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Truncated FGFR2 is a clinically actionable oncogene in multiple cancers.

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Truncated fibroblast growth factor receptor 2 (FGFR2) exon 18 alterations are potent cancer drivers. These FGFR2 variants represent actionable therapeutic targets for FGFR-targeted therapies in multiple cancers.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Fibroblast growth factor receptor 2 (FGFR2) alterations, including mutations, amplifications, and fusions, are implicated in various cancers.
  • Clinical responses to FGFR inhibitors are variable, highlighting the need to identify specific oncogenic FGFR2 alterations.

Purpose of the Study:

  • To investigate the oncogenic potential of different FGFR2 alterations.
  • To identify specific FGFR2 variants that are therapeutically targetable.

Main Methods:

  • Transposon-based screening and murine tumor modeling were employed.
  • Functional in vitro and in vivo assays were used to examine FGFR2 variants.
  • Human oncogenomic datasets were analyzed.

Main Results:

  • Truncation of exon 18 (E18) of Fgfr2 (FGFR2ΔE18) was identified as a potent driver mutation.
  • Diverse FGFR2 alterations, including rearrangements and nonsense/frameshift mutations, lead to FGFR2ΔE18.
  • FGFR2-E18 truncation acts as a single-driver alteration, while full-length FGFR2 amplifications require cooperating genes.

Conclusions:

  • Genomic alterations generating stable FGFR2ΔE18 variants are actionable therapeutic targets.
  • Preclinical and clinical data support targeting FGFR2ΔE18.
  • Cancers with any FGFR2 variant featuring E18 truncation should be considered for FGFR-targeted therapies.