Abstract
Hypoxia that originates from disturbed growth of solid tumors initiates a cascade of intracellular events engaging hypoxia-inducible factors, HIF-1 and HIF-2. Overexpression of HIF has been confirmed in solid tumors and was unfortunately accompanied with chemo- and radioresistance observed in many patients. Multiple cellular pathways resulting in HIF activation could be successfully inhibited by use of different kinds of drugs (e.g. topotecan, heat shock protein 90 and mTOR inhibitors, YC-1, pleurotin or 2-methoxyestradiol), which are being subjected into intensive investigation in clinical trials.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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2-Methoxyestradiol
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Animals
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Antineoplastic Agents* / pharmacology
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Antineoplastic Agents* / therapeutic use
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Basic Helix-Loop-Helix Transcription Factors* / antagonists & inhibitors
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Basic Helix-Loop-Helix Transcription Factors* / metabolism
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Cell Hypoxia / drug effects
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Cell Hypoxia / physiology
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Clinical Trials as Topic
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Estradiol / analogs & derivatives
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Estradiol / pharmacology
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Estradiol / therapeutic use
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Humans
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Hypoxia-Inducible Factor 1* / antagonists & inhibitors
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Hypoxia-Inducible Factor 1* / metabolism
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Indazoles / pharmacology
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Indazoles / therapeutic use
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Mice
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NF-kappa B / antagonists & inhibitors
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NF-kappa B / metabolism
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Neoplasms* / drug therapy
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Neoplasms* / metabolism
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Neoplasms* / physiopathology
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Topotecan / pharmacology
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Topotecan / therapeutic use
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Transcription Factors / antagonists & inhibitors
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Transcription Factors / metabolism
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Tumor Cells, Cultured
Substances
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Antineoplastic Agents
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Basic Helix-Loop-Helix Transcription Factors
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Hypoxia-Inducible Factor 1
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Indazoles
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NF-kappa B
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Transcription Factors
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3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole
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endothelial PAS domain-containing protein 1
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Estradiol
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2-Methoxyestradiol
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Topotecan