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Solid tumors with areas of low oxygen tension (hypoxia) have a poor prognosis, as cells in this environment often survive radiation and chemotherapy. In this report we describe how this hypoxic environment can be used to activate heterologous gene expression driven by a hypoxia-responsive element (HRE), which interacts with the transcriptional complex hypoxia-inducible factor-1 (HIF-1). Our results demonstrate that the HIF-1/HRE system of gene regulation is active in hypoxic tumor cells and show the potential of exploiting tumor-specific conditions for the targeted expression of diagnostic or therapeutic genes in cancer therapy.

Original publication

DOI

10.1038/nm0597-515

Type

Journal article

Journal

Nat Med

Publication Date

05/1997

Volume

3

Pages

515 - 520

Keywords

Animals, Antimetabolites, Antineoplastic, Cell Hypoxia, Cytosine Deaminase, DNA-Binding Proteins, Fibrosarcoma, Flucytosine, Fluorouracil, Gene Expression Regulation, Neoplastic, Genes, Reporter, Humans, Hypoxia-Inducible Factor 1, Hypoxia-Inducible Factor 1, alpha Subunit, Mice, Mice, Nude, Misonidazole, Neoplasm Transplantation, Nuclear Proteins, Nucleoside Deaminases, Oxygen, Phosphoglycerate Kinase, Prodrugs, Promoter Regions, Genetic, Recombinant Fusion Proteins, Transcription Factors, Tumor Cells, Cultured