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They differ from their adult counterparts, showing extensive clinical and molecular heterogeneity as well as a challenging histopathological spectrum that often impairs accurate diagnosis. Here, we use DNA methylation-based CNS tumor classification in combination with copy number, RNA-seq, and ChIP-seq analysis to characterize a newly identified CNS tumor type. In addition, we report histology, patient characteristics, and survival data in this tumor type. We describe a biologically distinct pediatric CNS tumor type (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u200931 cases) that is characterized by focal high-level amplification and resultant overexpression of either\n                    <jats:italic>PLAGL1<\/jats:italic>\n                    or\n                    <jats:italic>PLAGL2<\/jats:italic>\n                    , and an absence of recurrent genetic alterations characteristic of other pediatric CNS tumor types. Both genes act as transcription factors for a regulatory subset of imprinted genes (IGs), components of the Wnt\/\u03b2-Catenin pathway, and the potential drug targets\n                    <jats:italic>RET<\/jats:italic>\n                    and\n                    <jats:italic>CYP2W1<\/jats:italic>\n                    , which are also specifically overexpressed in this tumor type. A derived PLAGL-specific gene expression signature indicates dysregulation of imprinting control and differentiation\/development. These tumors occurred throughout the neuroaxis including the cerebral hemispheres, cerebellum, and brainstem, and were predominantly composed of primitive embryonal-like cells lacking robust expression of markers of glial or neuronal differentiation (e.g., GFAP, OLIG2, and synaptophysin). Tumors with\n                    <jats:italic>PLAGL1<\/jats:italic>\n                    amplification were typically diagnosed during adolescence (median age 10.5\u00a0years), whereas those with\n                    <jats:italic>PLAGL2<\/jats:italic>\n                    amplification were diagnosed during early childhood (median age 2\u00a0years). The 10-year overall survival was 66% for\n                    <jats:italic>PLAGL1<\/jats:italic>\n                    -amplified tumors, 25% for\n                    <jats:italic>PLAGL2<\/jats:italic>\n                    -amplified tumors, 18% for male patients, and 82% for female patients. In summary, we describe a new type of biologically distinct CNS tumor characterized by\n                    <jats:italic>PLAGL1\/2<\/jats:italic>\n                    amplification that occurs predominantly in infants and toddlers (\n                    <jats:italic>PLAGL2<\/jats:italic>\n                    ) or adolescents (\n                    <jats:italic>PLAGL1<\/jats:italic>\n                    ) which we consider best classified as a CNS embryonal tumor and which is associated with intermediate survival. The cell of origin and optimal treatment strategies remain to be defined.\n                  <\/jats:p>","DOI":"10.1007\/s00401-022-02516-2","type":"journal-article","created":{"date-parts":[[2022,11,27]],"date-time":"2022-11-27T16:31:58Z","timestamp":1669566718000},"page":"49-69","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["Amplification of the PLAG-family genes\u2014PLAGL1 and PLAGL2\u2014is\u00a0a key feature of the novel tumor type CNS embryonal tumor with PLAGL amplification"],"prefix":"10.1007","volume":"145","author":[{"given":"Michaela-Kristina","family":"Keck","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Sill","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrea","family":"Wittmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Piyush","family":"Joshi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Damian","family":"Stichel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pengbo","family":"Beck","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Konstantin","family":"Okonechnikow","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philipp","family":"Sievers","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Annika K.","family":"Wefers","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Federico","family":"Roncaroli","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shivaram","family":"Avula","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin G.","family":"McCabe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James T.","family":"Hayden","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pieter","family":"Wesseling","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ingrid","family":"\u00d8ra","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Monica","family":"Nist\u00e9r","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mari\u00ebtte E. 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