Abstract
Metastasis remains the primary cause of patient morbidity and mortality in solid tumors and is due to the action of a large number of tumor-autonomous and non-autonomous factors. Here we report the results of a genome-wide integrated strategy to identify novel metastasis susceptibility candidate genes and molecular pathways in breast cancer metastasis. This analysis implicates a number of transcriptional regulators and suggests cell-mediated immunity is an important determinant. Moreover, the analysis identified novel or FDA-approved drugs as potentially useful for anti-metastatic therapy. Further explorations implementing this strategy may therefore provide a variety of information for clinical applications in the control and treatment of advanced neoplastic disease.
Publication types
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Research Support, N.I.H., Intramural
MeSH terms
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Animals
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Cell Adhesion Molecules / genetics
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Cell Line, Tumor
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Female
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Gene Expression Profiling
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Gene Expression Regulation, Neoplastic
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Genetic Predisposition to Disease*
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Genome-Wide Association Study
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Kruppel-Like Transcription Factors / biosynthesis
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Kruppel-Like Transcription Factors / genetics
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Lung Neoplasms / secondary*
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Mammary Neoplasms, Animal / diagnosis
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Mammary Neoplasms, Animal / genetics*
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Mammary Neoplasms, Animal / pathology
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Mice
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Mice, Inbred NZB
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Mice, Transgenic
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Nectins
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Promyelocytic Leukemia Zinc Finger Protein
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RNA Interference
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RNA, Small Interfering / genetics
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Rosiglitazone
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Thiazolidinediones / pharmacology
Substances
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Cell Adhesion Molecules
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Kruppel-Like Transcription Factors
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Nectins
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Promyelocytic Leukemia Zinc Finger Protein
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RNA, Small Interfering
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Thiazolidinediones
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Zbtb16 protein, mouse
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Rosiglitazone