Concurrence of FGFR1 mutations modulates oncogenesis in glioneuronal tumors

ABSTRACT: FGFR1 genetic alterations are associated with brain maligancies, including FGFR1 mutations in familial and sporadic cases of low-grade glioneuronal tumors, suggesting intrinsic mechanisms of selective pressure toward FGFR1 multiple events arising in the context of a quiet genome. To decipher the molecular mechanisms triggered by multiple concurrent FGFR1 mutations, we have mapped the proximal interactome of wild-type, single- and double-mutant FGFR1 proteins through a BioID-MS approach. Our data reveal novel oncogenic functionality for the two hotspot mutations N546K and K656E, linked to evasion of lysosomal degradation. Further, we identified a modulatory tumor-suprressive role for the susceptibility variant R661P, which hampers the oncogenic potential of both hotspot N546K and K656E muta

SUBMITTER: Jacopo Boni 

PROVIDER: S-SCDT-10_1038-S44318-025-00600-3 | biostudies-other |

REPOSITORIES: biostudies-other