ライフサイエンスコーパス: IDH

1 IDH mutant gliomas thus manifest a CpG island methylator

2 IDH mutation has been found to be an inciting event in g

3 IDH mutation is a central and defining event in the deve

4 IDH mutation is an early event in gliomagenesis and has

5 IDH mutational status identified patients with oligodend

6 IDH mutational status was also of prognostic significanc

7 IDH status was evaluable in 210 of 291 patients; 156 (74

8 IDH(m-codel) gliomas demonstrated a significant positive

9 IDH, by 2017 ACC/AHA (systolic BP <130 mm Hg, diastolic

10 IDH-mt tumors have a more favorable prognosis, and tumor

11 IDH-mutant cancer cells show an inability to differentia

12 IDH-mutant patients with 2HG levels >200 at complete rem

13 IDH-wt tumors are not a homogeneous entity and warrant f

14 d-type, 107 IDH mutant/1p19q intact, and 101 IDH mutant/1p19q codeleted gliomas.

15 69 male patients) with 82 IDH wild-type, 107 IDH mutant/1p19q intact, and 101 IDH mutant/1p19q codele

16 stemic cancers, 31 other CNS-tumors, and 120 IDH-mutant cartilaginous tumors, we identified that the

17 on subsequent mutational analysis of the 13 IDH wild-type samples with 2HG levels >700 ng/mL, 9 were

18 ild type, 21 IDH mutant/1p19q intact, and 19 IDH mutant/1p19q codeleted), the classification accuracy

19 ations in isocitrate dehydrogenases 1 and 2 (IDH(mut)) are present in a variety of cancers, including

20 sample of 49 gliomas (nine IDH wild type, 21 IDH mutant/1p19q intact, and 19 IDH mutant/1p19q codelet

21 nge, 33-52 years; 169 male patients) with 82 IDH wild-type, 107 IDH mutant/1p19q intact, and 101 IDH

22 wever, the effects on DNA methylation across IDH mutant cancers and functionally different genome reg

23 Additionally, IDH(mut) caused a greater degree of hypermethylation in

24 n and immune response were suppressed in all IDH(mut) cancers.

25 and transcriptome profiles, would vary among IDH(mut) cancers, especially gliomas.

26 s have chromosomes 1p/19q co-deletion and an IDH mutation.

27 Results Nine patients had an IDH-1 mutation and 61 had IDH-1 wild type.

28 enesis and tumor maintenance and identify an IDH-independent strategy to target these cancers therape

29 make a presumptive molecular diagnosis of an IDH mutation in gliomas technically unable to undergo a

30 pects of this phenotype in the absence of an IDH mutation.

31 Patients who had lower-grade gliomas with an IDH mutation and 1p/19q codeletion had the most favorabl

32 Lower-grade gliomas with an IDH mutation either had 1p/19q codeletion or carried a T

33 e majority of lower-grade gliomas without an IDH mutation had genomic aberrations and clinical behavi

34 Most lower-grade gliomas without an IDH mutation were molecularly and clinically similar to

35 er than those observed in samples without an IDH mutation, similar to what was observed in the origin

36 cluded indirect hyperbilirubinemia (12%) and IDH-inhibitor-associated differentiation syndrome (7%).

37 irubinemia (10%), thrombocytopenia (7%), and IDH differentiation syndrome (6%).

38 ld stress promotes the expression of ACS and IDH which may increase the synthesis of citrate, cis-aco

39 patients, virtually all 1p19q codeleted and IDH mutated (59 of 60).

40 = .029) in the IDH-mutant/non-codeleted and IDH-mutant/codeleted subgroups, respectively.

41 ations in the metabolic enzymes SDH, FH, and IDH can result in cancer and, more broadly, for how alte

42 aracterization may be useful for grading and IDH mutation detection of gliomas and requires only 7 mi

43 y, combination of CNTFRalpha methylation and IDH mutation significantly (p < 0.05) improved the progn

44 isocitrate dehydrogenase (IDH-1)-mutated and IDH-1 wild-type glioblastomas.

45 i.e., were triple-positive), 5% had TERT and IDH mutations, 45% had only IDH mutations, 7% were tripl

46 han 1% were triple-positive, 2% had TERT and IDH mutations, 7% had only IDH mutations, 17% were tripl

47 As expected, TET2 and IDH mutated patients had significantly lower levels of 5

48 Results: For IDH(wt) and IDH(m-noncodel) gliomas, nSUV demonstrated significant p

49 is divided into IDH wild-type ( IDH-wt) and IDH-mt tumors.

50 -Olff-Fresco multi-model selection approach, IDH testing was done.

51 h prognostic relevance further designated as IDH, high (H), medium (M), and low (L) alteration groups

52 ed to study new tumor tissue markers such as IDH mutations.

53 Cancer-associated IDH mutations alter the enzymes such that they reduce 2O

54 LGG-associated IDH mutations confer gain-of-function activity by conver

55 1p19q co-deleted (n = 81); (2) astrocytoma, IDH-mutant and 1p19q non-codeleted (n = 54); (3) astrocy

56 19q non-codeleted (n = 54); (3) astrocytoma, IDH-wildtype (n = 20).

57 ssociation was only retained in astrocytoma, IDH-wildtype.

58 added prognostic information in astrocytoma, IDH-wildtype.

59 acy of vaccine immunotherapy in mice bearing IDH-MUT gliomas.

60 We establish a firm association between IDH mutations and serum 2HG concentration in AML, and co

61 vivo (1)H-MRS spectra discriminated between IDH-mutant tumors and healthy tissue, and separated IDH1

62 se studies provide a functional link between IDH mutations, hepatic cell fate, and IHCC pathogenesis,

63 Differences in bulk profiles between IDH-mutant astrocytoma and oligodendroglioma can be prim

64 godendroglioma requires the presence of both IDH-mt and 1p/19q co-deletion, whereas anaplastic astroc

65 glioma that were captured more accurately by IDH, 1p/19q, and TP53 status than by histologic class.

66 n recurrent gliomas and was characterized by IDH mutation but without co-deletion of chromosome arms

67 ctive modulation of relevant cancer genes by IDH mutations.

68 nt of D2HGA and suggest that 2HG produced by IDH mutant tumors has the potential to provoke a paraneo

69 L10 and T cell accumulation were reversed by IDH-C35, a specific inhibitor of mutant IDH1.

70 tion with kinetic data on IDHKP to calculate IDH activity at a range of total IDH levels and find tha

71 (m-noncodel)], and 16 with mutant codeleted [IDH(m-codel)]).

72 was identical to that of other GBM cohorts (IDH wild-type [WT], 95%; EGFR amplified, approximately 5

73 E. coli IDH is regulated by reversible phosphorylation catalyzed

74 Conclusion IDH-mutated glioblastomas have a less invasive phenotype

75 Conclusion: IDH(m-codel) gliomas showed distinctive patterns of corr

76 e gene coding for isocitrate dehydrogenase ( IDH).

77 Mutant isocitrate dehydrogenase (IDH) 1 and 2 proteins alter the epigenetic landscape in

78 ibitors of mutated isocitrate dehydrogenase (IDH) 1 and IDH2, antibody-based therapies, and cell-base

79 rogression such as isocitrate dehydrogenase (IDH) 1, IDH2, EZH2, serine/arginine-rich splicing factor

80 Mutations in isocitrate dehydrogenase (IDH) are the most prevalent genetic abnormalities in low

81 ions involving the isocitrate dehydrogenase (IDH) enzymes.

82 haracterization of isocitrate dehydrogenase (IDH) gene mutation status of gliomas.

83 onal status of the isocitrate dehydrogenase (IDH) gene were determined.

84 Isocitrate dehydrogenase (IDH) genes 1 and 2 are frequently mutated in acute myelo

85 c mutations in the isocitrate dehydrogenase (IDH) genes IDH1 and IDH2 occur frequently in acute myelo

86 synthase (ACS) and isocitrate dehydrogenase (IDH) genes in cold-treated tomato fruit.

87 the genes encoding isocitrate dehydrogenase (IDH) has uncovered a critical role for altered metabolis

88 e metabolic enzyme isocitrate dehydrogenase (IDH) in subsets of cancers, including secondary glioblas

89 er of novel genes, isocitrate dehydrogenase (IDH) is recurrently mutated in intrahepatic cholangiocar

90 hways disturbed in isocitrate dehydrogenase (IDH) mutant tumors revealed that the hallmark metabolic

91 en tumors harbored isocitrate dehydrogenase (IDH) mutations (91% in IDH-wild-type tumors, 67% in IDH-

92 Background Isocitrate dehydrogenase (IDH) mutations are highly frequent in glioma, producing

93 tions, such as the isocitrate dehydrogenase (IDH) mutations found in 15% of AML patients.

94 Cancer-associated isocitrate dehydrogenase (IDH) mutations produce the metabolite 2-hydroxyglutarate

95 lastomas harboring isocitrate dehydrogenase (IDH) mutations, but metabolic alterations in glioblastom

96 ling, but not with isocitrate dehydrogenase (IDH) mutations, suggesting a distinct mechanism for incr

97 vior arises in the isocitrate dehydrogenase (IDH) regulatory system of Escherichia coli, which was sh

98 ers for predicting isocitrate dehydrogenase (IDH) status in patients with glioma.

99 hydratase (FH) and isocitrate dehydrogenase (IDH), advancing and challenging our understanding of cel

100 CoA, which unlocks isocitrate dehydrogenase (IDH)-dependent reductive carboxylation, producing the re

101 hese influences in isocitrate dehydrogenase (IDH)-mutant gliomas by combining 14,226 single-cell RNA

102 nalysis identifies isocitrate dehydrogenase (IDH)-mutant gliomas misassigned to 1p/19q codeletion sta

103 nsferase (OGT) and isocitrate dehydrogenase (IDH).

104 hosphate-dependent isocitrate dehydrogenase (IDH)1 and IDH2 frequently arise in human leukemias and o

105 Oncogenic isocitrate dehydrogenase (IDH)1 and IDH2 mutations at three hotspot arginine resid

106 n of mitochondrial isocitrate dehydrogenase (IDH)2, a tricarboxylic acid cycle enzyme mutated in subs

107 on and activity of isocitrate dehydrogenase (IDH); and, via 13C-labeling studies, demonstrated that a

108 phenotypes of both isocitrate dehydrogenase (IDH-1)-mutated and IDH-1 wild-type glioblastomas.

109 verse flux through isocitrate dehydrogenase, IDH).

110 Isocitrate dehydrogenases (IDH) convert isocitrate to alpha-ketoglutarate (alpha-KG

111 factors: mutated isocitrate dehydrogenases (IDH), succinate dehydrogenase (SDH), and fumarate hydrat

112 were no differences in patient demographics, IDH/MGMT mutation status, or treatment.

113 for artificial valve replacement, developed IDH and esophagogastroduodenal pneumatosis after endosco

114 a noninvasive clinical imaging biomarker for IDH-mutated gliomas.

115 ds-ratios were 9.25 (5.17-16.52; 95% CI) for IDH-mutated gliomas and 12.85 (5.94-27.83; 95% CI) for I

116 d gliomas and 12.85 (5.94-27.83; 95% CI) for IDH-mutated, 1p/19q co-deleted gliomas.

117 r samples underwent immunohistochemistry for IDH-1 R132H mutations.

118 2HG represents a valuable imaging marker for IDH-mutated human glioma.

119 Our work provides a unifying model for IDH-mutant gliomas and a general framework for dissectin

120 howed the highest diagnostic performance for IDH gene mutation detection in low-grade glioma (AUC, 0.

121 t differences can regulate the potential for IDH mutations to produce 2HG in cells.

122 V or ADC may result in a worse prognosis for IDH(wt) gliomas.

123 Results: For IDH(wt) and IDH(m-noncodel) gliomas, nSUV demonstrated s

124 ation that can improve patient selection for IDH-targeted therapies.

125 omas (LGGs) are fundamentally different from IDH-mutant LGGs occurring in adults, because they rarely

126 ed replication plan of key experiments from "IDH mutation impairs histone demethylation and results i

127 Gain-of-function IDH mutations are initiating events that define major cl

128 Furthermore, IDH-C35 enhanced the efficacy of vaccine immunotherapy i

129 vents of special interest included all-grade IDH differentiation syndrome (17%), all-grade electrocar

130 ne patients had an IDH-1 mutation and 61 had IDH-1 wild type.

131 levels >700 ng/mL, 9 were identified to have IDH mutations.

132 Among those newly classified as having IDH, an estimated 0.6% (95% CI, 0.5%-0.6%) also met the

133 Intramural duodenal hematoma (IDH) rarely occurs after endoscopic intervention.

134 However, IDH was not significantly associated with increased risk

135 Here we show that human IDH mutant gliomas exhibit hypermethylation at cohesin a

136 finition of isolated diastolic hypertension (IDH).

137 The Improving the Detection of Hypertension (IDH) study, a community-based observational study, enrol

138 The Intermediate Disturbance Hypothesis (IDH) is well-known in ecology providing an explanation f

139 tations (91% in IDH-wild-type tumors, 67% in IDH-mutant tumors, P < 0.001).

140 itrate dehydrogenase (IDH) mutations (91% in IDH-wild-type tumors, 67% in IDH-mutant tumors, P < 0.00

141 r mechanism that defines chemosensitivity in IDH-mutated gliomas.

142 a-inducible chemokines, including CXCL10, in IDH-mutated (IDH-MUT) tumors compared with IDH-WT tumors

143 mutations have been recurrently detected in IDH-mutated AML samples.

144 from 10 to 30 000 ng/mL and were elevated in IDH-mutants (median, 3004 ng/mL), compared to wild-type

145 demonstrate a mechanism of immune evasion in IDH-MUT gliomas and suggest that specific inhibitors of

146 Molecular events in IDH WT GBMs were stable in approximately 80% of events,

147 and 4% of CpG sites were hypermethylated in IDH(mut) AML, melanoma, and cholangiocarcinoma, relative

148 sites, 70,591 (19%) were hypermethylated in IDH(mut) gliomas compared to wild-type (IDH(wt)) gliomas

149 trategy to map D-2HG and tumor metabolism in IDH-mutated human glioma.

150 SPR-mediated disruption of the CTCF motif in IDH wild-type gliomaspheres upregulates PDGFRA and incre

151 Hotspot mutations in IDH isoforms 1 or 2 occur in approximately 15% of intrah

152 mutations in the TERT promoter, mutations in IDH, and codeletion of chromosome arms 1p and 19q (1p/19

153 Mutations in IDH, TP53, and ATRX and codeletion of chromosome arms 1p

154 ests that IDH may be a therapeutic target in IDH-mutant gliomas.

155 ereas anaplastic astrocytoma is divided into IDH wild-type ( IDH-wt) and IDH-mt tumors.

156 for the IDH1(R132H) mutation exhibited less IDH-mediated production of NADPH, such that after exposu

157 We leveraged IDH wild-type glioblastomas, derivative neurospheres, an

158 lar to previous reports on related mammalian IDH enzymes.

159 istinct clusters termed H3-Pons, H3-Medulla, IDH, and PA-like, each associated with unique genomic an

160 e predictive performance of MGMT methylation IDH mutations, 1p/19q co-deletion, and ATRX mutations.

161 We introduce molecular (MGMT methylation, IDH mutation, 1p/19q co-deletion, ATRX mutation, and TER

162 The prediction models of MGMT methylation, IDH mutations, 1p/19q co-deletion, ATRX mutation, and TE

163 evels by positively modulating mitochondrial IDH activity and inducing IDH2 expression.

164 anner independent of wild-type mitochondrial IDH function.

165 monoallelic IDH1 mutation when mitochondrial IDH flux was diverted to the cytosol.

166 Moreover, IDH and Kras mutations, genetic alterations that co-exis

167 Mutant IDH produces 2-hydroxyglutarate (2HG), which induces his

168 Mutant IDH protein produces a new onco-metabolite, 2-hydroxyglu

169 Mutant IDH proteins in IHCC and other malignancies acquire an a

170 gression-free survival after CRT, and mutant IDH was associated with longer overall survival (9.4 v 5

171 cular mechanisms of transformation by mutant IDH and discuss their implications for the development o

172 For AML, low-grade glioma and CC, mutant IDH status is associated with a DNA hypermethylation phe

173 ly engineered mouse models expressing mutant IDH in the adult liver show an aberrant response to hepa

174 ial implications for understanding of mutant IDH function and for optimizing therapeutic approaches t

175 strating that continued expression of mutant IDH is required to maintain this phenotype.

176 d suggest that specific inhibitors of mutant IDH may improve the efficacy of immunotherapy in patient

177 ansformation, but the contribution of mutant IDH proteins to maintenance and progression of AML in vi

178 propagating downstream the effects of mutant IDH, leading to malignant transformation of cells.

179 roxyglutarate, supporting the role of mutant IDH-produced 2-hydroxyglutarate as an inhibitor of TET-m

180 Here we show that mutant IDH blocks liver progenitor cells from undergoing hepato

181 P = .037) in low-grade glioma with a mutated IDH gene, and MTI was significantly increased in glioma

182 hemokines, including CXCL10, in IDH-mutated (IDH-MUT) tumors compared with IDH-WT tumors.

183 o the presence or absence of IDH mutations ( IDH-mt) and combined 1p/19q loss.

184 In the test sample of 49 gliomas (nine IDH wild type, 21 IDH mutant/1p19q intact, and 19 IDH mu

185 rs lived longest, patients with noncodeleted IDH-mutated tumors also lived longer after CRT.

186 DH(wt)], 16 with mutant 1p/19q noncodeleted [IDH(m-noncodel)], and 16 with mutant codeleted [IDH(m-co

187 rily according to the presence or absence of IDH mutations ( IDH-mt) and combined 1p/19q loss.

188 on of spatiotemporal genomic architecture of IDH-wild-type multifocal glioblastomas (M-GBMs) suggests

189 tic performance for grading and detection of IDH gene mutation status.

190 ed an obligatory factor for the diagnosis of IDH.

191 oped to specifically inhibit mutant forms of IDH (mIDH1 and mIDH2).

192 te relationship between the phospho-forms of IDH.

193 s, and the neomorphic, oncogenic function of IDH mutations affects several epigenetic and gene regula

194 A demethylation and poor outcome; a group of IDH-wild-type diffuse glioma showed molecular similarity

195 of the system (including homodimerization of IDH and bifunctionality of IDHKP) that provide a potenti

196 tality in the 2 external cohorts (eg, HRs of IDH by the 2017 ACC/AHA definition were 1.17 [95% CI, 0.

197 athway and offer insights into the impact of IDH mutation and D-2HG on metazoan tissues.

198 findings, we have investigated the impact of IDH mutations on the immunological milieu in LGG.

199 dditionally, we observed that independent of IDH mutation status, methylation of CNTFRalpha was signi

200 FN-driven IL-10 contributes to inhibition of IDH activity and itaconate synthesis in LPS-stimulated m

201 y as being responsible for the inhibition of IDH in LPS-stimulated macrophages.

202 kinase/phosphatase (IDHKP), and the level of IDH activity determines whether carbon flux is directed

203 porating 2HG MRS into clinical management of IDH-mutated gliomas.

204 novel genetically engineered mouse model of IDH-driven malignancy.

205 endroglioma is characterized by mutations of IDH and CIC, 1p/19q loss, and slow growth.

206 The onset of IDH may occur earlier than reported in the literature.

207 reviously been linked to the pathogenesis of IDH mutant tumors.

208 that is highly dependent on the presence of IDH mutation.

209 ted CpG sites were higher in the presence of IDH-mutation.

210 HA guideline based solely on the presence of IDH.

211 The estimated prevalence of IDH in the NHANES was 6.5% by the 2017 ACC/AHA definitio

212 Weighted estimates for prevalence of IDH in US adults and prevalence of US adults recommended

213 is of US adults, the estimated prevalence of IDH was more common when defined by the 2017 ACC/AHA BP

214 defective in both of the normal reactions of IDH.

215 Here we discuss the relevance of IDH mutations to leukemia pathogenesis, therapy, and out

216 Elucidation of the role of IDH mutations and (R)-2HG in leukemogenesis has been ham

217 To further understand the role of IDH mutations in cancer, we conducted mechanistic studie

218 In order to investigate the role of IDH mutations in immune response, we created a syngeneic

219 D-driven model was used to study the role of IDH mutations in the differentiation of mesenchymal cell

220 A subtype of IDH mutant glioma was associated with DNA demethylation

221 data suggest that the extent and targets of IDH(mut)-induced genomic hypermethylation vary greatly a

222 Treatment of IDH mutant gliomaspheres with a demethylating agent part

223 dings may have implications for treatment of IDH-mutant leukemia.

224 lassification system: (1) oligodendroglioma, IDH-mutant and 1p19q co-deleted (n = 81); (2) astrocytom

225 CpG sites were found for oligodendroglioma, IDH-mutant and 1p19q co-deleted.

226 t advances in glioma classification based on IDH mutation and 1p/19q co-deletion status were recapitu

227 associations with overall survival for only IDH(wt) gliomas.

228 , 2% had TERT and IDH mutations, 7% had only IDH mutations, 17% were triple-negative, and 74% had onl

229 5% had TERT and IDH mutations, 45% had only IDH mutations, 7% were triple-negative, and 10% had only

230 rs) among patients who had gliomas with only IDH mutations and was highest (59 years) among patients

231 without 1p/19q co-deletion [IDHmt/codel], or IDH wild type [IDHwt]; p=0.013).

232 ted almost entirely of patients with TET2 or IDH mutations.

233 cells with defective mitochondria, oxidative IDH flux persists and may exceed the reductive flux.

234 ompared with normotensive ARIC participants, IDH by the 2017 ACC/AHA definition was not significantly

235 y automated method was useful for predicting IDH mutations (sensitivity = 0.93, specificity = 0.88),

236 arge cohort of matched primary and recurrent IDH WT tumors establishes the frequency of GBM driver in

237 -2-hydroxyglutarate was sufficient to reduce IDH-mediated NADPH production and increase IR sensitivit

238 n, although we cannot rule out net reductive IDH flux in some compartments.

239 by spreading of label without net reductive IDH flux.

240 treating AML and other cancers by targeting IDH mutant proteins, it remains unclear how these mutant

241 and monitoring treatment response targeting IDH mutations.

242 timizing therapeutic approaches to targeting IDH-mutant tumors.

243 l. propose in this issue of Cancer Cell that IDH-wild-type glioblastomas initiate years pre-diagnosis

244 ng of chondrosarcoma biopsies and found that IDH mutations were associated with DNA hypermethylation

245 Early evidence suggests that IDH may be a therapeutic target in IDH-mutant gliomas.

246 Our study suggests that IDH mutations promote gliomagenesis by disrupting chromo

247 The IDH group consisted of all samples with IDH1 or IDH2 mut

248 Among the IDH-1 wild-type tumors, 42 of 61 (69%) were diffusively

249 , 0.38; P = .013; HR, 0.21; P = .029) in the IDH-mutant/non-codeleted and IDH-mutant/codeleted subgro

250 was observed with the addition of PCV in the IDH-wild-type subgroup.

251 Accordingly, lowest numbers were seen in the IDH-wildtype subpopulation.

252 nt studies have shown that expression of the IDH mutant enzymes results in high levels of 2HG and a b

253 ma cultures recapitulates the effects of the IDH mutation on intrinsic apoptosis, shuts down oxidativ

254 nifies much of the known biochemistry of the IDH regulatory system into a single quantitative framewo

255 Here we show that the IDH variants in CS are also associated with a hypermethy

256 ty and forest disturbance expected under the IDH; instead diversity peaked in old-growth forests.

257 Here, we used the IDH as a framework to describe the role of forest distur

258 H mutation (P = .013) when compared with the IDH wild-type counterparts.

259 holangiocarcinoma, relative to each of their IDH(wt) counterparts.

260 Therefore, IDH flux may not be a net contributor to acetyl-CoA prod

261 The three IDH isoforms (nicotinamide adenine dinucleotide phosphat

262 rine type I IFN controls carbon flow through IDH in LPS-activated macrophages.

263 silenced in oligodendrogliomas secondary to IDH-associated hypermethylation and 1p allelic loss.

264 ntified that the association was specific to IDH-mutant gliomas.

265 -malignant genes that appear to be unique to IDH(mut) gliomas.

266 o calculate IDH activity at a range of total IDH levels and find that our model predicts robustness.

267 e development of targeted therapies to treat IDH mutant malignancies.

268 (median, 3004 ng/mL), compared to wild-type IDH (median, 61 ng/mL) (P < .0005).

269 alterations in glioblastomas with wild-type IDH are poorly understood.

270 astrocytoma is divided into IDH wild-type ( IDH-wt) and IDH-mt tumors.

271 d in IDH(mut) gliomas compared to wild-type (IDH(wt)) gliomas, and only 3%, 2%, and 4% of CpG sites w

272 (36 with isocitrate dehydrogenase wild-type [IDH(wt)], 16 with mutant 1p/19q noncodeleted [IDH(m-nonc

273 The following search terms were used: IDH, IDH1, IDH2, and isocitrate dehydrogenase, in conjun

274 olecular groups (n = 106/251), 26 (24%) were IDH-wild type, 43 (41%) were IDH-mutant/non-codeleted, a

275 e IDH-mutant/non-codeleted, and 37(35%) were IDH-mutant/codeleted.

276 , 26 (24%) were IDH-wild type, 43 (41%) were IDH-mutant/non-codeleted, and 37(35%) were IDH-mutant/co

277 iew of the literature dating from 2008, when IDH mutation was discovered to be clinically significant

278 However, the molecular pathways by which IDH mutations lead to tumour formation remain unclear.

279 he cellular context and may help explain why IDH(mut) is only a favorable prognostic marker in glioma

280 gion at 8q24.21, is strongly associated with IDH-mutant glioma development and was suggested to be a

281 with high D-2HG levels in cancer cells with IDH mutations.

282 s are relatively common in PMF, cluster with IDH mutations, and are independently predictive of poor

283 have a less invasive phenotype compared with IDH wild type.

284 n IDH-mutated (IDH-MUT) tumors compared with IDH-WT tumors.

285 grade gliomas that were more concordant with IDH, 1p/19q, and TP53 status than with histologic class.

286 eloid leukemia (AML) patients correlate with IDH mutations, and whether diagnostic or remission 2HG m

287 ously published criteria and correlated with IDH-1 mutation status by using the Freeman-Halton extens

288 Nearly all lower-grade gliomas with IDH mutations and no 1p/19q codeletion had mutations in

289 viable therapeutic strategy for gliomas with IDH mutations.Significance: These findings show that the

290 ificantly increased in glioma grade III with IDH mutation (P = .013) when compared with the IDH wild-

291 tral profiles were observed for lesions with IDH-mutated genotypes, between astrocytoma and oligodend

292 , there exist relatively few cell lines with IDH mutations.

293 All of the patients with IDH-1 mutation had a minimally invasive DT imaging pheno

294 e efficacy of immunotherapy in patients with IDH-MUT gliomas.

295 lysis supports the notion that patients with IDH-mutant high-risk LGG regardless of codeletion status

296 Materials and Methods Data in patients with IDH-mutant lower-grade gliomas (World Health Organizatio

297 ar differentiation that can be reversed with IDH mutant-specific small-molecule inhibitors.

298 Those with IDH-1 wild-type were more likely to show no activity on

299 timally segregated patients with and without IDH mutations, and on subsequent mutational analysis of

300 associated with higher grade tumors without IDH mutations.