with advanced GIST, intolerant to or experienced progression on >= 1 l

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

18 a large population of patients with advanced GIST.

19 prognostic factor in patients with advanced GIST.

20 further clinical evaluation in the advanced GISTs.

21 irst-line therapy for patients with advanced GISTs.

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

23 PD-1 and PD-L1 expressing tumors across all GIST mutational subtypes, which may provide insight into

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

25 Although GISTs are often initially sensitive to imatinib or other

26 s containing both gastric adenocarcinoma and GIST.

27 Unfortunately, CML and GIST have high rates of recurrence in the absence of the

28 hancer essential for KIT gene expression and GIST cell viability.

29 hronous gastric adenocarcinoma with GIST and GIST alone.

30 of 15a were also demonstrated in GIST430 and GIST patient-derived xenograft models.

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

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

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

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

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

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

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 Six patients with histologically confirmed GIST and unresectable primary lesion or metastases under

41 , 19-94 years) with pathologically confirmed GIST who were identified with a natural language process

42 ed insulator that normally partitions a core GIST super-enhancer from the FGF4 oncogene.

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

44 erived xenograft (PDX) from an SDH-deficient GIST that faithfully maintains the epigenetics of the pa

45 lator alters locus topology in SDH-deficient GISTs, allowing aberrant physical interaction between en

46 ation replaced CTCF binding in SDH-deficient GISTs.

47 KIT-mutant, PDGFRA-mutant and SDH-deficient GISTs.

48 s also highly expressed across SDH-deficient GISTs.

49 BBI treatment in KIT-dependent GIST cells produced genome-wide changes in the H3K27ac e

50 ng of LMTK3 with siRNA delayed KIT-dependent GIST growth in a xenograft model.

51 y low in two of three parental KIT-dependent GIST lines, whereas cyclin D1 expression was high in eac

52 al or transcutaneous biopsies for diagnosing GIST do not significantly alter the risk of local recurr

53 tive biopsies are widely used for diagnosing GIST.

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

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

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

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

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

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

60 sophageal gastrointestinal stromal tumors (E-GISTs).

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

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

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

64 sion, fostering cell cycle activity in early GISTs.

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

66 vercome imatinib-resistant of KIT-expressing GISTs.

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

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

69 new drugs targeting these gene mutations for GIST therapy.

70 by cabozantinib as an effective strategy for GIST treatment.

71 yzed 1000 patients who underwent surgery for GIST at our institution from 1982 to 2016.

72 , 400 patients who had undergone surgery for GISTs with a high risk of recurrence were randomized to

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

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

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

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

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

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

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

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

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

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

83 We performed RNA sequencing of 75 human GIST tumors from 75 patients, comprising the largest coh

84 al responses to RAF inhibition seen in human GIST.

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

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

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

88 eir effectiveness and mechanism of action in GIST.

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

90 Resistance to select BBI in GIST was attributable to drug efflux pumps.

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

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

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

94 for targeting oncogenic kinase dependency in GIST.

95 me machinery with bortezomib is effective in GIST cells through a dual mechanism of KIT transcription

96 , while also showing therapeutic efficacy in GIST-bearing xenograft mice following surgical resection

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

98 d with enhanced NFKBIB protein expression in GIST cells.

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

100 esistance is an increasing clinical issue in GIST patients receiving front-line imatinib therapy.

101 s without knowing the role of nuclear KIT in GIST tumorigenesis.

102 therapeutic opportunities and limitations in GIST.

103 riven NFKBIB-RELA-KIT autoregulatory loop in GIST tumorigenesis, which are potential targets for deve

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

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

106 alization of KIT with DAPI-stained nuclei in GIST cells without knowing the role of nuclear KIT in GI

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

108 ation associated with imatinib resistance in GIST and the first in vivo demonstration that cell-auton

109 ising strategy to overcome TKI resistance in GIST, while highlighting the complexity of the ubiquitin

110 , and cell death, with unique sensitivity in GIST cells arising from attenuation of the KIT enhancer

111 ts KIT and has been a mainstay of therapy in GIST.

112 le or double mutations of c-KIT developed in GISTs.

113 ppo, and cyclin D1 as oncogenic mediators in GISTs that have converted, during TKI-therapy, to a KIT-

114 th in KIT-dependent, but not KIT-independent GIST and melanoma cell lines.

115 sion was high in each of the KIT-independent GIST sublines.

116 Cyclin D1 inhibition in KIT-independent GISTs had anti-proliferative and pro-apoptotic effects,

117 iologic mechanisms unique to KIT-independent GISTs were identified by transcriptome sequencing, qRT-P

118 duction restores p16 expression and inhibits GIST proliferation.

119 e corresponding CTCF motifs in an SDH-intact GIST model disrupted the boundary between enhancer and o

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

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

122 We developed isogenic GIST lines in which the parental forms were KIT oncoprot

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

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

125 1 (85.9%) had centrally confirmed, localized GISTs with mutation analysis for KIT and PDGFRA performe

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

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

128 tandard of care for patients with metastatic GIST.

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

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

131 Most GISTs are caused by activating mutations in the KIT rece

132 However, most GISTs develop imatinib resistance through secondary KIT

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

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

135 tify novel therapeutic targets in KIT-mutant GIST and melanoma cells using a human tyrosine kinome si

136 role as a novel KIT regulator in KIT-mutant GIST and melanoma cells.

137 apoptosis by targeting c-KIT in c-KIT-mutant GIST cell lines.

138 The treatment of KIT-mutant GIST has been revolutionized with the advent of KIT-dire

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

140 oth of which may contribute to PDGFRA-mutant GIST immunogenicity.

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

142 immune infiltrates of KIT and PDGFRA-mutant GIST.

143 tly higher level when compared to KIT-mutant GISTs and exhibited more diverse driver-derived neoepito

144 tolytic activity when compared to KIT-mutant GISTs.

145 PDGFRA-mutant GISTs expressed many chemokines, such as CXCL14, at a si

146 flow cytometry, we found that PDGFRA-mutant GISTs harbored more immune cells with increased cytolyti

147 ble of differentiating KIT and PDGFRA-mutant GISTs, and also identified additional immune features of

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

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

150 sufficient to drive ICC hyperplasia but not GIST tumorigenesis.

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

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

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

154 Given the dependence of GIST upon enhancer-driven expression of RTKs, we hypothe

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

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

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

158 , are associated with the natural history of GIST.

159 KIT is essential for driving the majority of GIST neoplasms, which can be therapeutically targeted us

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

161 inib has radically changed the management of GIST, yet the magnitude of impact on outcome across the

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

163 Using a mouse model of GIST and human specimens, we show that intratumoral muri

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

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

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

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

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

169 of impact on outcome across the spectrum of GIST presentation and relevance of historical prognostic

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

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

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

173 Treatment of GIST cells with BBIs led to cell-cycle arrest, apoptosis

174 ranscription/expression and the viability of GIST cells.

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

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

177 5 patients, comprising the largest cohort of GISTs sequenced to date, in order to discover difference

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

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

180 FS improves over time following resection of GISTs.

181 tential anticancer drug for the treatment of GISTs and AML.

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

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

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

185 atients who underwent resection of a primary GIST between 1996 and 2014 were identified from 2 databa

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

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

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

189 and the Hippo pathway coordinately regulate GIST cyclin D1 expression.

190 elative cell viability of imatinib-resistant GIST cells.

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

192 of imatinib-sensitive and imatinib-resistant GIST.

193 th imatinib-sensitive and imatinib-resistant GIST.

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

195 KIT mutants in patients with drug-resistant GISTs.

196 tures in KIT-independent, imatinib-resistant GISTs as a step towards identifying drug targets in thes

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 h those of intermediate or low/very low-risk GISTs.

201 Clinically, high NCCN risk GISTs had significantly higher mean expression levels of

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

203 KIT mutants and the proliferation of several GIST cell lines.

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

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

206 Most small GISTs are cured with surgery.

207 However, some GISTs lose expression of KIT oncoproteins, and therefore

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

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

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

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

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

213 H-Dots not only target GIST for image-guided surgery, but also tailor the fate

214 by markedly downregulated expression of the GIST biomarker, protein kinase C-theta (PRKCQ).

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

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

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

218 opy and grid inhomogeneous solvation theory (GIST) analyses.

219 y using grid inhomogeneous solvation theory (GIST).

220 on of mutant KIT in the ICC lineage leads to GIST.

221 advanced tyrosine-kinase inhibitors-treated GIST using PET/CT.

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

223 s, including gastrointestinal stromal tumor (GIST) and subsets of melanoma, are caused by somatic KIT

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

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

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

227 Gastrointestinal stromal tumor (GIST) is a mesenchymal neoplasm characterized by activat

228 Gastrointestinal stromal tumor (GIST) is driven by an activating mutation in the KIT pro

229 Gastrointestinal stromal tumor (GIST) is the most common human sarcoma and arises in the

230 Gastrointestinal stromal tumor (GIST) is the most common human sarcoma, frequently chara

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

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

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

234 In advanced gastrointestinal stromal tumor (GIST), there is an unmet need for therapies that target

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

236 atients with gastrointestinal stromal tumor (GIST).

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

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

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

240 therapy of gastrointestinal stromal tumors (GIST) using nonsticky and renal clearable theranostic na

241 ometastatic gastrointestinal stromal tumors (GIST).

242 a (CML) and gastrointestinal stromal tumors (GIST).

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

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

245 majority of gastrointestinal stromal tumors (GISTs) are driven by oncogenic KIT signaling and can the

246 Gastrointestinal stromal tumors (GISTs) are frequently driven by auto-activated, mutant K

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

248 Gastrointestinal stromal tumors (GISTs) are prototypes of stem cell factor receptor (c-KI

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

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

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

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

256 ets in most gastrointestinal stromal tumors (GISTs), and the KIT inhibitor, imatinib, is therefore st

257 icularly in gastrointestinal stromal tumors (GISTs), in which the heterogeneity of drug-resistant KIT

258 nagement of gastrointestinal stromal tumors (GISTs), renal cell carcinoma (RCC), and pancreatic cance

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

260 tients with gastrointestinal stromal tumors (GISTs).

261 lation with gastrointestinal stromal tumors (GISTs).

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

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

264 subset of gastrointestinal stromal tumours (GISTs) lack canonical kinase mutations but instead have

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

266 rs in most gastrointestinal stromal tumours (GISTs).

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

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

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

270 lting in efficient treatment of unresectable GIST.

271 ically confirmed, metastatic or unresectable GISTs.

272 nterstitial cells of Cajal (ICCs) from which GISTs presumably originate, and (b) temporally through t

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 ent-emergent adverse events in patients with GIST receiving ripretinib 150 mg once daily (n = 142) we

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

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

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

284 an effective therapy for many patients with GIST, disease progression from kinase-resistant mutation

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

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.