Truncated FGFR2 is a clinically actionable oncogene in multiple cancers.

ABSTRACT: Somatic hotspot mutations and structural amplifications and fusions that affect fibroblast growth factor receptor 2 (encoded by FGFR2) occur in multiple types of cancer¹. However, clinical responses to FGFR inhibitors have remained variable^1-9, emphasizing the need to better understand which FGFR2 alterations are oncogenic and therapeutically targetable. Here we apply transposon-based screening^10,11 and tumour modelling in mice^12,13, and find that the truncation of exon 18 (E18) of Fgfr2 is a potent driver mutation. Human oncogenomic datasets revealed a diverse set of FGFR2 alterations, including rearrangements, E1-E17 partial amplifications, and E18 nonsense and frameshift mutations, each causing the transcription of E18-truncated FGFR2 (FGFR2

SUBMITTER: Zingg D 

PROVIDER: S-EPMC9436779 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature