Advances in the molecular classification of pediatric brain tumors: a guide to the galaxy.


Journal

The Journal of pathology
ISSN: 1096-9896
Titre abrégé: J Pathol
Pays: England
ID NLM: 0204634

Informations de publication

Date de publication:
07 2020
Historique:
received: 03 02 2020
revised: 31 03 2020
accepted: 04 05 2020
pubmed: 12 5 2020
medline: 18 11 2020
entrez: 12 5 2020
Statut: ppublish

Résumé

Central nervous system (CNS) tumors are the most common solid tumor in pediatrics, accounting for approximately 25% of all childhood cancers, and the second most common pediatric malignancy after leukemia. CNS tumors can be associated with significant morbidity, even those classified as low grade. Mortality from CNS tumors is disproportionately high compared to other childhood malignancies, although surgery, radiation, and chemotherapy have improved outcomes in these patients over the last few decades. Current therapeutic strategies lead to a high risk of side effects, especially in young children. Pediatric brain tumor survivors have unique sequelae compared to age-matched patients who survived other malignancies. They are at greater risk of significant impairment in cognitive, neurological, endocrine, social, and emotional domains, depending on the location and type of the CNS tumor. Next-generation genomics have shed light on the broad molecular heterogeneity of pediatric brain tumors and have identified important genes and signaling pathways that serve to drive tumor proliferation. This insight has impacted the research field by providing potential therapeutic targets for these diseases. In this review, we highlight recent progress in understanding the molecular basis of common pediatric brain tumors, specifically low-grade glioma, high-grade glioma, ependymoma, embryonal tumors, and atypical teratoid/rhabdoid tumor (ATRT). © 2020 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Identifiants

pubmed: 32391583
doi: 10.1002/path.5457
doi:

Substances chimiques

Biomarkers, Tumor 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

249-261

Subventions

Organisme : CIHR
Pays : Canada

Informations de copyright

© 2020 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Références

Gajjar A, Pfister SM, Taylor MD, et al. Molecular insights into pediatric brain tumors have the potential to transform therapy. Clin Cancer Res 2014; 20: 5630-5640.
Capper D, Jones DTW, Sill M, et al. DNA methylation-based classification of central nervous system tumours. Nature 2018; 555: 469-474.
Khatua S, Wang J, Rajaram V. Review of low-grade gliomas in children - evolving molecular era and therapeutic insights. Childs Nerv Syst 2015; 31: 643-652.
Raabe E, Kieran MW, Cohen KJ. New strategies in pediatric gliomas: molecular advances in pediatric low-grade gliomas as a model. Clin Cancer Res 2013; 19: 4553-4558.
Sievert AJ, Fisher MJ. Pediatric low-grade gliomas. J Child Neurol 2009; 24: 1397-1408.
Diamandis P, Aldape K. World Health Organization 2016 classification of central nervous system tumors. Neurol Clin 2018; 36: 439-447.
Gutmann DH, Donahoe J, Brown T, et al. Loss of neurofibromatosis 1 (NF1) gene expression in NF1-associated pilocytic astrocytomas. Neuropathol Appl Neurobiol 2000; 26: 361-367.
Lau N, Feldkamp MM, Roncari L, et al. Loss of neurofibromin is associated with activation of RAS/MAPK and PI3-K/AKT signaling in a neurofibromatosis 1 astrocytoma. J Neuropathol Exp Neurol 2000; 59: 759-767.
Chen YH, Gutmann DH. The molecular and cell biology of pediatric low-grade gliomas. Oncogene 2014; 33: 2019-2026.
Zhang J, Wu G, Miller CP, et al. Whole-genome sequencing identifies genetic alterations in pediatric low-grade gliomas. Nat Genet 2013; 45: 602-612.
Ryall S, Zapotocky M, Fukuoka K, et al. Integrated molecular and clinical analysis of 1,000 pediatric low-grade gliomas. Cancer Cell 2020; 37: 569-583.e565.
Fukuoka K, Mamatjan Y, Tatevossian R, et al. Clinical impact of combined epigenetic and molecular analysis of pediatric low grade gliomas. Neuro Oncol 2020. https://doi.org/10.1093/neuonc/noaa077 [Epub ahead of print].
Dougherty MJ, Santi M, Brose MS, et al. Activating mutations in BRAF characterize a spectrum of pediatric low-grade gliomas. Neuro Oncol 2010; 12: 621-630.
Rubin JB, Finlay JL. Pediatric low-grade gliomas: a brave new world. Neuro Oncol 2018; 20: 149-150.
Yang RR, Aibaidula A, Wang WW, et al. Pediatric low-grade gliomas can be molecularly stratified for risk. Acta Neuropathol 2018; 136: 641-655.
Fangusaro J, Onar-Thomas A, Young Poussaint T, et al. Selumetinib in paediatric patients with BRAF-aberrant or neurofibromatosis type 1-associated recurrent, refractory, or progressive low-grade glioma: a multicentre, phase 2 trial. Lancet Oncol 2019; 20: 1011-1022.
Banerjee A, Jakacki RI, Onar-Thomas A, et al. A phase I trial of the MEK inhibitor selumetinib (AZD6244) in pediatric patients with recurrent or refractory low-grade glioma: a pediatric brain tumor consortium (PBTC) study. Neuro Oncol 2017; 19: 1135-1144.
Lassaletta A, Zapotocky M, Mistry M, et al. Therapeutic and prognostic implications of BRAF V600E in pediatric low-grade gliomas. J Clin Oncol 2017; 35: 2934-2941.
Lassaletta A, Scheinemann K, Zelcer SM, et al. Phase II weekly vinblastine for chemotherapy-naive children with progressive low-grade glioma: a Canadian pediatric brain tumor consortium study. J Clin Oncol 2016; 34: 3537-3543.
Ater JL, Zhou T, Holmes E, et al. Randomized study of two chemotherapy regimens for treatment of low-grade glioma in young children: a report from the Children's Oncology Group. J Clin Oncol 2012; 30: 2641-2647.
Curatolo P, Bombardieri R, Jozwiak S. Tuberous sclerosis. Lancet 2008; 372: 657-668.
Devinsky O. Everolimus for epilepsy in paediatric tuberous sclerosis complex. Lancet Child Adolesc Health 2018; 2: 467-469.
Franz DN, Belousova E, Sparagana S, et al. Everolimus for subependymal giant cell astrocytoma in patients with tuberous sclerosis complex: 2-year open-label extension of the randomised EXIST-1 study. Lancet Oncol 2014; 15: 1513-1520.
French JA, Lawson JA, Yapici Z, et al. Adjunctive everolimus therapy for treatment-resistant focal-onset seizures associated with tuberous sclerosis (EXIST-3): a phase 3, randomised, double-blind, placebo-controlled study. Lancet 2016; 388: 2153-2163.
Mukherjee D, Sarmiento JM, Ly D, et al. Everolimus for astrocytomas in tuberous sclerosis. Lancet 2013; 381: 1274-1275.
Northrup H. The mTOR inhibitor revolution rolls on. Lancet Oncol 2014; 15: 1418-1419.
Anderson MD, Gilbert MR. Clinical discussion of the management of anaplastic oligodendroglioma/oligoastrocytoma (both codeleted and nondeleted). J Natl Compr Canc Netw 2014; 12: 665-672.
Bender S, Gronych J, Warnatz H-J, et al. Recurrent MET fusion genes represent a drug target in pediatric glioblastoma. Nat Med 2016; 22: 1314-1320.
Liu KW, Pajtler KW, Worst BC, et al. Molecular mechanisms and therapeutic targets in pediatric brain tumors. Sci Signal 2017; 10: eaaf7593.
Rodriguez FJ, Vizcaino MA, Lin MT. Recent advances on the molecular pathology of glial neoplasms in children and adults. J Mol Diagn 2016; 18: 620-634.
Sturm D, Bender S, Jones DT, et al. Paediatric and adult glioblastoma: multiform (epi)genomic culprits emerge. Nat Rev Cancer 2014; 14: 92-107.
Sturm D, Witt H, Hovestadt V, et al. Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma. Cancer Cell 2012; 22: 425-437.
Sumerauer D, Krskova L, Vicha A, et al. Rare IDH1 variants are common in pediatric hemispheric diffuse astrocytomas and frequently associated with Li-Fraumeni syndrome. Acta Neuropathol 2020; 139: 795-797.
Heaphy CM, de Wilde RF, Jiao Y, et al. Altered telomeres in tumors with ATRX and DAXX mutations. Science 2011; 333: 425.
Johanns TM, Ferguson CJ, Grierson PM, et al. Rapid clinical and radiographic response with combined dabrafenib and trametinib in adults with BRAF-mutated high-grade glioma. J Natl Compr Canc Netw 2018; 16: 4-10.
Planchard D, Besse B, Groen HJM, et al. Dabrafenib plus trametinib in patients with previously treated BRAFV600E-mutant metastatic non-small cell lung cancer: an open-label, multicentre phase 2 trial. Lancet Oncol 2016; 17: 984-993.
Laetsch TW, DuBois SG, Mascarenhas L, et al. Larotrectinib for paediatric solid tumours harbouring NTRK gene fusions: phase 1 results from a multicentre, open-label, phase 1/2 study. Lancet Oncol 2018; 19: 705-714.
Doebele RC, Drilon A, Paz-Ares L, et al. Entrectinib in patients with advanced or metastatic NTRK fusion-positive solid tumours: integrated analysis of three phase 1-2 trials. Lancet Oncol 2020; 21: 271-282.
Khuong-Quang DA, Buczkowicz P, Rakopoulos P, et al. K27M mutation in histone H3.3 defines clinically and biologically distinct subgroups of pediatric diffuse intrinsic pontine gliomas. Acta Neuropathol 2012; 124: 439-447.
Schwartzentruber J, Korshunov A, Liu XY, et al. Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma. Nature 2012; 482: 226-231.
Duffner PK, Horowitz ME, Krischer JP, et al. The treatment of malignant brain tumors in infants and very young children: an update of the Pediatric Oncology Group experience. Neuro Oncol 1999; 1: 152-161.
Guerreiro Stucklin AS, Ryall S, Fukuoka K, et al. Alterations in ALK/ROS1/NTRK/MET drive a group of infantile hemispheric gliomas. Nat Commun 2019; 10: 4343.
Clarke M, Mackay A, Ismer B, et al. Infant high grade gliomas comprise multiple subgroups characterized by novel targetable gene fusions and favorable outcomes. Cancer Discov 2020. https://doi.org/10.1158/2159-8290.CD-19-1030 [Epub ahead of print].
Bouffet E, Larouche V, Campbell BB, et al. Immune checkpoint inhibition for hypermutant glioblastoma multiforme resulting from germline biallelic mismatch repair deficiency. J Clin Oncol 2016; 34: 2206-2211.
Finlay JL, Boyett JM, Yates AJ, et al. Randomized phase III trial in childhood high-grade astrocytoma comparing vincristine, lomustine, and prednisone with the eight-drugs-in-1-day regimen. J Clin Oncol 1995; 13: 112-123.
Grill J, Massimino M, Bouffet E, et al. Phase II, open-label, randomized, multicenter trial (HERBY) of bevacizumab in pediatric patients with newly diagnosed high-grade glioma. J Clin Oncol 2018; 36: 951-958.
Hong TS, Mehta MP, Boyett JM, et al. Patterns of treatment failure in infants with primitive neuroectodermal tumors who were treated on CCG-921: a phase III combined modality study. Pediatr Blood Cancer 2005; 45: 676-682.
Jones C, Karajannis MA, Jones DTW, et al. Pediatric high-grade glioma: biologically and clinically in need of new thinking. Neuro Oncol 2017; 19: 153-161.
Tihan T, Zhou T, Holmes E, et al. The prognostic value of histological grading of posterior fossa ependymomas in children: a Children's Oncology Group study and a review of prognostic factors. Mod Pathol 2008; 21: 165-177.
Guerreiro Stucklin AS, Ramaswamy V, Daniels C, et al. Review of molecular classification and treatment implications of pediatric brain tumors. Curr Opin Pediatr 2018; 30: 3-9.
Ramaswamy V, Taylor MD. Treatment implications of posterior fossa ependymoma subgroups. Chin J Cancer 2016; 35: 93.
Parker M, Mohankumar KM, Punchihewa C, et al. C11orf95-RELA fusions drive oncogenic NF-κB signalling in ependymoma. Nature 2014; 506: 451-455.
Johnson RA, Wright KD, Poppleton H, et al. Cross-species genomics matches driver mutations and cell compartments to model ependymoma. Nature 2010; 466: 632-636.
Pajtler KW, Witt H, Sill M, et al. Molecular classification of ependymal tumors across all CNS compartments, histopathological grades, and age groups. Cancer Cell 2015; 27: 728-743.
Fukuoka K, Kanemura Y, Shofuda T, et al. Significance of molecular classification of ependymomas: C11orf95-RELA fusion-negative supratentorial ependymomas are a heterogeneous group of tumors. Acta Neuropathol Commun 2018; 6: 134.
Mack SC, Witt H, Piro RM, et al. Epigenomic alterations define lethal CIMP-positive ependymomas of infancy. Nature 2014; 506: 445-450.
Witt H, Mack SC, Ryzhova M, et al. Delineation of two clinically and molecularly distinct subgroups of posterior fossa ependymoma. Cancer Cell 2011; 20: 143-157.
Witt H, Korshunov A, Pfister SM, et al. Molecular approaches to ependymoma: the next step(s). Curr Opin Neurol 2012; 25: 745-750.
Pajtler KW, Wen J, Sill M, et al. Molecular heterogeneity and CXorf67 alterations in posterior fossa group A (PFA) ependymomas. Acta Neuropathol 2018; 136: 211-226.
Cavalli FMG, Hubner JM, Sharma T, et al. Heterogeneity within the PF-EPN-B ependymoma subgroup. Acta Neuropathol 2018; 136: 227-237.
Ramaswamy V, Hielscher T, Mack SC, et al. Therapeutic impact of cytoreductive surgery and irradiation of posterior fossa ependymoma in the molecular era: a retrospective multicohort analysis. J Clin Oncol 2016; 34: 2468-2477.
Zapotocky M, Beera K, Adamski J, et al. Survival and functional outcomes of molecularly defined childhood posterior fossa ependymoma: cure at a cost. Cancer 2019; 125: 1867-1876.
Merchant TE, Bendel AE, Sabin ND, et al. Conformal radiation therapy for pediatric ependymoma, chemotherapy for incompletely resected ependymoma, and observation for completely resected, supratentorial ependymoma. J Clin Oncol 2019; 37: 974-983.
Lin FY, Chintagumpala M. Advances in management of pediatric ependymomas. Curr Oncol Rep 2015; 17: 47.
Kim JH, Huang Y, Griffin AS, et al. Ependymoma in children: molecular considerations and therapeutic insights. Clin Transl Oncol 2013; 15: 759-765.
Grundy RG, Wilne SH, Robinson KJ, et al. Primary postoperative chemotherapy without radiotherapy for treatment of brain tumours other than ependymoma in children under 3 years: results of the first UKCCSG/SIOP CNS 9204 trial. Eur J Cancer 2010; 46: 120-133.
Strother DR, Lafay-Cousin L, Boyett JM, et al. Benefit from prolonged dose-intensive chemotherapy for infants with malignant brain tumors is restricted to patients with ependymoma: a report of the Pediatric Oncology Group randomized controlled trial 9233/34. Neuro Oncol 2014; 16: 457-465.
Bouffet E, Foreman N. Chemotherapy for intracranial ependymomas. Childs Nerv Syst 1999; 15: 563-570.
Bouffet E, Hawkins CE, Ballourah W, et al. Survival benefit for pediatric patients with recurrent ependymoma treated with reirradiation. Int J Radiat Oncol Biol Phys 2012; 83: 1541-1548.
Liu AK, Foreman NK, Gaspar LE, et al. Maximally safe resection followed by hypofractionated re-irradiation for locally recurrent ependymoma in children. Pediatr Blood Cancer 2009; 52: 804-807.
Crawford JR, MacDonald TJ, Packer RJ. Medulloblastoma in childhood: new biological advances. Lancet Neurol 2007; 6: 1073-1085.
Eberhart CG, Kratz J, Wang Y, et al. Histopathological and molecular prognostic markers in medulloblastoma: c-myc, N-myc, TrkC, and anaplasia. J Neuropathol Exp Neurol 2004; 63: 441-449.
Judkins AR, Mauger J, Ht A, et al. Immunohistochemical analysis of hSNF5/INI1 in pediatric CNS neoplasms. Am J Surg Pathol 2004; 28: 644-650.
Pomeroy SL, Tamayo P, Gaasenbeek M, et al. Prediction of central nervous system embryonal tumour outcome based on gene expression. Nature 2002; 415: 436-442.
Sturm D, Orr BA, Toprak UH, et al. New brain tumor entities emerge from molecular classification of CNS-PNETs. Cell 2016; 164: 1060-1072.
Korshunov A, Sturm D, Ryzhova M, et al. Embryonal tumor with abundant neuropil and true rosettes (ETANTR), ependymoblastoma, and medulloepithelioma share molecular similarity and comprise a single clinicopathological entity. Acta Neuropathol 2014; 128: 279-289.
Taylor MD, Northcott PA, Korshunov A, et al. Molecular subgroups of medulloblastoma: the current consensus. Acta Neuropathol 2012; 123: 465-472.
Hovestadt V, Smith KS, Bihannic L, et al. Resolving medulloblastoma cellular architecture by single-cell genomics. Nature 2019; 572: 74-79.
Vladoiu MC, El-Hamamy I, Donovan LK, et al. Childhood cerebellar tumours mirror conserved fetal transcriptional programs. Nature 2019; 572: 67-73.
Jessa S, Blanchet-Cohen A, Krug B, et al. Stalled developmental programs at the root of pediatric brain tumors. Nat Genet 2019; 51: 1702-1713.
Ellison DW, Kocak M, Dalton J, et al. Definition of disease-risk stratification groups in childhood medulloblastoma using combined clinical, pathologic, and molecular variables. J Clin Oncol 2011; 29: 1400-1407.
Ellison DW, Onilude OE, Lindsey JC, et al. β-Catenin status predicts a favorable outcome in childhood medulloblastoma: the United Kingdom Children's Cancer Study Group Brain Tumour Committee. J Clin Oncol 2005; 23: 7951-7957.
Northcott PA, Buchhalter I, Morrissy AS, et al. The whole-genome landscape of medulloblastoma subtypes. Nature 2017; 547: 311-317.
Surun A, Varlet P, Brugières L, et al. Medulloblastomas associated with an APC germline pathogenic variant share the good prognosis of CTNNB1-mutated medulloblastomas. Neuro Oncol 2020; 22: 128-138.
Waszak SM, Northcott PA, Buchhalter I, et al. Spectrum and prevalence of genetic predisposition in medulloblastoma: a retrospective genetic study and prospective validation in a clinical trial cohort. Lancet Oncol 2018; 19: 785-798.
Northcott PA, Jones DT, Kool M, et al. Medulloblastomics: the end of the beginning. Nat Rev Cancer 2012; 12: 818-834.
Gibson P, Tong Y, Robinson G, et al. Subtypes of medulloblastoma have distinct developmental origins. Nature 2010; 468: 1095-1099.
Perreault S, Ramaswamy V, Achrol AS, et al. MRI surrogates for molecular subgroups of medulloblastoma. Am J Neuroradiol 2014; 35: 1263-1269.
Gajjar AJ, Robinson GW. Medulloblastoma-translating discoveries from the bench to the bedside. Nat Rev Clin Oncol 2014; 11: 714-722.
Xing Z, Lin C, Yang L. Unraveling the therapeutic potential of the LncRNA-dependent noncanonical Hedgehog pathway in cancer. Mol Cell Oncol 2015; 2: e998900.
Kool M, Jones DT, Jäger N, et al. Genome sequencing of SHH medulloblastoma predicts genotype-related response to smoothened inhibition. Cancer Cell 2014; 25: 393-405.
Jabarkheel R, Amayiri N, Yecies D, et al. Molecular correlates of cerebellar mutism syndrome in medulloblastoma. Neuro Oncol 2020; 22: 290-297.
Suzuki H, Kumar SA, Shuai S, et al. Recurrent noncoding U1 snRNA mutations drive cryptic splicing in SHH medulloblastoma. Nature 2019; 574: 707-711.
Bandopadhayay P, Bergthold G, Nguyen B, et al. BET bromodomain inhibition of MYC-amplified medulloblastoma. Clin Cancer Res 2014; 20: 912-925.
Sharma T, Schwalbe EC, Williamson D, et al. Second-generation molecular subgrouping of medulloblastoma: an international meta-analysis of Group 3 and Group 4 subtypes. Acta Neuropathol 2019; 138: 309-326.
Cavalli FMG, Remke M, Rampasek L, et al. Intertumoral heterogeneity within medulloblastoma subgroups. Cancer Cell 2017; 31: 737-754.
Morfouace M, Shelat A, Jacus M, et al. Pemetrexed and gemcitabine as combination therapy for the treatment of Group3 medulloblastoma. Cancer Cell 2014; 25: 516-529.
Ramaswamy V, Remke M, Bouffet E, et al. Recurrence patterns across medulloblastoma subgroups: an integrated clinical and molecular analysis. Lancet Oncol 2013; 14: 1200-1207.
Pugh TJ, Weeraratne SD, Archer TC, et al. Medulloblastoma exome sequencing uncovers subtype-specific somatic mutations. Nature 2012; 488: 106-110.
Jones DT, Jager N, Kool M, et al. Dissecting the genomic complexity underlying medulloblastoma. Nature 2012; 488: 100-105.
Northcott PA, Lee C, Zichner T, et al. Enhancer hijacking activates GFI1 family oncogenes in medulloblastoma. Nature 2014; 511: 428-434.
Packer RJ, Gajjar A, Vezina G, et al. Phase III study of craniospinal radiation therapy followed by adjuvant chemotherapy for newly diagnosed average-risk medulloblastoma. J Clin Oncol 2006; 24: 4202-4208.
Mulhern RK, Palmer SL, Merchant TE, et al. Neurocognitive consequences of risk-adapted therapy for childhood medulloblastoma. J Clin Oncol 2005; 23: 5511-5519.
Dufour C, Kieffer V, Varlet P, et al. Tandem high-dose chemotherapy and autologous stem cell rescue in children with newly diagnosed high-risk medulloblastoma or supratentorial primitive neuro-ectodermic tumors. Pediatr Blood Cancer 2014; 61: 1398-1402.
Ramaswamy V, Remke M, Bouffet E, et al. Risk stratification of childhood medulloblastoma in the molecular era: the current consensus. Acta Neuropathol 2016; 131: 821-831.
Rutkowski S, Gerber NU, von Hoff K, et al. Treatment of early childhood medulloblastoma by postoperative chemotherapy and deferred radiotherapy. Neuro Oncol 2009; 11: 201-210.
Remke M, Ramaswamy V. Infant medulloblastoma - learning new lessons from old strata. Nat Rev Clin Oncol 2018; 15: 659-660.
Leary SE, Olson JM. The molecular classification of medulloblastoma: driving the next generation clinical trials. Curr Opin Pediatr 2012; 24: 33-39.
Gajjar A, Stewart CF, Ellison DW, et al. Phase I study of vismodegib in children with recurrent or refractory medulloblastoma: a pediatric brain tumor consortium study. Clin Cancer Res 2013; 19: 6305-6312.
Spence T, Sin-Chan P, Picard D, et al. CNS-PNETs with C19MC amplification and/or LIN28 expression comprise a distinct histogenetic diagnostic and therapeutic entity. Acta Neuropathol 2014; 128: 291-303.
Lambo S, Grobner SN, Rausch T, et al. The molecular landscape of ETMR at diagnosis and relapse. Nature 2019; 576: 274-280.
Versteege I, Sévenet N, Lange J, et al. Truncating mutations of hSNF5/INI1 in aggressive paediatric cancer. Nature 1998; 394: 203-206.
Eaton KW, Tooke LS, Wainwright LM, et al. Spectrum of SMARCB1/INI1 mutations in familial and sporadic rhabdoid tumors. Pediatr Blood Cancer 2011; 56: 7-15.
Foulkes WD, Kamihara J, Evans DGR, et al. Cancer surveillance in Gorlin syndrome and rhabdoid tumor predisposition syndrome. Clin Cancer Res 2017; 23: e62-e67.
Hasselblatt M, Gesk S, Oyen F, et al. Nonsense mutation and inactivation of SMARCA4 (BRG1) in an atypical teratoid/rhabdoid tumor showing retained SMARCB1 (INI1) expression. Am J Surg Pathol 2011; 35: 933-935.
Ho B, Johann PD, Grabovska Y, et al. Molecular subgrouping of atypical teratoid/rhabdoid tumors (ATRT) - a reinvestigation and current consensus. Neuro Oncol 2019; 22: 613-624.
Johann PD, Erkek S, Zapatka M, et al. Atypical teratoid/rhabdoid tumors are comprised of three epigenetic subgroups with distinct enhancer landscapes. Cancer Cell 2016; 29: 379-393.
Lafay-Cousin L, Hawkins C, Carret AS, et al. Central nervous system atypical teratoid rhabdoid tumours: the Canadian Paediatric Brain Tumour Consortium experience. Eur J Cancer 2012; 48: 353-359.
Hilden JM, Meerbaum S, Burger P, et al. Central nervous system atypical teratoid/rhabdoid tumor: results of therapy in children enrolled in a registry. J Clin Oncol 2004; 22: 2877-2884.
Fruhwald MC, Hasselblatt M, Nemes K, et al. Age and DNA-methylation subgroup as potential independent risk factors for treatment stratification in children with atypical teratoid/rhabdoid tumors (ATRT). Neuro Oncol 2019. https://doi.org/10.1093/neuonc/noz244 [Epub ahead of print].
Reddy A, Strother D, Judkins A, et al. Treatment of atypical teratoid rhabdoid tumors (ATRT) of the central nervous system with surgery, intensive chemotherapy, and 3-D conformal radiation (ACNS0333). A report from the Children's Oncology Group. Neuro Oncol 2016; 18(suppl 3): iii2.
Kim KH, Kim W, Howard TP, et al. SWI/SNF-mutant cancers depend on catalytic and non-catalytic activity of EZH2. Nat Med 2015; 21: 1491-1496.

Auteurs

Chantel Cacciotti (C)

Division of Pediatric Hematology/Oncology, McMaster Children's Hospital, Hamilton, ON, Canada.
Dana Farber/Boston Children's Cancer and Blood Disorder Center, Boston, MA, USA.

Adam Fleming (A)

Division of Pediatric Hematology/Oncology, McMaster Children's Hospital, Hamilton, ON, Canada.

Vijay Ramaswamy (V)

Division of Haematology/Oncology, Department of Pediatrics, University of Toronto and The Hospital for Sick Children, Toronto, ON, Canada.
Programme in Developmental and Stem Cell Biology, Arthur and Sonia Labatt Brain Tumor Research Centre, Hospital for Sick Children, Toronto, ON, Canada.
Department of Medical Biophysics and Pediatrics, University of Toronto, Toronto, ON, Canada.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH