Expression of miR-200c in claudin-low breast cancer alters stem cell functionality, enhances chemosensitivity and reduces metastatic potential

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Predicting Drug Responsiveness in Human Cancers Using Genetically Engineered Mice

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Epigenetic modulation of the miR-200 family is associated with transition to a breast cancer stem-cell-like state

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Down Regulation of miR200c Promotes Radiation-Induced Thymic Lymphoma by Targeting BMI1

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The miRNA-200 family and miRNA-9 exhibit differential expression in primary versus corresponding metastatic tissue in breast cancer

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EZH2 Promotes Expansion of Breast Tumor Initiating Cells through Activation of RAF1-β-Catenin Signaling

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MicroRNA-200c Represses Migration and Invasion of Breast Cancer Cells by Targeting Actin-Regulatory Proteins FHOD1 and PPM1F

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An autocrine TGF-β/ZEB/miR-200 signaling network regulates establishment and maintenance of epithelial-mesenchymal transition

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miR-200 Inhibits Lung Adenocarcinoma Cell Invasion and Metastasis by Targeting Flt1/VEGFR1

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Characterization of a Naturally Occurring Breast Cancer Subset Enriched in Epithelial-to-Mesenchymal Transition and Stem Cell Characteristics

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Downregulation of miRNA-200c Links Breast Cancer Stem Cells with Normal Stem Cells

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Epithelial-Mesenchymal Transitions in Development and Disease

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miR-200 Enhances Mouse Breast Cancer Cell Colonization to Form Distant Metastases

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Loss of E-Cadherin Promotes Metastasis via Multiple Downstream Transcriptional Pathways

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Identification of Tumor-Initiating Cells in a p53-Null Mouse Model of Breast Cancer

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Lentiviral Transduction of Mammary Stem Cells for Analysis of Gene Function during Development and Cancer

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The miR-200 family determines the epithelial phenotype of cancer cells by targeting the E-cadherin repressors ZEB1 and ZEB2

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The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1

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