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Pathogenetic pathways leading to glioblastoma multiforme: association between gene expressions and resistance to

Sarah Löw1, Vassilios I Vougioukas, Thomas Hielscher

  • 1Department of Neurosurgery, Ruprecht Karls University, Im Neuenheimer Feld 400, D-69120 Heidelberg, Germany.

Anticancer Research
|February 5, 2009
PubMed
Abstract

Insights

Erlotinib resistance in glioblastoma multiforme (GBM) is complex. Two genes, IGF1 and PIK3C2B, were identified as potentially conferring resistance to erlotinib in GBM.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Glioblastoma multiforme (GBM) exhibits variable response to erlotinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor.
  • EGFR expression levels do not predict erlotinib response in GBM, suggesting other genetic factors are involved.

Purpose of the Study:

  • To identify specific genes within primary and secondary GBM pathogenesis pathways that mediate cellular response to erlotinib.
  • To elucidate the molecular basis of erlotinib resistance in human glioblastoma.

Main Methods:

  • Gene expression profiling using CodeLink Human Whole Genome Bioarrays.
  • Analysis of complementary (c)RNAs from GBM cell lines with varying sensitivity to erlotinib.

Main Results:

  • Expression analysis of 104 genes related to GBM pathogenesis pathways was performed.
  • Two genes, IGF1 and PIK3C2B, showed significant correlation with cellular resistance to erlotinib.

Conclusions:

  • IGF1 and PIK3C2B are candidate genes potentially conferring resistance to erlotinib in GBM.
  • GBM resistance to erlotinib may develop through natural genetic evolution of the tumor.

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