Abstract
At the doses used clinically, chemotherapy is believed to kill melanoma by a final common 'mitochondrial' pathway that leads to apoptosis. Similarly, several natural defence mechanisms kill melanoma by the same pathways. A corollary to the latter is that survival of melanoma in the host is due to the development of anti-apoptotic mechanisms in melanoma cells. What are these mechanisms? And how might we bypass them to improve the treatment of melanoma?
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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Antineoplastic Agents / therapeutic use
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Apoptosis / drug effects
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Apoptosis / physiology*
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Apoptosis Regulatory Proteins
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Caspase 9
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Caspases / physiology
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Cytochrome c Group / physiology
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DNA Damage
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Enzyme Activation
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Fas Ligand Protein
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Gene Expression Regulation, Neoplastic
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Humans
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Killer Cells, Natural / immunology
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MAP Kinase Signaling System
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Macromolecular Substances
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Melanoma / immunology
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Melanoma / pathology*
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Melanoma / therapy
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Membrane Glycoproteins / physiology*
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Mitochondria / physiology
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Models, Biological
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NF-kappa B / physiology
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Neoplasm Proteins / physiology
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Receptors, Tumor Necrosis Factor / drug effects
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Receptors, Tumor Necrosis Factor / physiology
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Signal Transduction
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T-Lymphocyte Subsets / immunology
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TNF-Related Apoptosis-Inducing Ligand
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Tumor Cells, Cultured
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Tumor Necrosis Factor-alpha / physiology*
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Tumor Suppressor Protein p53 / physiology
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fas Receptor / physiology
Substances
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Antineoplastic Agents
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Apoptosis Regulatory Proteins
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Cytochrome c Group
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FASLG protein, human
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Fas Ligand Protein
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Macromolecular Substances
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Membrane Glycoproteins
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NF-kappa B
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Neoplasm Proteins
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Receptors, Tumor Necrosis Factor
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TNF-Related Apoptosis-Inducing Ligand
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TNFSF10 protein, human
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Tumor Necrosis Factor-alpha
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Tumor Suppressor Protein p53
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fas Receptor
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CASP9 protein, human
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Caspase 9
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Caspases