{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,7,21]],"date-time":"2024-07-21T20:32:22Z","timestamp":1721593942308},"reference-count":28,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["PED"],"published-print":{"date-parts":[[2010,3]]},"abstract":"<jats:sec>\n<jats:title>Object<\/jats:title>\n<jats:p>In this paper the authors' goal was to investigate the genetic characteristics of primary brain tumors in children and determine their influence on clinical outcome.<\/jats:p><\/jats:sec>\n<jats:sec>\n<jats:title>Methods<\/jats:title>\n<jats:p>The authors performed high-resolution comparative genomic hybridization studies in 14 low-grade and 12 high-grade brain neoplasms in 26 children who underwent surgery between 2005 and 2007.<\/jats:p><\/jats:sec>\n<jats:sec>\n<jats:title>Results<\/jats:title>\n<jats:p>Complex comparative genomic hybridization alterations were observed in 2 (14.3%) of the 14 lowgrade lesions and in 8 (66.6%) of the 12 high-grade lesions. High-level amplifications of DNA were detected in 3 cases, namely in a desmoplastic medulloblastoma where a <jats:italic>c-Myc<\/jats:italic> amplification was found. Gains of 1q were detected in 2 low-grade and 6 high-grade lesions that were classified as ependymomas, astrocytomas, oligodendrogliomas, oligoastrocytomas, and gangliogliomas. When the authors correlated genetics with outcome, they noted that among the low-grade neoplasms only the 2 patients who presented with complex comparative genomic hybridization alterations had to undergo reoperation because of recurrent disease. The patient with <jats:italic>c-Myc<\/jats:italic> amplification died of progressive disease. Gains of 1q were only observed in tumor cases with progressive disease.<\/jats:p><\/jats:sec>\n<jats:sec>\n<jats:title>Conclusions<\/jats:title>\n<jats:p>Complex genetic alterations are indicative of a less favorable outcome in low-grade tumors. In these cases, closer follow-up should be pursued. The authors corroborate that <jats:italic>c-Myc<\/jats:italic> amplification is a marker of poor prognosis in medulloblastomas. In this study, they were able to verify that a 1q gain correlates with a poor clinical outcome, independent of tumor grade and histological type. The authors propose that it may be considered a common marker of poor prognosis in these neoplasms.<\/jats:p><\/jats:sec>","DOI":"10.3171\/2009.10.peds09240","type":"journal-article","created":{"date-parts":[[2010,3,1]],"date-time":"2010-03-01T15:04:10Z","timestamp":1267455850000},"page":"263-270","source":"Crossref","is-referenced-by-count":21,"title":["Pediatric brain tumors: genetics and clinical outcome"],"prefix":"10.3171","volume":"5","author":[{"given":"Claudia","family":"Faria","sequence":"first","affiliation":[{"name":"Departments of Neurosurgery and"}]},{"given":"Jos\u00e9","family":"Migu\u00e9ns","sequence":"additional","affiliation":[{"name":"Departments of Neurosurgery and"}]},{"given":"Jo\u00e3o Lobo","family":"Antunes","sequence":"additional","affiliation":[{"name":"Departments of Neurosurgery and"}]},{"given":"Duarte","family":"Salgado","sequence":"additional","affiliation":[{"name":"Department of Neurology and"}]},{"given":"Sofia","family":"Nunes","sequence":"additional","affiliation":[{"name":"Department of Neurology and"}]},{"given":"C\u00e2ndida","family":"Barroso","sequence":"additional","affiliation":[{"name":"Neuropathology, Hospital de Santa Maria; and"}]},{"given":"Maria do Carmo","family":"Martins","sequence":"additional","affiliation":[{"name":"Cytogenetic Laboratory (CIPM), Instituto Portugu\u00eas de Oncologia, Lisbon, Portugal"}]},{"given":"Vasco Moura","family":"Nunes","sequence":"additional","affiliation":[{"name":"Cytogenetic Laboratory (CIPM), Instituto Portugu\u00eas de Oncologia, Lisbon, Portugal"}]},{"given":"L\u00facia","family":"Roque","sequence":"additional","affiliation":[{"name":"Cytogenetic Laboratory (CIPM), Instituto Portugu\u00eas de Oncologia, Lisbon, Portugal"}]}],"member":"1754","reference":[{"key":"b1-0050263","series-title":"Cancer","doi-asserted-by":"publisher","first-page":"396","DOI":"10.1002\/cncr.21612","article-title":"Functional outcome after low-grade astrocytoma treatment in childhood","volume":"106","author":"Aarsen","year":"2006"},{"key":"b2-0050263","series-title":"J Neuropathol Exp Neurol","doi-asserted-by":"publisher","first-page":"878","DOI":"10.1097\/NEN.0b013e3181845622","article-title":"Frequent gains at chromosome 7q34 involving BRAF in pilocytic astrocytoma","volume":"67","author":"Bar","year":"2008"},{"key":"b3-0050263","series-title":"JAMA","doi-asserted-by":"publisher","first-page":"261","DOI":"10.1001\/jama.2009.997","article-title":"A network model of a cooperative genetic landscape in brain tumors","volume":"302","author":"Bredel","year":"2009"},{"key":"b4-0050263","series-title":"Nature","doi-asserted-by":"publisher","first-page":"1061","DOI":"10.1038\/nature07385","article-title":"Comprehensive genomic characterization defines human glioblastoma genes and core pathways","volume":"455","author":"Cancer Genome Atlas Research Network","year":"2008"},{"key":"b5-0050263","series-title":"Oncogene","doi-asserted-by":"publisher","first-page":"4741","DOI":"10.1038\/sj.onc.1208641","article-title":"KIF14 is a candidate oncogene in the 1q minimal region of genomic gain in multiple cancers","volume":"24","author":"Corson","year":"2005"},{"key":"b6-0050263","series-title":"Neuro Oncol","doi-asserted-by":"publisher","first-page":"1040","DOI":"10.1215\/15228517-2008-059","article-title":"Biological background of pediatric medulloblastoma and ependymoma: a review from a translational research perspective","volume":"10","author":"de Bont","year":"2008"},{"key":"b7-0050263","series-title":"Proc Natl Acad Sci U S A","doi-asserted-by":"publisher","first-page":"10833","DOI":"10.1073\/pnas.0400690101","article-title":"REN(KCTD11) is a suppressor of Hedgehog signaling and is deleted in human medulloblastoma","volume":"101","author":"Di Marcotullio","year":"2004"},{"key":"b8-0050263","series-title":"J Neuropathol Exp Neurol","doi-asserted-by":"publisher","first-page":"441","DOI":"10.1093\/jnen\/63.5.441","article-title":"Histopathological and molecular prognostic markers in medulloblastoma: c-myc, N-myc, TrC, and anaplasia","volume":"63","author":"Eberhart","year":"2004"},{"key":"b9-0050263","series-title":"Brain Tumors","first-page":"3","article-title":"Epidemiology of brain tumors","author":"El-Zein","year":"2005"},{"key":"b10-0050263","series-title":"J Neurosurg Pediatr","doi-asserted-by":"publisher","first-page":"99","DOI":"10.3171\/PED-08\/01\/099","article-title":"Genetic alterations in a papillary glioneuronal tumor. 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