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Amplification of the PLAG-family genes-PLAGL1 and PLAGL2-is a key feature of the novel tumor type CNS embryonal tumor with PLAGL amplification
MK. Keck, M. Sill, A. Wittmann, P. Joshi, D. Stichel, P. Beck, K. Okonechnikow, P. Sievers, AK. Wefers, F. Roncaroli, S. Avula, MG. McCabe, JT. Hayden, P. Wesseling, I. Øra, M. Nistér, MEG. Kranendonk, BBJ. Tops, M. Zapotocky, J. Zamecnik, A....
Jazyk angličtina Země Německo
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
ProQuest Central
od 1997-01-01 do Před 1 rokem
Health & Medicine (ProQuest)
od 1997-01-01 do Před 1 rokem
Psychology Database (ProQuest)
od 1997-01-01 do Před 1 rokem
- MeSH
- dítě MeSH
- DNA vazebné proteiny genetika metabolismus MeSH
- kojenec MeSH
- lidé MeSH
- metylace DNA MeSH
- nádorové supresorové proteiny genetika MeSH
- nádory centrálního nervového systému * genetika MeSH
- předškolní dítě MeSH
- primitivní neuroektodermové nádory * genetika MeSH
- proteiny buněčného cyklu genetika MeSH
- proteiny vázající RNA genetika MeSH
- signální dráha Wnt genetika MeSH
- transkripční faktory genetika metabolismus MeSH
- Check Tag
- dítě MeSH
- kojenec MeSH
- lidé MeSH
- mužské pohlaví MeSH
- předškolní dítě MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Pediatric central nervous system (CNS) tumors represent the most common cause of cancer-related death in children aged 0-14 years. 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 = 31 cases) that is characterized by focal high-level amplification and resultant overexpression of either PLAGL1 or PLAGL2, 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/β-Catenin pathway, and the potential drug targets RET and CYP2W1, 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 PLAGL1 amplification were typically diagnosed during adolescence (median age 10.5 years), whereas those with PLAGL2 amplification were diagnosed during early childhood (median age 2 years). The 10-year overall survival was 66% for PLAGL1-amplified tumors, 25% for PLAGL2-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 PLAGL1/2 amplification that occurs predominantly in infants and toddlers (PLAGL2) or adolescents (PLAGL1) 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.
Department of Developmental Neurobiology St Jude Children's Research Hospital Memphis TN USA
Department of Oncology Pathology Karolinska Institutet Stockholm Sweden
Department of Pathology and Laboratory Medicine The Aga Khan University Karachi Pakistan
Department of Pathology and Laboratory Medicine The University of British Colombia Vancouver Canada
Department of Pathology NYU Langone Medical Center New York NY USA
Department of Pathology Rigshospitalet Copenhagen Denmark
Department of Pediatric Hematology Oncology Valley Children's Hospital Madera CA USA
Department of Radiology Alder Hey Children's NHS Foundation Trust Liverpool UK
Division of Pediatric Glioma Research Im Neuenheimer Feld 280 69120 Heidelberg Germany
Division of Pediatric Hematology and Oncology University Medical Center Göttingen Göttingen Germany
Division of Pediatric Neurooncology German Cancer Consortium Heidelberg Germany
Faculty of Biosciences Heidelberg University Heidelberg Germany
Hopp Children's Cancer Center Heidelberg Im Neuenheimer Feld 280 69120 Heidelberg Germany
Institute of Neuropathology University Medical Center Hamburg Eppendorf Hamburg Germany
Princess Máxima Center for Pediatric Oncology Utrecht The Netherlands
Research Institute Children's Cancer Center Hamburg Hamburg Germany
Citace poskytuje Crossref.org
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- $a Amplification of the PLAG-family genes-PLAGL1 and PLAGL2-is a key feature of the novel tumor type CNS embryonal tumor with PLAGL amplification / $c MK. Keck, M. Sill, A. Wittmann, P. Joshi, D. Stichel, P. Beck, K. Okonechnikow, P. Sievers, AK. Wefers, F. Roncaroli, S. Avula, MG. McCabe, JT. Hayden, P. Wesseling, I. Øra, M. Nistér, MEG. Kranendonk, BBJ. Tops, M. Zapotocky, J. Zamecnik, A. Vasiljevic, T. Fenouil, D. Meyronet, K. von Hoff, U. Schüller, H. Loiseau, D. Figarella-Branger, CM. Kramm, D. Sturm, D. Scheie, T. Rauramaa, J. Pesola, J. Gojo, C. Haberler, S. Brandner, T. Jacques, A. Sexton Oates, R. Saffery, E. Koscielniak, SJ. Baker, S. Yip, M. Snuderl, N. Ud Din, D. Samuel, K. Schramm, M. Blattner-Johnson, F. Selt, J. Ecker, T. Milde, A. von Deimling, A. Korshunov, A. Perry, SM. Pfister, F. Sahm, DA. Solomon, DTW. Jones
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