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Journal Article
Journal Article
American Journal of Pathology, The, ISSN 0002-9440, 2010, Volume 177, Issue 3, pp. 1053 - 1064
Journal Article
Nature, ISSN 0028-0836, 11/2015, Volume 527, Issue 7579, pp. 525 - 530
Diagnosis of pancreatic ductal adenocarcinoma (PDAC) is associated with a dismal prognosis despite current best therapies; therefore new treatment strategies... 
STEM-CELLS | REPRESSION | DUCTAL ADENOCARCINOMA | MULTIDISCIPLINARY SCIENCES | GENE-EXPRESSION | RESISTANCE | TUMOR-CELLS | PROLIFERATION | EMT | SNAIL | BETA | Adenocarcinoma - pathology | Pancreatic Neoplasms - metabolism | Transcription Factors - deficiency | Carcinoma, Pancreatic Ductal - metabolism | Deoxycytidine - pharmacology | Male | Nucleoside Transport Proteins - metabolism | Twist-Related Protein 1 - deficiency | Pancreatic Neoplasms - drug therapy | Deoxycytidine - therapeutic use | Adenocarcinoma - metabolism | Neoplasm Invasiveness - pathology | Epithelial-Mesenchymal Transition | Female | Snail Family Transcription Factors | Disease Models, Animal | Pancreatic Neoplasms - pathology | Pancreatic Neoplasms - genetics | Transcription Factors - genetics | Adenocarcinoma - drug therapy | Carcinoma, Pancreatic Ductal - pathology | Disease Progression | Transcription Factors - metabolism | Carcinoma, Pancreatic Ductal - drug therapy | Animals | Neoplasm Metastasis - pathology | Survival Analysis | Twist-Related Protein 1 - genetics | Cell Proliferation - drug effects | Mice | Twist-Related Protein 1 - metabolism | Deoxycytidine - analogs & derivatives | Drug Resistance, Neoplasm - drug effects | Care and treatment | Prognosis | Diagnosis | Pancreatic cancer | Analysis | Cancer cells | Studies | Cell growth | Chemotherapy | Transcription factors | Medical prognosis | Metastasis | Gene expression | Cancer therapies | Tumors | Apoptosis | Index Medicus
Journal Article
Nature Cell Biology, ISSN 1465-7392, 03/2010, Volume 12, Issue 3, pp. 247 - 256
MicroRNAs (miRNAs) are increasingly implicated in regulating the malignant progression of cancer. Here we show that miR-9, which is upregulated in breast... 
ADHESION | STEM-CELLS | INVASION | N-MYC | C-MYC | TUMOR ANGIOGENESIS | HUMAN BREAST-CANCER | MESENCHYMAL TRANSITION | EXPRESSION | MAMMARY EPITHELIAL-CELLS | CELL BIOLOGY | Oncogene Proteins - genetics | RNA, Small Interfering - genetics | Protein Binding - genetics | Cell Proliferation | MicroRNAs - antagonists & inhibitors | Cadherins - metabolism | Gene Expression - genetics | Humans | 3' Untranslated Regions - genetics | Vascular Endothelial Growth Factor A - genetics | N-Myc Proto-Oncogene Protein | Cadherins - genetics | Oncogene Proteins - metabolism | Vascular Endothelial Growth Factor A - blood | Epithelial Cells - pathology | DNA - metabolism | Neuroblastoma - diagnosis | beta Catenin - metabolism | Down-Regulation - genetics | Cell Line, Tumor | Mice, Inbred NOD | Mice | Mice, Inbred BALB C | Neovascularization, Pathologic - metabolism | Neuroblastoma - metabolism | Proto-Oncogene Proteins c-myc - genetics | Histones - metabolism | MicroRNAs - physiology | Neoplasms - metabolism | Epithelial Cells - metabolism | Vimentin - metabolism | Lung Neoplasms - pathology | Breast Neoplasms - metabolism | Neovascularization, Pathologic - pathology | Neoplasms - blood | Transfection | Lung Neoplasms - secondary | Neoplasm Invasiveness - pathology | Female | Nuclear Proteins - genetics | Gene Expression Regulation, Neoplastic - physiology | Neuroblastoma - pathology | Cell Line | Neuroblastoma - genetics | Nuclear Proteins - metabolism | Gene Dosage | Mice, SCID | Proto-Oncogene Proteins c-myc - metabolism | beta Catenin - genetics | Neoplasm Metastasis - genetics | Animals | Breast Neoplasms - pathology | Neoplasm Metastasis - pathology | Signal Transduction - physiology | Transplantation, Heterologous - pathology | Neoplasm Invasiveness - genetics | Neoplasms - pathology | MicroRNA | Physiological aspects | Cadherins | Development and progression | Genetic aspects | Metastasis | Research | Oncogenes | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 11/2015, Volume 527, Issue 7579, pp. 472 - 476
The role of epithelial-to-mesenchymal transition (EMT) in metastasis is a longstanding source of debate, largely owing to an inability to monitor transient and... 
CANCER-CELLS | STEM-CELLS | THERAPY | MULTIDISCIPLINARY SCIENCES | RESISTANCE | INDUCTION | MODEL | MIR-200 FAMILY | EXPRESSION | BREAST | PLASTICITY | Lung Neoplasms - drug therapy | Apoptosis - drug effects | Antineoplastic Agents, Alkylating - pharmacology | Epithelial-Mesenchymal Transition - drug effects | Lung Neoplasms - pathology | Male | Epithelial-Mesenchymal Transition - genetics | Cyclophosphamide - therapeutic use | Mammary Neoplasms, Experimental - genetics | Cell Tracking | Lung Neoplasms - secondary | Neoplasm Metastasis - drug therapy | Mammary Neoplasms, Experimental - pathology | Female | Disease Models, Animal | Mammary Neoplasms, Experimental - drug therapy | Lung Neoplasms - genetics | Reproducibility of Results | Disease Progression | Antineoplastic Agents, Alkylating - therapeutic use | Cell Lineage | Neoplasm Metastasis - genetics | Drug Resistance, Neoplasm - genetics | Animals | Neoplasm Metastasis - pathology | Cyclophosphamide - pharmacology | Cell Proliferation - drug effects | Mice | MicroRNAs - genetics | Drug Resistance, Neoplasm - drug effects | Development and progression | Metastasis | Drug resistance | Cell differentiation | Health aspects | Lung cancer | Chemotherapy | Analysis | Stem cells | Cancer | Studies | Genotype & phenotype | Transgenic animals | Rodents | Morphology | Fibroblasts | Breast cancer | Cancer therapies | Tumors | Index Medicus
Journal Article