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Rare amplicons implicate frequent deregulation of cell fate specification pathways in oral squamous cell carcinoma

Antoine M Snijders1, Brian L Schmidt, Jane Fridlyand

  • 1Cancer Research Institute, University of California San Francisco, Box 0808, San Francisco, CA 94143-0808, USA.

Oncogene
|April 13, 2005
PubMed

Insights

This study identifies key amplified genes in oral squamous cell carcinoma (SCC) development. Findings highlight the role of integrin, hedgehog, and notch pathways in oral cancer progression and cell fate.

Area of Science:

  • Genomics
  • Cancer Biology
  • Molecular Oncology

Background:

  • Genomic aberrations, including copy number alterations, are hallmarks of solid tumors.
  • Identifying specific driver genes within large amplified regions in oral squamous cell carcinoma (SCC) is challenging.

Purpose of the Study:

  • To pinpoint critical genetic pathways involved in oral SCC development by focusing on narrow gene amplification regions.
  • To identify candidate driver genes within amplicons <3 Mb.

Main Methods:

  • Utilized array comparative genomic hybridization (array CGH) to define minimum common amplified regions.
  • Employed expression analysis to identify overexpressed candidate genes within these amplicons.

Main Results:

  • Identified amplification and overexpression of genes in integrin signaling (TLN1), survival (YAP1, BIRC2), and cell adhesion/migration (TLN1, LAMA3, MMP7).
  • Found amplification and overexpression of key members of the hedgehog (GLI2) and notch (JAG1, RBPSUH, FJX1) signaling pathways.
  • Detected deregulation of additional hedgehog (HHIP, SMO) and notch (DLL1, NOTCH4) pathway members.

Conclusions:

  • Amplified and overexpressed genes in oral SCC are involved in crucial cellular processes including signaling, survival, adhesion, and migration.
  • Deregulation of developmental pathways, specifically hedgehog and notch signaling, is implicated in oral SCC pathogenesis.
  • Aberrations in these pathways suggest a role in cell fate misspecification during oral cancer development.

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