No amplifications of hypoxia-inducible factor-1α gene in invasive breast cancer: A tissue microarray study

Marije M. Vleugel, Reinhard Bos, Horst Buerger, Petra Van Der Groep, Outi R. Saramäki, Tapio Visakorpi, Elsken Van Der Wall, Paul J. Van Diest

Research output: Contribution to journalArticle

Abstract

Objective: Hypoxia Inducible Factor-1 (HIF-1) is an important transcription factor that stimulates tumour growth and metastases via several pathways, including angiogenesis and altered metabolism. Activation of HIF-1 depends on the levels of its α-subunit, which increase during hypoxia. Recent studies showed that the HIF-1α gene was amplified in prostate cancer, leading to overexpression of HIF-1α at normoxia. The aim of this study was to evaluate the presence of HIF-1α gene amplifications in invasive breast cancer as an explanation for HIF-1α protein overexpression. Methods: Protein and gene expression of HIF-1α were analyzed on a tissue microarray of 94 breast cancers by immunohistochemistry and fluorescent in situ hybridization (FISH), respectively. Results: Overexpression of HIF-1α protein was found in 58/94 (62%) of patients. No amplifications of the HIF-1α gene were detected. Conclusion: Increased protein levels of HIF-1α are not associated with amplification of the HIF-1α gene in human breast cancer. Therefore, other mechanisms than gene amplification must be responsible for HIF-α overexpression at normoxia.

Original languageEnglish (US)
Pages (from-to)347-351
Number of pages5
JournalCellular Oncology
Volume26
Issue number5-6
StatePublished - Dec 1 2004

Keywords

  • Amplification
  • Breast cancer
  • FISH
  • Gene expression
  • HIF-1α
  • Immunohistochemistry

ASJC Scopus subject areas

  • Molecular Medicine
  • Oncology
  • Cancer Research

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  • Cite this

    Vleugel, M. M., Bos, R., Buerger, H., Van Der Groep, P., Saramäki, O. R., Visakorpi, T., Van Der Wall, E., & Van Diest, P. J. (2004). No amplifications of hypoxia-inducible factor-1α gene in invasive breast cancer: A tissue microarray study. Cellular Oncology, 26(5-6), 347-351.