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Integrated Molecular and Clinical Analysis of 1,000 Pediatric Low-Grade Gliomas. 2020
Scott Ryall, and
Michal Zapotocky, and
Kohei Fukuoka, and
Liana Nobre, and
Ana Guerreiro Stucklin, and
Julie Bennett, and
Robert Siddaway, and
Christopher Li, and
Sanja Pajovic, and
Anthony Arnoldo, and
Paul E Kowalski, and
Monique Johnson, and
Javal Sheth, and
Alvaro Lassaletta, and
Ruth G Tatevossian, and
Wilda Orisme, and
Ibrahim Qaddoumi, and
Lea F Surrey, and
Marilyn M Li, and
Angela J Waanders, and
Stephen Gilheeney, and
Marc Rosenblum, and
Tejus Bale, and
Derek S Tsang, and
Normand Laperriere, and
Abhaya Kulkarni, and
George M Ibrahim, and
James Drake, and
Peter Dirks, and
Michael D Taylor, and
James T Rutka, and
Suzanne Laughlin, and
Manohar Shroff, and
Mary Shago, and
Lili-Naz Hazrati, and
Colleen D'Arcy, and
Vijay Ramaswamy, and
Ute Bartels, and
Annie Huang, and
Eric Bouffet, and
Matthias A Karajannis, and
Mariarita Santi, and
David W Ellison, and
Uri Tabori, and
Cynthia Hawkins
Arthur and Sonia Labatt Brain Tumour Research Centre, The Hospital for Sick Children, 555 University Avenue, Toronto, ON M5G 1X8, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
Pediatric low-grade gliomas (pLGG) are frequently driven by genetic alterations in the RAS-mitogen-activated protein kinase (RAS/MAPK) pathway yet show unexplained variability in their clinical outcome. To address this, we characterized a cohort of >1,000 clinically annotated pLGG. Eighty-four percent of cases harbored a driver alteration, while those without an identified alteration also often exhibited upregulation of the RAS/MAPK pathway. pLGG could be broadly classified based on their alteration type. Rearrangement-driven tumors were diagnosed at a younger age, enriched for WHO grade I histology, infrequently progressed, and rarely resulted in death as compared with SNV-driven tumors. Further sub-classification of clinical-molecular correlates stratified pLGG into risk categories. These data highlight the biological and clinical differences between pLGG subtypes and opens avenues for future treatment refinement.
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