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<p>Gliomas are a major cause of cancer-related deaths in adolescents and young adults (AYAs; ages 15–39 years). Different molecular alterations drive gliomas in children and adults, leading to distinct biology and clinical consequences, but the implications of pediatric- versus adult-type alterations in AYAs are unknown. Our population-based analysis of 1,456 clinically and molecularly characterized gliomas in patients aged 0–39 years addresses this gap. Pediatric-type alterations were found in 31% of AYA gliomas and conferred superior outcomes compared to adult-type alterations. AYA low-grade gliomas with specific RAS–MAPK alterations exhibited senescence, tended to arise in different locations and were associated with superior outcomes compared to gliomas in children, suggesting different cellular origins. Hemispheric IDH-mutant, BRAF p.V600E and <i>FGFR</i>-altered gliomas were associated with the risk of malignant transformation, having worse outcomes with increased age. These insights into gliomagenesis may provide a rationale for earlier intervention for certain tumors to disrupt the typical behavior, leading to improved outcomes.</p>

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A population-based analysis of the molecular landscape of glioma in adolescents and young adults reveals insights into gliomagenesis

  • 期刊论文

  • 发表日期：

    2025年5月7日

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  • Julie Bennett,
  • Adrian B. Levine,
  • Liana Nobre,
  • Logine Negm,
  • Jiil Chung,
  • Karen Fang,
  • Monique Johnson,
  • Martin Komosa,
  • Stacey Krumholtz,
  • Nuno Miguel Nunes,
  • Mansuba Rana,
  • Scott Ryall,
  • Javal Sheth,
  • Robert Siddaway,
  • Tejus A. Bale,
  • Eric Bouffet,
  • Michael D. Cusimano,
  • Sunit Das,
  • Jay Detsky,
  • Peter Dirks,
  • Matthias A. Karajannis,
  • Paul Kongkham,
  • Alexandra Giantini-Larsen,
  • Bryan Kincheon Li,
  • Mary Jane Lim-Fat,
  • Andrew L. Lin,
  • Warren P. Mason,
  • Alexandra Miller,
  • James R. Perry,
  • Arjun Sahgal,
  • Sameer Farouk Sait,
  • Derek S. Tsang,
  • Gelareh Zadeh,
  • Normand Laperriere,
  • Lananh Nguyen,
  • Andrew Gao,
  • Julia Keith,
  • David G. Munoz,
  • Uri Tabori,
  • Cynthia Hawkins

摘要

Gliomas are a major cause of cancer-related deaths in adolescents and young adults (AYAs; ages 15–39 years). Different molecular alterations drive gliomas in children and adults, leading to distinct biology and clinical consequences, but the implications of pediatric- versus adult-type alterations in AYAs are unknown. Our population-based analysis of 1,456 clinically and molecularly characterized gliomas in patients aged 0–39 years addresses this gap. Pediatric-type alterations were found in 31% of AYA gliomas and conferred superior outcomes compared to adult-type alterations. AYA low-grade gliomas with specific RAS–MAPK alterations exhibited senescence, tended to arise in different locations and were associated with superior outcomes compared to gliomas in children, suggesting different cellular origins. Hemispheric IDH-mutant, BRAF p.V600E and FGFR-altered gliomas were associated with the risk of malignant transformation, having worse outcomes with increased age. These insights into gliomagenesis may provide a rationale for earlier intervention for certain tumors to disrupt the typical behavior, leading to improved outcomes.