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Cancer genomics and genetics of FGFR2 (Review)

Masaru Katoh1

  • 1Genetics and Cell Biology Section, National Cancer Center Research Institute, Chuo-ward, Tokyo 104-0045, Japan. mkatoh-kkr@umin.ac.jp

International Journal of Oncology
|July 19, 2008
PubMed

Insights

Fibroblast Growth Factor Receptor 2 (FGFR2) gene alterations are linked to various cancers. FGFR2ome analysis can guide targeted therapies, with AZD2171 showing promise as an anti-cancer drug.

Area of Science:

  • Genomics and Genetics
  • Cancer Biology
  • Pharmacology

Background:

  • The FGFR2 gene produces FGFR2b and FGFR2c receptors, crucial for cell signaling.
  • FGFR2 alterations, including SNPs and mutations, are implicated in breast, gastric, lung, ovarian, and endometrial cancers.
  • Aberrant FGFR2 signaling, driven by genetic changes or isoform switching, promotes cancer development.

Purpose of the Study:

  • To review the genomics and genetics of FGFR2.
  • To discuss therapeutics targeting FGFR2.
  • To define and advocate for FGFR2ome analysis for clinical application.

Main Methods:

  • Literature review of FGFR2 genomics, genetics, and targeted therapies.
  • Analysis of genetic alterations (SNPs, amplification, mutation) and their functional consequences.
  • Evaluation of FGFR inhibitors (PD173074, SU5402, AZD2171).

Main Results:

  • FGFR2 SNPs increase breast cancer risk; mutations/amplifications occur in multiple cancer types.
  • Genetic alterations lead to FGFR2 signaling activation and potentially more malignant phenotypes via FGFR2b to FGFR2c switching.
  • AZD2171 demonstrates the most promise among evaluated FGFR inhibitors.

Conclusions:

  • Comprehensive FGFR2ome analysis across diverse populations and tumor types is essential.
  • An integrated FGFR2 database will enable rational clinical application of FGFR2-targeted cancer therapies.
  • Understanding FGFR2 signaling interplay with WNT pathways is critical for specific cancer types.

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