Abstract
The process of chronic inflammation is a common link which connects different kinds of environmental pollutants and infections with tumorigenesis. Transcription factor NF-κB is a common final target for many inflammatory and cell proliferation pathways, independent of the source of stimuli (e.g., cytokines, growth factors, environmental carcinogens, radiation, hypoxia, bacteria, and viruses). Over-activation of NF-κB has been confirmed in many tumors, resulting in worse prognosis for patient survival. Therefore, inhibition of cellular pathways for NF-κB activation is nowadays considered as a promising anti-cancer therapy and is extensively studied in clinical trials, or even has been adopted as an approved therapy in some kinds of cancer.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology
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Boronic Acids / pharmacology
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Boronic Acids / therapeutic use
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Bortezomib
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Cell Line, Tumor
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Cell Proliferation
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Clinical Trials as Topic
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Cytokines / metabolism
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Gene Expression Regulation
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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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Inflammation / drug therapy
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Inflammation / genetics
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Inflammation / physiopathology*
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Mice
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Models, Biological
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NF-kappa B* / antagonists & inhibitors
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NF-kappa B* / genetics
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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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Pyrazines / pharmacology
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Pyrazines / therapeutic use
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Signal Transduction
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Transcription Factors / genetics
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Transcription Factors / metabolism
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Tumor Suppressor Protein p53 / agonists
Substances
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Antineoplastic Agents
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Boronic Acids
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Cytokines
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Hypoxia-Inducible Factor 1
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NF-kappa B
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Pyrazines
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Transcription Factors
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Tumor Suppressor Protein p53
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Bortezomib