A clinicopathologic study of diencephalic pediatric low-grade gliomas with BRAF V600 mutation

Acta Neuropathol. 2015 Oct;130(4):575-85. doi: 10.1007/s00401-015-1467-3. Epub 2015 Aug 12.

Abstract

Among brain tumors, the BRAF (V600E) mutation is frequently associated with pleomorphic xanthoastrocytomas (PXAs) and gangliogliomas (GGs). This oncogenic mutation is also detected in ~5 % of other pediatric low-grade gliomas (LGGs) including pilocytic astrocytomas (PAs) and diffuse astrocytomas. In the current multi-institutional study of 56 non-PXA/non-GG diencephalic pediatric LGGs, the BRAF (V600) mutation rate is 36 %. V600-mutant tumors demonstrate a predilection for infants and young children (<age 3) and have a higher tendency for multicentricity. On neuroimaging, BRAF (V600)-mutant tumors appear as nodular, yet infiltrative contrast-enhancing masses. Morphologic examination reveals a monophasic, predominantly compact and partially infiltrative architecture. Due to the lack of classic morphologic features associated with PAs, pilomyxoid astrocytomas (PMAs), or diffuse astrocytomas, 75 % of the BRAF (V600)-mutant tumors could not be definitively classified on initial histopathologic evaluation. At a median follow-up of 55 months, the 5-year progression-free survival (PFS) rate for BRAF (V600)-mutant diencephalic low-grade astrocytomas (LGAs) was 22 ± 12 %, shorter than BRAF (V600)-WT PAs (52 ± 13 %) but higher than PMAs (10 ± 6 %). Of note, long-term PFS was observed in several adolescent patients with BRAF (V600)-mutant tumors. In children aged 0-12 years, 5-year PFS rate and median PFS in BRAF (V600)-mutant LGAs are 9 ± 9 % and 19 months (95 % CI 3-37 months), respectively. The PFS is comparable to that in BRAF (V600)-WT PMAs (5-year PFS rate: 10 ± 9 %; median PFS: 15 months, 95 % CI 3-32 months; p = 0.96) and significantly shorter than BRAF (V600)-WT PAs (5-year PFS rate: 46 ± 13 %; median PFS: 51 months, 95 % CI 20-∞ months; p < 0.05). In summary, diencephalic BRAF (V600)-mutant pediatric LGAs are associated with unique clinicopathologic features and have a more aggressive clinical course, especially in children under age 13. The low rate of CDKN2A deletion also suggests that these tumors are molecularly distinct from secondary pediatric high-grade gliomas.

Keywords: BRAF; Diencephalic; Hypothalamic; Low-grade glioma; Pilocytic astrocytoma; Pilomyxoid astrocytoma; V600E.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Age Factors
  • Brain Neoplasms / epidemiology
  • Brain Neoplasms / genetics*
  • Brain Neoplasms / pathology*
  • Brain Neoplasms / therapy
  • Child
  • Child, Preschool
  • Cohort Studies
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics
  • Diencephalon / pathology*
  • Disease-Free Survival
  • Female
  • Follow-Up Studies
  • Glioma / epidemiology
  • Glioma / genetics*
  • Glioma / pathology*
  • Glioma / therapy
  • Humans
  • Infant
  • Magnetic Resonance Imaging
  • Male
  • Mutation
  • Neoplasm Grading
  • Proto-Oncogene Proteins B-raf / genetics*
  • Treatment Outcome

Substances

  • Cyclin-Dependent Kinase Inhibitor p16
  • BRAF protein, human
  • Proto-Oncogene Proteins B-raf