| Literature DB >> 31820118 |
Bryan K Li1,2,3, Alexandre Vasiljevic4,5, Christelle Dufour6, Fupan Yao2,7, Ben L B Ho2, Mei Lu2, Eugene I Hwang8, Sridharan Gururangan9, Jordan R Hansford10, Maryam Fouladi11, Sumihito Nobusawa12, Annie Laquerriere13, Marie-Bernadette Delisle14, Jason Fangusaro15, Fabien Forest16, Helen Toledano17, Palma Solano-Paez2,18, Sarah Leary19, Diane Birks20, Lindsey M Hoffman21, Alexandru Szathmari22, Cécile Faure-Conter23, Xing Fan24, Daniel Catchpoole25, Li Zhou25, Kris Ann P Schultz26, Koichi Ichimura27, Guillaume Gauchotte28, Nada Jabado29, Chris Jones30, Delphine Loussouarn31, Karima Mokhtari32, Audrey Rousseau33, David S Ziegler34,35, Shinya Tanaka36, Scott L Pomeroy37, Amar Gajjar38, Vijay Ramaswamy1,2,7, Cynthia Hawkins2,3,39, Richard G Grundy40, D Ashley Hill41, Eric Bouffet1, Annie Huang42,43,44,45, Anne Jouvet5,46.
Abstract
Pineoblastomas (PBs) are rare, aggressive pediatric brain tumors of the pineal gland with modest overall survival despite intensive therapy. We sought to define the clinical and molecular spectra of PB to inform new treatment approaches for this orphan cancer. Tumor, blood, and clinical data from 91 patients with PB or supratentorial primitive neuroectodermal tumor (sPNETs/CNS-PNETs), and 2 pineal parenchymal tumors of intermediate differentiation (PPTIDs) were collected from 29 centres in the Rare Brain Tumor Consortium. We used global DNA methylation profiling to define a core group of PB from 72/93 cases, which were delineated into five molecular sub-groups. Copy number, whole exome and targeted sequencing, and miRNA expression analyses were used to evaluate the clinico-pathologic significance of each sub-group. Tumors designated as group 1 and 2 almost exclusively exhibited deleterious homozygous loss-of-function alterations in miRNA biogenesis genes (DICER1, DROSHA, and DGCR8) in 62 and 100% of group 1 and 2 tumors, respectively. Recurrent alterations of the oncogenic MYC-miR-17/92-RB1 pathway were observed in the RB and MYC sub-group, respectively, characterized by RB1 loss with gain of miR-17/92, and recurrent gain or amplification of MYC. PB sub-groups exhibited distinct clinical features: group 1-3 arose in older children (median ages 5.2-14.0 years) and had intermediate to excellent survival (5-year OS of 68.0-100%), while Group RB and MYC PB patients were much younger (median age 1.3-1.4 years) with dismal survival (5-year OS 37.5% and 28.6%, respectively). We identified age < 3 years at diagnosis, metastatic disease, omission of upfront radiation, and chr 16q loss as significant negative prognostic factors across all PBs. Our findings demonstrate that PB exhibits substantial molecular heterogeneity with sub-group-associated clinical phenotypes and survival. In addition to revealing novel biology and therapeutics, molecular sub-grouping of PB can be exploited to reduce treatment intensity for patients with favorable biology tumors.Entities:
Keywords: MYC; PNET; PPTID; Pineoblastoma; RB; miRNA
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Year: 2019 PMID: 31820118 PMCID: PMC7673644 DOI: 10.1007/s00401-019-02111-y
Source DB: PubMed Journal: Acta Neuropathol ISSN: 0001-6322 Impact factor: 17.088