| Literature DB >> 27263935 |
Jelte Helfferich1, Ronald Nijmeijer2, Oebele F Brouwer3, Maartje Boon3, Annemarie Fock3, Eelco W Hoving4, Lisethe Meijer5, Wilfred F A den Dunnen2, Eveline S J M de Bont6.
Abstract
Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder, associated with a variable clinical phenotype including café-au-lait spots, intertriginous freckling, Lisch nodules, neurofibromas, optic pathway gliomas and distinctive bony lesions. NF1 is caused by a mutation in the NF1 gene, which codes for neurofibromin, a large protein involved in the MAPK- and the mTOR-pathway through RAS-RAF signalling. NF1 is a known tumour predisposition syndrome, associated with different tumours of the nervous system including low grade gliomas (LGGs) in the paediatric population. The focus of this review is on grade I pilocytic astrocytomas (PAs), the most commonly observed histologic subtype of low grade gliomas in NF1. Clinically, these PAs have a better prognosis and show different localisation patterns than their sporadic counterparts, which are most commonly associated with a KIAA1549:BRAF fusion. In this review, possible mechanisms of tumourigenesis in LGGs with and without NF1 will be discussed, including the contribution of different signalling pathways and tumour microenvironment. Furthermore we will discuss how increased understanding of tumourigenesis may lead to new potential targets for treatment.Entities:
Keywords: BRAF:KIAA1549 fusion; Low grade glioma; NF1 gene; Neurofibromatosis; Pilocytic astrocytoma
Mesh:
Year: 2016 PMID: 27263935 DOI: 10.1016/j.critrevonc.2016.05.008
Source DB: PubMed Journal: Crit Rev Oncol Hematol ISSN: 1040-8428 Impact factor: 6.312