| Tumor hypoxia and cancer progression. | |
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MedLine Citation:
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PMID: 16002209 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Aerobic life consumes oxygen for efficient production of high energy compounds. The ability to sense and respond to changes in oxygen partial pressure represents a fundamental property to assure the cellular oxygen supply to be within a narrow range that balances the risks of oxidative damage vs. oxygen deficiency. The discovery of hypoxia-inducible factor-1 (HIF-1) allowed the identification of molecular mechanisms by which changes in oxygenation are transduced to adequate intracellular adaptive responses. It became apparent that hypoxia can initiate cell demise by apoptosis/necrosis but also prevent cell death by provoking adaptive responses that, in turn, facilitate cell proliferation or angiogenesis, thus contributing to tumor progression. Considering that activation of HIF-1 provokes pro-survival as well as pro-death decisions under hypoxia, it will be crucial to understand decision making processes in regulating cell death, adaptation and chemoresistance. Likely, secondary stressors such as pH changes, i.e. acidosis, and the context of genetic alterations will shape the role of HIF-1 to affect susceptibility of cells to undergo hypoxia-induced cell death or to allow adaptation and progression towards malignancy. Understanding the mechanisms by which HIF-1 affects the expression and/or function of key apoptotic regulators such as Bcl-2 family members or p53 will help to uncover how HIF-1 induces cell death and the manner in which cells can overcome such signals and thus determine which of its Janus faces prevail. |
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Authors:
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Jie Zhou; Tobias Schmid; Steffen Schnitzer; Bernhard Brüne |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review Date: 2005-07-05 |
Journal Detail:
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Title: Cancer letters Volume: 237 ISSN: 0304-3835 ISO Abbreviation: Cancer Lett. Publication Date: 2006 Jun |
Date Detail:
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Created Date: 2006-05-22 Completed Date: 2006-07-26 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 7600053 Medline TA: Cancer Lett Country: Ireland |
Other Details:
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Languages: eng Pagination: 10-21 Citation Subset: IM |
Affiliation:
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Institute of Biochemistry I, Faculty of Medicine, Johann Wolfgang Goethe-University, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Angiogenic Proteins
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genetics,
metabolism Animals Apoptosis / genetics* Aryl Hydrocarbon Receptor Nuclear Translocator / metabolism Cell Hypoxia / genetics* Cell Proliferation Disease Progression Drug Resistance, Neoplasm / genetics Gene Expression Regulation, Neoplastic* Humans Hypoxia-Inducible Factor 1, alpha Subunit / metabolism Membrane Proteins / genetics, metabolism Neoplasms / blood supply, genetics*, metabolism Neovascularization, Pathologic / genetics, metabolism Proto-Oncogene Proteins / genetics, metabolism Tumor Suppressor Protein p53 / genetics, metabolism Tumor Suppressor Proteins / genetics, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Angiogenic Proteins; 0/BNIP3 protein, human; 0/BNIP3L protein, human; 0/Hypoxia-Inducible Factor 1, alpha Subunit; 0/Membrane Proteins; 0/Proto-Oncogene Proteins; 0/Tumor Suppressor Protein p53; 0/Tumor Suppressor Proteins; 138391-32-9/Aryl Hydrocarbon Receptor Nuclear Translocator |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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