ライフサイエンスコーパス: medulloblastoma

1 and brain tumors (gliomas, ependymomas, and medulloblastomas).

2 we enrolled patients aged 3-21 years who had medulloblastoma.

3 ic response in mice with primary, Shh-driven medulloblastoma.

4 tumor-initiating cells and in human SHH-type medulloblastoma.

5 ve agents in children with neuroblastoma and medulloblastoma.

6 tors of PI3K/AKT signaling and metastasis in medulloblastoma.

7 the Fbxl17-Sufu axis in the pathogenesis of medulloblastoma.

8 alue target for clinical trials in high risk medulloblastoma.

9 ed with proton radiotherapy in children with medulloblastoma.

10 ationale for the upregulation of ARHGAP36 in medulloblastoma.

11 in neuroblastoma, breast cancer, DLBCL, and medulloblastoma.

12 ical and biologic risk factors in metastatic medulloblastoma.

13 luster, we identify 12 different subtypes of medulloblastoma.

14 argetable component of PI3K/AKT signaling in medulloblastoma.

15 cally tractable cancers such as Group 3 (G3) medulloblastoma.

16 ts aberrant activation is a leading cause of medulloblastoma.

17 rvival of patients with WIP1 high-expressing medulloblastoma.

18 ted and could contribute to tumorigenesis of medulloblastoma.

19 o seen in the hGFAP-Cre:SmoM2 mouse model of medulloblastoma.

20 expression of p73 in a proportion of non-WNT medulloblastoma.

21 represents a key step in the development of medulloblastoma.

22 ase DDX3X is frequently mutated in pediatric medulloblastoma.

23 nostic biomarker for the improved therapy of medulloblastoma.

24 rs (CGNP) and for the growth of CGNP-derived medulloblastoma.

25 e as a marker of sonic hedgehog (SHH)-driven medulloblastoma.

26 02V and G325E, are associated with pediatric medulloblastoma.

27 s when mutated, and sustains tumor growth in medulloblastoma.

28 fective therapy for patients with SHH-driven medulloblastoma.

29 to empower chemotherapeutic responses in G3 medulloblastoma.

30 rlin syndrome and a PTCH1 mutation developed medulloblastoma.

31 igm for treatment of sonic hedgehog subgroup medulloblastoma.

32 intellectual outcome in patients treated for medulloblastoma.

33 ng a pathway that is aberrantly activated in medulloblastoma.

34 ve network that could be further targeted in medulloblastoma.

35 the growth of HH-dependent cancers, such as medulloblastoma.

36 l proliferation in various cancers including medulloblastoma.

37 and more tailored therapies for a subset of medulloblastoma.

38 orylation could provide a viable therapy for medulloblastoma.

39 ted therapeutic targets in cancer, including medulloblastoma.

40 low as 50-60% for Sonic Hedgehog (Shh)-type medulloblastoma.

41 as an adjuvant treatment for p73-expressing medulloblastoma.

42 consistently in recurrent and metastatic SHH medulloblastoma.

43 nd brain, resembling xenografts of human SHH medulloblastoma.

44 ferent genetic mouse models of Hh-associated medulloblastoma.

45 bellum predisposed to oncogenic induction of medulloblastoma.

46 c targets for the treatment of patients with medulloblastoma.

47 etastasis of granule precursor-derived human medulloblastoma.

48 neity within the four molecular subgroups of medulloblastoma.

49 d Atoh1 dosage and modifications in Shh-type medulloblastoma.

50 ignaling-driven growth of the cerebellum and medulloblastoma.

51 based treatment protocols for patients with medulloblastoma.

52 expression in CGNPs and mouse Shh-associated medulloblastomas.

53 erful target for therapeutic intervention in medulloblastomas.

54 brain cancer; ASC is also expressed in human medulloblastomas.

55 or causing glutamine addiction in aggressive medulloblastomas.

56 aggressive Sonic hedgehog (SHH)-driven human medulloblastomas.

57 vation are up-regulated in a subset of human medulloblastomas.

58 tion of the sonic hedgehog subgroup of human medulloblastomas.

59 cell population in Pten/Trp53 double mutant medulloblastomas.

60 s an adjuvant treatment for TAp73-expressing medulloblastomas.

61 ere first identified in 216 subgrouped human medulloblastomas (50 MBSHH, 28 Wnt/Wingless, 44 Group 3

62 We included 787 patients with medulloblastoma (86 with WNT tumours, 242 with SHH tumou

63 Medulloblastoma, a clinically challenging, malignant chi

64 Current therapies for medulloblastoma, a highly malignant childhood brain tumo

65 In contrast, SHH-medulloblastoma, a less curable disease subtype, contain

66 Moreover, Eya1 drives the growth of medulloblastoma, a Shh-dependent hindbrain tumor.

67 Group 3 and group 4 subgroup medulloblastomas account for most paediatric cases; yet,

68 d survival from centres participating in the Medulloblastoma Advanced Genomics International Consorti

69 ative radiotherapy deferral in children with medulloblastoma ages 3 to 8 years.

70 ations for overall survival in patients with medulloblastoma ages 3 to 8 years.

71 In mouse medulloblastoma allografts, PDE4D inhibitors suppress Hh

72 g from four independent murine models of Shh medulloblastoma, alongside any role in tumorigenesis usi

73 been described in several tumors, including medulloblastoma, ameloblastoma, and basal cell carcinoma

74 Medulloblastoma, an aggressive cancer of the cerebellum,

75 signals driven by mutant beta-catenin in WNT-medulloblastoma, an essentially curable form of the dise

76 essed at highly increased levels in human G3 medulloblastoma and a mouse model of this disease.

77 edgehog-driven tumors (basal cell carcinoma, medulloblastoma and atypical teratoid rhabdoid tumor) re

78 of Shh signaling is particularly evident in medulloblastoma and basal cell carcinoma (BCC), where in

79 patients who had a histological diagnosis of medulloblastoma and complete data about extent of resect

80 vestigated a transgenic model of MYCN-driven medulloblastoma and found spontaneous development of Trp

81 toposide- and cisplatin-induced apoptosis in medulloblastoma and glioblastoma cell lines is mediated

82 ptosis induced by cisplatin and etoposide in medulloblastoma and glioblastoma cell lines.

83 mouse brain, resulting in the development of medulloblastoma and glioblastoma, respectively.

84 re highly correlated with longer survival in medulloblastoma and glioma patients, suggesting their tu

85 gnaling and an important target for treating medulloblastoma and other cancers driven by HH signaling

86 gs highlight two novel prometastatic loci in medulloblastoma and point to the JPO2:LEDGF/p75 protein

87 Analysis of mouse medulloblastoma and precursor-cell methylation demonstra

88 n mice repressed the growth of Hh-associated medulloblastoma and prolonged survival through inhibitio

89 signaling to the most aggressive subtype of medulloblastoma and this axis in medulloblastoma therapy

90 l molecular subgroups exist within childhood medulloblastoma and whether these could be used to impro

91 /nodular and 45.97 for large-cell/anaplastic medulloblastoma) and nonresponse to the first chemothera

92 ics during pregnancy/infancy for 43 PNET, 34 medulloblastoma, and 106 astrocytoma cases and 30,569 co

93 T-lineage acute lymphoblastic leukaemia and medulloblastoma, and a paucity of mutations in low-grade

94 ted pathways are conserved in human Shh-type medulloblastoma, and Brg1 is important for the growth of

95 olyamines are elevated in Hedgehog-dependent medulloblastoma, and genetic or pharmacological inhibiti

96 FBW7 is either mutated or downregulated in medulloblastoma, and in cases where FBW7 mRNA levels are

97 rate increased WIP1 expression in metastatic medulloblastomas, and inferior progression-free and over

98 to Ptch1(+/-) mice, which develop SHH-driven medulloblastoma, animals with Atoh1 transgene expression

99 tients with incomplete surgical resection of medulloblastoma are controversially regarded as having a

100 Medulloblastomas are among the most common malignant bra

101 Approximately one-third of medulloblastomas are associated with misactivation of th

102 We suggest that medulloblastomas are typically sensitive to DNA-damaging

103 Medulloblastoma arising from the cerebellum is the most

104 tors in clinical trials for the treatment of medulloblastoma, as well as other cancers driven by SHH

105 nsgene expression developed highly penetrant medulloblastoma at a young age with extensive leptomenin

106 ule in vivo, against the HH-dependent cancer medulloblastoma, attenuating its growth and reducing the

107 t cranial radiation extended the survival of medulloblastoma-bearing mice and induced widespread apop

108 ospective review of 113 patients treated for medulloblastoma between 1983 and 2011 who were seen for

109 led novel, clinically relevant insights into medulloblastoma biology.

110 nical and biological investigation of serial medulloblastoma biopsies obtained at diagnosis and relap

111 pinal axis is standard-of-care for pediatric medulloblastoma but is associated with long-term morbidi

112 ve been reported in basal cell carcinoma and medulloblastoma, but are largely absent in most tumor ty

113 ive in treatment of basal cell carcinoma and medulloblastoma, but fail therapeutically or accelerate

114 re led to explore the bioactivity of IGF1 in medulloblastoma by elevated CSF levels of IGF1, IGF-sequ

115 s a promising therapeutic drug candidate for medulloblastoma by inhibiting persistent STAT3 signaling

116 Epigenetic alterations also affected novel medulloblastoma candidate genes (for example, LIN28B), r

117 Risk or presence of metastasis in medulloblastoma causes substantial treatment-related mor

118 activity is required for sustaining CGNP and medulloblastoma cell (MBC) proliferation.

119 on and chromatin-binding analysis in a human medulloblastoma cell line to characterize direct, evolut

120 Brg1 is important for the growth of a human medulloblastoma cell line.

121 In medulloblastoma cell lines (DAOY and UW228) engineered t

122 osphorylation and induced apoptosis in human medulloblastoma cell lines expressing constitutive STAT3

123 Transcriptional profiling of medulloblastoma cells expressing a degradation-resistant

124 growth and invasion of WIP1 high-expressing medulloblastoma cells in a p53-dependent manner.

125 elerated migration/adhesion in MYC amplified medulloblastoma cells in the context of appropriate matr

126 y blocks Hedgehog-dependent proliferation of medulloblastoma cells in vitro and in vivo.

127 Medulloblastoma cells not arising from granule precursor

128 9 in a GSK3/FBW7-dependent manner, rendering medulloblastoma cells sensitive to cytostatic treatment.

129 ing the G protein-coupled receptor CXCR4, in medulloblastoma cells with high WIP1 expression.

130 lization of CXCR4 and promoted the growth of medulloblastoma cells with low WIP1 expression.

131 into the cerebellum of immunodeficient mice, medulloblastoma cells with stable or endogenous high WIP

132 -1, IGF-2, and leukemia inhibitory factor in medulloblastoma cells, but did not inhibit STAT1 and STA

133 ppressed the HH activity-dependent growth of medulloblastoma cells, in vitro and in vivo.

134 a2 depletion impaired the growth of cultured medulloblastoma cells, which was rescued by Gli overexpr

135 f mice xenografted with WIP1 high-expressing medulloblastoma cells.

136 in the inhibition of cell viability in human medulloblastoma cells.

137 mall molecule, named LY5, to target STAT3 in medulloblastoma cells.

138 XCR4 and inhibited the growth of WIP1-stable medulloblastoma cells.

139 targets required for the growth of the human medulloblastoma cells.

140 neuron progenitors (CGNPs) and SmoM2-driven medulloblastoma cells.

141 We ascertained all cases of medulloblastoma, central nervous system primitive neuroe

142 t with cisplatin, a component of the current medulloblastoma chemotherapy.

143 ile molecular subgrouping has revolutionized medulloblastoma classification, the extent of heterogene

144 rom the most recently completed pan-European medulloblastoma clinical trial, refractory to analysis b

145 -Light II cells, and inhibited the growth of medulloblastoma D283 cells at nanomolar concentrations.

146 3 pairs of human diagnostic and post-therapy medulloblastomas demonstrated substantial genetic diverg

147 homologue 1 (Atoh1) is required for Shh-type medulloblastoma development in mice.

148 nscriptional program underlying the Shh-type medulloblastoma development.

149 th Ptch1 prevented BCC formation and delayed medulloblastoma development.

150 is signature was evaluated in neuroblastoma, medulloblastoma, diffuse large B-cell lymphoma (DLBCL),

151 eveal novel survival differences between the medulloblastoma disease subgroups with significant poten

152 Shh-type medulloblastoma displays distinct H3K27me3 properties.

153 In mice, an mTORC1 inhibitor suppressed medulloblastoma driven by a mutant SMO that is inherentl

154 genome sequencing (WGS) we characterized the medulloblastoma-driving Ptch1 deletions in detail and sh

155 The medulloblastoma-endothelial cell paracrine axis can be m

156 All medulloblastomas, ependymomas, and high-grade gliomas th

157 e PKM1 isoform, while neural progenitors and medulloblastomas exclusively expressed the less active P

158 R4 pathways in a murine model of SHH-subtype medulloblastoma exerts potent antitumor effects.

159 Genetic events in recurrent murine medulloblastoma exhibit a very poor overlap with those i

160 tionally redundant, but Myc- and MycN-driven medulloblastomas exhibit distinct phenotypes.

161 e Smoothened (ND2:SmoA1) transgenic model of medulloblastoma exhibited a profound reduction in medull

162 graft or transgenic models of metastatic SHH medulloblastoma, foretinib administration reduced the gr

163 Nestin levels increased progressively during medulloblastoma formation, resulting in enhanced tumor g

164 ons in those developmental processes lead to medulloblastoma formation, the most common malignant bra

165 actor during both cerebellar development and medulloblastoma formation, up-to-date detailed mechanism

166 7me3 modifiers to regulate the expression of medulloblastoma genes.

167 Thus, medulloblastoma genotype dictates tumor vessel phenotype

168 ntaining 1 (PID1; NYGGF4) inhibits growth of medulloblastoma, glioblastoma and atypical teratoid rhab

169 WIP1 or CXCR4 knockdown inhibited medulloblastoma growth and invasion.

170 program that specifically regulates Shh-type medulloblastoma growth.

171 f Neuropilins to control Hh transduction and medulloblastoma growth.

172 tenance, and its abrogation markedly reduced medulloblastoma growth.

173 2) disrupts CGNP proliferation and restricts medulloblastoma growth.

174 Cerebellar medulloblastoma has been described in a single affected

175 Recent publications in medulloblastoma have revolved largely around the recogni

176 and tumor suppressors that are required for medulloblastoma identity and proliferation.

177 Consequently, Huwe1 loss in mouse SHH medulloblastoma illustrates the disruption of this devel

178 diagnosed as having histologically confirmed medulloblastoma in 2004 to 2012, without distant metasta

179 Our study redefines the risk of medulloblastoma in Gorlin syndrome, dependent on the und

180 Previous reports have found a 5% risk of medulloblastoma in Gorlin syndrome.

181 ising therapeutic approach for Hh-associated medulloblastoma in humans.

182 lar progenitor model for the Shh subgroup of medulloblastoma in mice, we show for the first time that

183 gnaling, and Aspm is expressed in Shh-driven medulloblastoma in mice.

184 JPO2 overexpression induced metastatic medulloblastoma in vivo through two synergistic feed-for

185 or the aggressive phenotype of a subclass of medulloblastomas in children.

186 levels were elevated in HH signaling-driven medulloblastomas in mice and humans.

187 l proliferation, and induce apoptosis in SHH medulloblastomas in vitro and in vivo.

188 loblastoma exhibited a profound reduction in medulloblastoma incidence and a delayed tumor onset.

189 The childhood brain tumor, medulloblastoma, includes four subtypes with very differ

190 Genetic alterations driving medulloblastoma initiation and progression remain poorly

191 large-scale genomic studies have classified medulloblastoma into four subtypes: Wnt, Shh, Group 3 an

192 pid changes in our biologic understanding of medulloblastoma into the next generation of upfront clin

193 Medulloblastoma is a highly malignant paediatric brain t

194 Medulloblastoma is a highly malignant paediatric brain t

195 Recurrence of medulloblastoma is a nearly universally fatal event, wit

196 reased extent of resection for patients with medulloblastoma is attenuated after molecular subgroup a

197 reased extent of resection for patients with medulloblastoma is attenuated after molecular subgroup a

198 rgical removal of small residual portions of medulloblastoma is not recommended when the likelihood o

199 rance of morbidity in treating patients with medulloblastoma is secondary to the treatment or prophyl

200 Medulloblastoma is the most common malignant pediatric b

201 Medulloblastoma is the most common solid primary brain t

202 of origin for the SHH-associated subgroup of medulloblastoma, is driven by Sonic hedgehog (Shh) and i

203 ng of the common pediatric brain tumors (ie, medulloblastoma, low- and high-grade gliomas, diffuse in

204 Medulloblastoma (</= 30 cases) was associated with prena

205 survival, suggesting that patients with SHH medulloblastoma may benefit from MET-targeted therapy.

206 Microcephaly and medulloblastoma may both result from mutations that comp

207 s enriched at the trailing edge of migrating medulloblastoma (MB) cells to regulate local cell volume

208 g, corroborating to tube-inducing ability of medulloblastoma (MB) cells.

209 Medulloblastoma (MB) is a highly malignant brain tumor t

210 Medulloblastoma (MB) is a highly malignant pediatric bra

211 Medulloblastoma (MB) is the most common malignant brain

212 Medulloblastoma (MB) is the most common paediatric brain

213 cal trials for SONIC HEDGEHOG (SHH)-subgroup medulloblastoma (MB) patients.

214 tmitotic neurons and in many cancers, allows medulloblastoma (MB) to evade immune elimination.

215 DDX3X mutations in numerous tumors including medulloblastoma (MB), but the physiological impact of th

216 GF-beta signaling blockade on progression of medulloblastoma (MB), the most common pediatric brain tu

217 alignant progression of the cerebellar tumor medulloblastoma (MB).

218 ened (SMO), in pediatric and adult recurrent medulloblastoma (MB).

219 ed for neurogenesis and tumor suppression of medulloblastoma (MB).

220 Group3 medulloblastoma (MBG3) that predominantly occur in young

221 Four distinct subgroups of cerebellar medulloblastomas (MBs) differ in their histopathology, m

222 atase PPM1D (WIP1) is present in a subset of medulloblastomas (MBs) that have an expression profile c

223 Medulloblastomas (MBs), but not high-grade gliomas (HGGs

224 enic events in Sonic Hedgehog (SHH) subgroup medulloblastomas (MBSHH) will be essential for the devel

225 ic ATOH1-driven molecular cascade underlying medulloblastoma metastasis that offers possible therapeu

226 l and temporal intratumoral heterogeneity as medulloblastoma metastasizes to leptomeninges and as it

227 In human medulloblastoma, misactivation of Hh signaling was assoc

228 In this study, we used mouse medulloblastoma models to explore the relationship of tu

229 Using new medulloblastoma models, we identify two distinct paradig

230 International consensus recognises four medulloblastoma molecular subgroups: WNT (MBWNT), SHH (M

231 Here we have tested whether medulloblastomas must be competent for apoptosis to be s

232 nts and Methods A total of 121 patients with medulloblastoma (n = 51, Group 4; n = 25, Group 3; n = 2

233 we identify a mutation in Sufu, occurring in medulloblastoma of patients with Gorlin syndrome, which

234 t can be found consistently across Shh-group medulloblastomas of disparate cellular and anatomical or

235 on factor Gli3 to mediate the development of medulloblastomas of the hedgehog subtype.

236 ion, metastasis, and treatment resistance in medulloblastoma, one of the most common childhood brain

237 onditioned media of metastatic MYC amplified medulloblastoma or leptomeningeal cells, we were led to

238 ic astrocytomas, but not other astrocytomas, medulloblastomas, or ependymomas.

239 f Pten and Trp53 resulted in fully penetrant medulloblastoma originating from the perivascular niche,

240 , 0 to 83) for large-cell/anaplastic (n = 5) medulloblastoma ( P < .001 for EFS; P = .001 for OS).

241 of transcription and genome organization in medulloblastoma pathogenesis, which are probably also of

242 genome and transcriptome, and its effects on medulloblastoma pathophysiology.

243 sitive to radiation and chemotherapy; 80% of medulloblastoma patients survive long-term after treatme

244 the cerebrospinal fluid (CSF) of metastatic medulloblastoma patients with factors also in conditione

245 revolved largely around the recognition that medulloblastoma per se does not exist, but rather, that

246 for cell autonomous growth in MYC amplified medulloblastoma prioritized IGF1R inhibitors.

247 Pkm2 deletion accelerated tumor formation in medulloblastoma-prone ND2:SmoA1 mice, indicating the dis

248 tic deletion of Atr blocked tumorigenesis in medulloblastoma-prone SmoM2 mice.

249 Deletion of Aspm in mice with Smo-induced medulloblastoma reduces tumor growth and increases DNA d

250 ur findings identify P53-MYC interactions at medulloblastoma relapse as biomarkers of clinically aggr

251 Mortality from medulloblastoma remains significant.

252 arge nonoverlapping cohorts of patients with medulloblastoma reveals MET kinase as a marker of sonic

253 e the somatic landscape across 491 sequenced medulloblastoma samples and the molecular heterogeneity

254 ective cohort study, we assessed 428 primary medulloblastoma samples collected from UK Children's Can

255 ed clinical trials for sonic-hedgehog-driven medulloblastoma (SHH-MB).

256 Whole-genome analyses of human medulloblastomas show that the dominant clone at relapse

257 Globally, genes associated with medulloblastoma-specific GLI1 binding sites are downregu

258 e cis-regulatory landscape across 28 primary medulloblastoma specimens.

259 In the setting of medulloblastoma, spontaneous or orthotopically implanted

260 In mouse medulloblastoma stem cells, 5 inhibited cell growth, whe

261 served that YB-1 is upregulated across human medulloblastoma subclasses as well as in other varieties

262 We established medulloblastoma subgroup affiliation by gene expression

263 sion is elevated in the Sonic Hedgehog (SHH) medulloblastoma subgroup originating from GNPs with pers

264 governing the transcriptional landscapes of medulloblastoma subgroups, and how this relates to their

265 st patients belonging to Group 3 and Group 4 medulloblastoma subgroups, greatly enhancing previous kn

266 enes and molecular processes that operate in medulloblastoma subgroups.

267 aining in part the disparate prognoses among medulloblastoma subtypes and suggesting an approach to e

268 factor ATOH1, which is present in aggressive medulloblastoma subtypes driven by aberrant Sonic Hedgeh

269 Medulloblastoma subtypes identified through integrative

270 sion and DNA methylation data to identify 12 medulloblastoma subtypes with distinct molecular and cli

271 ters of patients, supporting the presence of medulloblastoma subtypes.

272 fy a novel region of structural variation in medulloblastoma that leads to oncogenic activation of GF

273 als that Arhgap36 is overexpressed in murine medulloblastomas that acquire resistance to chemical Smo

274 -dependent diagnostic molecular subgroups of medulloblastoma (the most common malignant childhood bra

275 Medulloblastoma, the most common malignant brain tumor i

276 Treatment for medulloblastoma, the most common malignant brain tumor i

277 Recent studies suggest that medulloblastoma, the most common malignant brain tumor o

278 w that ASC is highly expressed in a model of medulloblastoma, the most common malignant pediatric bra

279 in the cerebellum and supports the growth of medulloblastoma, the most common malignant pediatric bra

280 lead to birth defects and cancers including medulloblastoma, the most common pediatric brain tumor.

281 subtype of medulloblastoma and this axis in medulloblastoma therapy.

282 tnatal development and in primary cerebellar medulloblastoma tissues.

283 th an impaired cancer cell proliferation and medulloblastoma tumor growth.

284 pected role for ASC in Sonic hedgehog-driven medulloblastoma tumorigenesis, thus identifying ASC as a

285 By screening ABC substrates against mouse G3 medulloblastoma tumorspheres in vitro, we found that Abc

286 y be exploited for treatment of CGNP-derived medulloblastoma using ATR inhibition.

287 f DDX3 to test the function of two recurrent medulloblastoma variants of DDX3 and find that both inac

288 of cancer, chronic lymphocytic leukaemia and medulloblastoma, we conduct a benchmarking exercise with

289 Using a mouse model of Shh-type medulloblastoma, we deleted Brg1 in precancerous progeni

290 ble primary molecular subgroups of childhood medulloblastoma were identified.

291 Current therapies for medulloblastoma were introduced primarily in the 1980s a

292 essed only during early embryogenesis and in medulloblastomas, where it functions as an oncogene.

293 FU-positive family included a single case of medulloblastoma, whereas only two (1.7%) of 115 individu

294 SNF further delineates group 3 from group 4 medulloblastoma, which is not as readily apparent throug

295 nalysed samples from patients with childhood medulloblastoma who were aged 0-16 years at diagnosis, a

296 stinguishing the four molecular subgroups of medulloblastoma-wingless (WNT), sonic hedgehog (SHH), gr

297 the four biologically distinct subgroups of medulloblastoma: wingless (WNT), sonic hedgehog (SHH), G

298 on-driven, functional genomic mouse model of medulloblastoma with 'humanized' in vivo therapy (micron

299 lear subtypes of infants with Sonic Hedgehog medulloblastoma with disparate outcomes and biology are

300 essed in Group 3 and 4 tumors, which contain medulloblastomas with the most aggressive clinical behav

301 ic sources may increase the risk of PNET and medulloblastoma, with limited support for increased risk