ライフサイエンスコーパス: medulloblastoma

1 ociated with poor prognosis in human group 3 medulloblastoma.

2 gin for the SHH-driven pediatric brain tumor medulloblastoma.

3 on normal cerebellar cells or SHH-associated medulloblastoma.

4 -cycle inhibitors with BETi in MYC-amplified medulloblastoma.

5 a and the most common pediatric brain tumor, medulloblastoma.

6 sent in the Sonic Hedgehog (SHH) subgroup of medulloblastoma.

7 hog (SHH) signaling has failed in SHH-driven medulloblastoma.

8 oth ex vivo and in vivo murine models of SHH medulloblastoma.

9 on whole brains from a mouse model of human medulloblastoma.

10 Ps and the pathological growth of SHH-driven medulloblastoma.

11 -up of post-pubertal and adult patients with medulloblastoma.

12 shown pre-clinical promise for MYC-amplified medulloblastoma.

13 ue to germline-mutated PTCH1, also generated medulloblastoma.

14 e PI3Kalpha selective inhibitor alpelisib in medulloblastoma.

15 an unexpected beneficial role of TAMs in SHH medulloblastoma.

16 and serve as the cells of origin for group 3 medulloblastoma.

17 promising therapeutic agents for Gfi1-driven medulloblastoma.

18 is also up-regulated in mouse and human SHH medulloblastoma.

19 f CNS-PNET and a rare model of group 3 and 4 medulloblastoma.

20 resource for dissecting genetic causation in medulloblastoma.

21 ted therapeutic targets in cancer, including medulloblastoma.

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

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

24 luster, we identify 12 different subtypes of medulloblastoma.

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

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

27 and more tailored therapies for a subset of medulloblastoma.

28 orylation could provide a viable therapy for medulloblastoma.

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

30 as an adjuvant treatment for p73-expressing medulloblastoma.

31 consistently in recurrent and metastatic SHH medulloblastoma.

32 nd brain, resembling xenografts of human SHH medulloblastoma.

33 ferent genetic mouse models of Hh-associated medulloblastoma.

34 bellum predisposed to oncogenic induction of medulloblastoma.

35 c targets for the treatment of patients with medulloblastoma.

36 etastasis of granule precursor-derived human medulloblastoma.

37 neity within the four molecular subgroups of medulloblastoma.

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

39 ignaling-driven growth of the cerebellum and medulloblastoma.

40 based treatment protocols for patients with medulloblastoma.

41 ed two families with a history of paediatric medulloblastoma.

42 rable survival rates than those with group 3 medulloblastoma.

43 y 7 in glioblastoma and isochromosome 17q in medulloblastoma.

44 essor BCOR are recurrent and enriched in SHH medulloblastoma.

45 ntage with PRT in the treatment of pediatric medulloblastoma.

46 d tumors in mouse cerebellum mimicking human medulloblastoma.

47 enriched in therapy-resistant and recurrent medulloblastomas.

48 effective treatment strategies in high-risk medulloblastomas.

49 snRNAs) in about 50% of Sonic hedgehog (SHH) medulloblastomas.

50 or causing glutamine addiction in aggressive medulloblastomas.

51 tion of the sonic hedgehog subgroup of human medulloblastomas.

52 cell population in Pten/Trp53 double mutant medulloblastomas.

53 s an adjuvant treatment for TAp73-expressing medulloblastomas.

54 expression in CGNPs and mouse Shh-associated medulloblastomas.

55 eptor gene Ptch1 resulted in fully penetrant medulloblastomas.

56 ncluding basal cell carcinoma and paediatric medulloblastoma(2).

57 3), ependymoma (32), high-grade glioma (25), medulloblastoma (22), ganglioglioma (18), craniopharyngi

58 of patients with the malignant brain tumour medulloblastoma(3).

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

60 Medulloblastoma, a malignant brain tumour primarily diag

61 es a multi-lateral network within the TME of medulloblastoma: a fraction of tumor cells trans-differe

62 In Sonic Hedgehog (SHH) subgroup medulloblastoma, aberrant activation of SHH signaling ca

63 Most ELP1-associated medulloblastomas also exhibited somatic alterations in P

64 Medulloblastoma, an aggressive cancer of the cerebellum,

65 ative cells of origin for the SHH subtype of medulloblastoma and aberrant SHH signaling is implicated

66 Medulloblastoma and central nervous system primitive neu

67 emble human Sonic hedgehog and group 3 and 4 medulloblastoma and CNS neuroblastoma with FOXR2 activat

68 es classified SB-driven tumors into distinct medulloblastoma and CNS-PNET subgroups, indicating they

69 drivers and potential therapeutic targets in medulloblastoma and CNS-PNET.

70 ied several promising therapeutic targets in medulloblastoma and CNS-PNET.

71 esis, we identified novel genetic drivers of medulloblastoma and CNS-PNET.

72 al PI3Kalpha and mTOR inhibition in SHH-type medulloblastoma and confirmed these results in HH-driven

73 this continued molecular characterization of medulloblastoma and contextualize this progress towards

74 Recurrent medulloblastoma and ependymoma are universally lethal, w

75 ected and killed GSCs and stem-like cells in medulloblastoma and ependymoma in a SOX2-dependent manne

76 ell as on the cerebellum from tumors such as medulloblastoma and ependymoma.

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

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

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

80 g is upregulated in basal cell carcinoma and medulloblastoma and Hh pathway inhibitors targeting the

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

82 or primary, metastatic and recurrent group 3 medulloblastoma and PFA ependymoma xenografts in mouse m

83 multiple metastatic mouse models of group 3 medulloblastoma and PFA ependymoma, thereby providing a

84 le PET imaging probe for the Shh subgroup of medulloblastoma and possibly other pediatric and adult b

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

86 These data may be relevant to studies of medulloblastoma and warrant further investigation.

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

88 ed number of bulk samples from patients with medulloblastoma and, more recently, for single medullobl

89 interleukin 13 receptor alpha2, expressed on medulloblastomas and ependymomas, but not expressed in t

90 Nearly all recurrent medulloblastomas and posterior fossa group A (PFA) epend

91 d metastatic CNS neuroblastoma, 57 (25%) had medulloblastoma, and 51 (23%) had other histologic types

92 s were not present across other subgroups of medulloblastoma, and we identified these hotspot mutatio

93 of progenitor pools in Sonic Hedgehog (SHH) medulloblastomas, and identified OLIG2-expressing glial

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

95 Roughly one-third of medulloblastoma are driven by aberrant activation of the

96 Hallmark mutations in WNT and SHH medulloblastoma are usually distinct, but DDX3X is often

97 Medulloblastomas are among the most common malignant bra

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

99 Sonic Hedgehog (SHH) medulloblastomas are brain tumours that arise in the pos

100 Medulloblastomas are the most common malignant brain can

101 Medulloblastoma arising from the cerebellum is the most

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

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

104 tumors specifically resembled human group 3 medulloblastoma based on histology and gene-expression p

105 GRK2 has not been implicated in medulloblastoma biology.

106 lopmental states underlying subtype-specific medulloblastoma biology.

107 multiple cancers, including ovarian cancer, medulloblastoma, breast cancer, colorectal cancer, and l

108 % of adolescents (subtype SHHalpha) with SHH medulloblastoma, but are largely absent from SHH medullo

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

110 children < 4 years of age with nonmetastatic medulloblastoma by systemic chemotherapy, intraventricul

111 robust cancer m/z model building to classify medulloblastoma cancer from healthy tissue without any m

112 ted in cancer margin assessments using human medulloblastoma cancers.

113 extended to genomes and epigenomes of 1,044 medulloblastoma cases from international multicenter coh

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

115 monstrated high [E1-3 (1)] or low [E1-7 (2)] medulloblastoma cell binding affinity were synthesized.

116 eveloping peptide-drug conjugates to inhibit medulloblastoma cell growth while minimizing off-target

117 ere, we investigate this question in a mouse medulloblastoma cell line, SMB55, that requires cilium-m

118 butes to proliferation and survival of these medulloblastoma cell lines and to their protection from

119 isplatin- and etoposide-induced apoptosis in medulloblastoma cell lines UW228-2 and Daoy.

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

121 Medulloblastoma cells not arising from granule precursor

122 Gene-expression analysis of MYC-driven medulloblastoma cells revealed altered glucose metabolic

123 he peptides to deliver a therapeutic drug to medulloblastoma cells with specificity was investigated

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

125 dulloblastoma and, more recently, for single medulloblastoma cells.

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

127 brary to identify heptapeptides that bind to medulloblastoma cells.

128 th peptide-drug conjugates were cytotoxic to medulloblastoma cells.

129 utic approach for a subset of aggressive SHH medulloblastomas characterised by reduced AHR pathway ac

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

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

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

133 d for nonresponders or patients with classic medulloblastoma (CMB) or large-cell/anaplastic medullobl

134 s were globally more representative of human medulloblastoma compared to a MYCN-driven genetically en

135 hich CPCs are maintained and expanded in SHH medulloblastoma could present novel therapeutic opportun

136 In mice predisposed to Wnt- or Shh medulloblastoma, Ddx3x sensed oncogenic stress and suppr

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

138 cer Survivor Study among 5-year survivors of medulloblastoma diagnosed between 1970 and 1999.

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

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

141 Shh-type medulloblastoma displays distinct H3K27me3 properties.

142 after diagnosis, patients with desmoplastic medulloblastoma (DMB) or medulloblastoma with extensive

143 nalysis of DNA sequencing revealed that most medulloblastomas do not have actionable mutations that p

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

145 Here we show that medulloblastomas driven by the transcription factor Gfi1

146 in syndrome patients, who are predisposed to medulloblastoma due to germline-mutated PTCH1, also gene

147 performed studies aimed to enhance the anti-medulloblastoma effects of alpelisib by simultaneous cat

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

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

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

151 ent of post-pubertal and adult patients with medulloblastoma, for patients and caregivers, and for he

152 A subset of group 3 medulloblastoma frequently harbors amplification or over

153 nervous system, including GTML/Trp53(KI/KI) medulloblastoma (G (d) = 3.5 +/- 0.2 kPa, G (l) = 2.3 +/

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

155 2) disrupts CGNP proliferation and restricts medulloblastoma growth.

156 Treatment of medulloblastoma has evolved from surgery and radiotherap

157 owever, the scarcity of genetic mutations in medulloblastoma has led to investigation of other mechan

158 Recent publications in medulloblastoma have revolved largely around the recogni

159 del for the sonic hedgehog (Shh) subgroup of medulloblastoma, here we evaluated the potential of the

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

161 lloblastoma, but are largely absent from SHH medulloblastoma in infants.

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

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

164 e tracing, we analyzed cellular diversity in medulloblastomas in transgenic, medulloblastoma-prone mi

165 positive role by impairing tumour growth in medulloblastoma, in contrast to the pro-tumoural role pl

166 patients can be used as a resource to model medulloblastoma initiation and progression and to identi

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

168 Medulloblastoma is a highly heterogeneous pediatric brai

169 Medulloblastoma is a malignant brain tumor diagnosed in

170 Medulloblastoma is a malignant childhood brain tumor ari

171 Medulloblastoma is a malignant childhood cerebellar tumo

172 Medulloblastoma is a malignant pediatric tumor that aris

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

174 Medulloblastoma is among the most common malignant brain

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

176 We hypothesize that each patient with medulloblastoma is sensitive to different therapies and

177 Medulloblastoma is the most common malignant brain tumor

178 Medulloblastoma is the most common solid primary brain t

179 In this study, we showed that medulloblastomas lacking the p53 tumor suppressor do not

180 dulloblastoma (CMB) or large-cell/anaplastic medulloblastoma (LCA).

181 nscriptomes onto this dataset shows that WNT medulloblastomas match the rhombic lip-derived mossy fib

182 clusively associated with the sonic hedgehog medulloblastoma (MB(SHH)) subgroup and accounted for 5%

183 Treatment for medulloblastoma (MB) - the most common malignant pediatr

184 Medulloblastoma (MB) comprises a biologically heterogene

185 Medulloblastoma (MB) is a highly malignant cerebellar tu

186 Medulloblastoma (MB) is a malignant pediatric brain tumo

187 Medulloblastoma (MB) is a pediatric malignant brain tumo

188 SHH-medulloblastoma (MB) is among the most frequent brain tu

189 Treatment of medulloblastoma (MB) is challenging due to diverse genet

190 Medulloblastoma (MB) is the most common malignant pediat

191 Medulloblastoma (MB) is the most common paediatric brain

192 Medulloblastoma (MB) is the most frequent malignant pedi

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

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

195 Medulloblastoma (MB), the most common malignant paediatr

196 Medulloblastoma (MB), the most frequent malignant childh

197 Group3 medulloblastoma (MBG3) that predominantly occur in young

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

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

200 In medulloblastomas (MBs), the expression and activity of R

201 R161) gene in six patients with infant-onset medulloblastoma (median age, 1.5 years).

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

203 the identification of lipids associated with medulloblastoma metastasis, including phosphatidic acids

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

205 aging was performed in tumor-bearing Smo/Smo medulloblastoma mice with constitutive actvation of the

206 up specific signalling circuits in high-risk medulloblastomas might be similarly important as targeti

207 In human medulloblastoma, misactivation of Hh signaling was assoc

208 Here we describe a medulloblastoma model using Induced pluripotent stem (iP

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

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

211 and validate a robust classifier to identify medulloblastoma molecular subtypes through the use of tr

212 thway as a potent tumour suppressor in a SHH medulloblastoma mouse model.

213 In cohorts of medulloblastomas (n = 2325), malignant rhabdoid tumors (

214 Nodular desmoplastic medulloblastoma (ND) and medulloblastoma with extensive

215 WNT and SHH medulloblastomas normally arise only in the lower and up

216 rain tumor, but whether DDX3X functions as a medulloblastoma oncogene or tumor suppressor gene is not

217 Families with childhood medulloblastoma, one of the most prevalent childhood mal

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

219 important subgroups in 10 seconds, providing medulloblastoma pathology in an actionable manner during

220 with the promise of better outcomes for SHH medulloblastoma patients.

221 n both Gorlin tNES cells and SHH-subgroup of medulloblastoma patients.

222 Despite recent advances in the treatment of medulloblastoma, patients in high-risk categories still

223 dentified LDHA as a novel target for group 3 medulloblastoma, paving the way for the development of e

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

225 dgehog (MB(SHH))(.) ELP1 was the most common medulloblastoma predisposition gene and increased the pr

226 at reduced AHR pathway activity promotes SHH medulloblastoma progression, consistent with a tumour su

227 diversity in medulloblastomas in transgenic, medulloblastoma-prone mice, and responses to the SHH-pat

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

229 co-deleting Gsk3a/b blocked tumor growth in medulloblastoma-prone SmoM2 mice.

230 ts treated between 2007 and 2018 on the same medulloblastoma protocols that differed only in radiothe

231 spite this heterogeneity, most patients with medulloblastoma receive similar therapies, including sur

232 s underlying tumor initiation and relapse in medulloblastomas remain elusive.

233 Mortality from medulloblastoma remains significant.

234 le cell hierarchy as expected, while group 3 medulloblastoma resembles Nestin(+) stem cells, group 4

235 toma resembles Nestin(+) stem cells, group 4 medulloblastoma resembles unipolar brush cells, and PFA/

236 glioma), U87 (human glioma) and Daoy (human medulloblastoma), respectively.

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

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

239 nable users to quickly and robustly classify medulloblastoma samples using transcriptomic data.

240 dentifying robust biomarkers for subgrouping medulloblastoma samples with data perturbation due to di

241 The sonic hedgehog subtype of medulloblastoma (SHH MB) is associated with treatment fa

242 ofiles of infantile sonic hedgehog-activated medulloblastoma (SHH-INF) were subdivided into iSHH-I an

243 rogression in the sonic hedgehog subgroup of medulloblastoma (SHH-MB).

244 Medulloblastoma showed significant and specific accumula

245 SHH-driven medulloblastomas similarly required GSK-3, as co-deletin

246 intra- and intertumoral heterogeneity in 25 medulloblastomas spanning all molecular subgroups.

247 In the setting of medulloblastoma, spontaneous or orthotopically implanted

248 ditionally blocked sphere-forming ability of medulloblastoma stem-like cancer cells in vitro.

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

250 We established medulloblastoma subgroup affiliation by gene expression

251 ELP1 in 14% of paediatric patients with the medulloblastoma subgroup Sonic Hedgehog (MB(SHH))(.) ELP

252 The Sonic Hedgehog medulloblastoma subgroup transcriptionally mirrors the g

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

254 enes and molecular processes that operate in medulloblastoma subgroups.

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

256 Medulloblastoma subtypes identified through integrative

257 oved this lineage restriction, enabling both medulloblastoma subtypes to arise in either germinal zon

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

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

260 icts the competence of cell lineages to form medulloblastoma subtypes.

261 hput drug screening identifies therapies for medulloblastoma that cannot be predicted by genomic or t

262 resolution in sonic hedgehog (SHH)-activated medulloblastomas that originate from unipotent granule n

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

264 was active against PDXs representing Group 3 medulloblastoma, the most aggressive form of the disease

265 ur in a wide range of human cancers, such as medulloblastoma, the most common brain malignancy in chi

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

267 ereas excessive CGNP proliferation can cause medulloblastoma, the most common malignant pediatric bra

268 pmental abnormalities and cancers, including medulloblastoma, the most common pediatric brain tumor,

269 ll gene expression data to investigate mouse medulloblastoma, the proposed method successfully remove

270 ss (WNT) and Sonic hedghog (SHH) subtypes of medulloblastoma-the commonest malignant childhood brain

271 Historical changes in medulloblastoma therapy that improved 5-year survival ha

272 ts that GSK-3 may be targeted for SHH-driven medulloblastoma therapy.

273 tnatal development and in primary cerebellar medulloblastoma tissues.

274 We anticipate this medulloblastoma transcriptomic subtype classifier will b

275 scores over time in patients with pediatric medulloblastoma treated with craniospinal PRT versus XRT

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

277 Thus, DDX3X is a medulloblastoma tumor suppressor that regulates hindbrai

278 rogenitors are tumor-initiating cells during medulloblastoma tumorigenesis and relapse, suggesting OL

279 -extracted lipids allow immediate grading of medulloblastoma tumors into prognostically important sub

280 anced the inhibitory effects of alpelisib on medulloblastoma tumour growth in vivo.

281 estigate two cell lines for glioblastoma and medulloblastoma (U87mg & DAOY, respectively), plated as

282 We transduced NES cells with MYCN, observing medulloblastoma upon orthotopic implantation in mice.

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

284 used for treatment of sarcoma but rarely for medulloblastoma, was active against PDXs representing Gr

285 view of the scarcity of data in adults with medulloblastoma, we base our recommendations on adult da

286 ome potential new biomarkers for subgrouping medulloblastoma were detected by our method.

287 ble primary molecular subgroups of childhood medulloblastoma were identified.

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

289 ELP1-associated medulloblastomas were restricted to the molecular SHHalp

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

291 Medulloblastoma, which is the most common malignant paed

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

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

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

295 odular desmoplastic medulloblastoma (ND) and medulloblastoma with extensive nodularity (MBEN) have be

296 s with desmoplastic medulloblastoma (DMB) or medulloblastoma with extensive nodularity (MBEN; n = 42)

297 ories between pediatric patients treated for medulloblastoma with PRT versus those treated with XRT o

298 c models of Sonic Hedgehog (SHH) subgroup of medulloblastoma with SUFU alterations, painting more nua

299 Human SHH medulloblastomas with high expression of the AHR repress

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