Response of recurrent BRAFV600E mutated ganglioglioma to Vemurafenib as single agent

  • Francesca del Bufalo
  • , Andrea Carai
  • , Lorenzo Figà-Talamanca
  • , Benedetta Pettorini
  • , Conor Mallucci
  • , Felice Giangaspero
  • , Manila Antonelli
  • , Manuela Badiali
  • , Loredana Moi
  • , Giuseppe Bianco
  • , Antonella Cacchione
  • , Franco Locatelli
  • , Elisabetta Ferretti*
  • , Angela Mastronuzzi
  • *Autore corrispondente per questo lavoro

Risultato della ricerca: Contributo in rivistaArticolo

Abstract

Background: Ganglioglioma (GG) and pilocytic astrocytoma (PA) represent the most frequent low-grade gliomas (LGG) occurring in paediatric age. LGGs not amenable of complete resection (CR) represent a challenging subgroup where traditional treatments often fail. Activation of the MAP Kinase (MAPK) pathway caused by the BRAFV600E mutation or the KIAA1549-BRAF fusion has been reported in pediatric GG and PA, respectively.Case presentation: We report on a case of BRAFV600E mutated cervicomedullary GG treated with standard chemotherapy and surgery. After multiple relapse, BRAF status was analyzed by immunohistochemistry and sequencing showing a BRAFV600E mutation. Treatment with Vemurafenib as single agent was started. For the first time, a radiological and clinical response was obtained after 3 months of treatment and sustained after 6 months.Conclusion: Our experience underline the importance of understanding the driver molecular alterations of LGG and suggests a role for Vemurafenib in the treatment of pediatric GG not amenable of complete surgical resection.
Lingua originaleInglese
pagine (da-a)N/A/-N/A
RivistaJournal of Translational Medicine
Volume12
Numero di pubblicazione1
DOI
Stato di pubblicazionePubblicato - 2014

All Science Journal Classification (ASJC) codes

  • Biochimica, Genetica, Biologia Molecolare Generali

Keywords

  • BRAF V600E
  • Ganglioglioma
  • Low Grade Glioma
  • MAP Kinase pathway
  • Vemurafenib

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