Abstract
The most common human cancers --lung, breast and prostate -- have a great avidity for bone, leading to painful and untreatable consequences. What makes some cancers, but not others, metastasize to bone, and how do they alter its physiology? Some of the molecular mechanisms that are responsible have recently been identified, and provide new molecular targets for drug development.
MeSH terms
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Bone Neoplasms / drug therapy
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Bone Neoplasms / metabolism
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Bone Neoplasms / secondary*
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Breast Neoplasms / pathology*
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Calcium / metabolism
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Carrier Proteins / metabolism
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Diphosphonates / metabolism
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Diphosphonates / therapeutic use
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Female
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Glycoproteins / metabolism
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Glycoproteins / therapeutic use
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Humans
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Lung Neoplasms / pathology*
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Male
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Membrane Glycoproteins / metabolism
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Osteoprotegerin
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Prostatic Neoplasms / pathology*
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RANK Ligand
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Receptor Activator of Nuclear Factor-kappa B
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Receptors, Cytoplasmic and Nuclear / metabolism
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Receptors, Cytoplasmic and Nuclear / therapeutic use
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Receptors, Tumor Necrosis Factor
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Vitamin D / metabolism
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Vitamin D / therapeutic use
Substances
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Carrier Proteins
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Diphosphonates
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Glycoproteins
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Membrane Glycoproteins
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Osteoprotegerin
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RANK Ligand
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Receptor Activator of Nuclear Factor-kappa B
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Receptors, Cytoplasmic and Nuclear
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Receptors, Tumor Necrosis Factor
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TNFRSF11A protein, human
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TNFRSF11B protein, human
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TNFSF11 protein, human
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Vitamin D
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Calcium