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The EMBO Journal, ISSN 0261-4189, 02/2011, Volume 30, Issue 4, pp. 770 - 782
Notch signalling is important for development and tissue homeostasis and activated in many human cancers. Nevertheless, mutations in Notch pathway components... 
miR‐200 | ZEB1 | EMT | Notch | stemness | miR-200 | STEM-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOWN-REGULATION | PHENOTYPE | E-CADHERIN | MIR-200 FAMILY | REPRESSORS ZEB1 | CELL BIOLOGY | EPITHELIAL-MESENCHYMAL TRANSITION | BREAST-CANCER | COLORECTAL-CANCER | Receptors, Notch - metabolism | Humans | Receptors, Notch - genetics | Gene Knockdown Techniques | Intercellular Signaling Peptides and Proteins - physiology | DNA-Binding Proteins - metabolism | Intercellular Signaling Peptides and Proteins - metabolism | Neoplasms - genetics | Membrane Proteins - physiology | Serrate-Jagged Proteins | Base Sequence | Membrane Proteins - metabolism | Nuclear Proteins - genetics | Jagged-1 Protein | Calcium-Binding Proteins - metabolism | Transcription Factors - physiology | DNA-Binding Proteins - antagonists & inhibitors | Membrane Proteins - genetics | Cells, Cultured | Intercellular Signaling Peptides and Proteins - genetics | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Signal Transduction - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Homeodomain Proteins - genetics | Transcription Factors - metabolism | Models, Biological | Calcium-Binding Proteins - physiology | Homeodomain Proteins - antagonists & inhibitors | Nuclear Proteins - antagonists & inhibitors | Signal Transduction - physiology | MicroRNAs - genetics | Feedback, Physiological - physiology | MicroRNAs - physiology | Homeodomain Proteins - physiology | Calcium-Binding Proteins - genetics | Zinc Finger E-box-Binding Homeobox 1 | Proteins | Signal transduction | Cellular biology | Molecular biology | Gene expression | Cancer | Index Medicus
Journal Article
Nature Medicine, ISSN 1078-8956, 08/2012, Volume 18, Issue 8, pp. 1239 - 1247
The inactivation of the p53 tumor suppressor pathway, which often occurs through mutations in TP53 (encoding tumor protein 53) is a common step in human... 
MEDICINE, RESEARCH & EXPERIMENTAL | N-RAS | BIOCHEMISTRY & MOLECULAR BIOLOGY | TUMOR-SUPPRESSOR ACTIVITY | STAPLED P53 | BRAF | MALIGNANT-MELANOMA | P53 PATHWAY | CELL-DEATH | CELL BIOLOGY | BREAST-CANCER | METASTATIC MELANOMA | IN-VIVO | Up-Regulation | Proto-Oncogene Proteins c-mdm2 - genetics | Tumor Suppressor Protein p53 - antagonists & inhibitors | Apoptosis - drug effects | Humans | Neoplasm Proteins - physiology | Gene Expression Regulation, Neoplastic | Recombinant Fusion Proteins - physiology | Skin Neoplasms - chemistry | Male | Melanocytes - metabolism | Neoplasm Proteins - antagonists & inhibitors | Cell Line, Tumor - transplantation | Proto-Oncogene Proteins - biosynthesis | Tumor Suppressor Protein p53 - physiology | Cell-Penetrating Peptides - pharmacology | Nuclear Proteins - biosynthesis | Female | Antineoplastic Agents - pharmacology | Neoplasm Proteins - genetics | Nuclear Proteins - genetics | Cell Line, Tumor - metabolism | Melanoma - chemistry | Proto-Oncogene Proteins c-mdm2 - biosynthesis | Proto-Oncogene Proteins - antagonists & inhibitors | Tumor Stem Cell Assay | Membrane Proteins - genetics | Neoplasm Proteins - biosynthesis | Melanoma, Experimental - etiology | Mice, Inbred C57BL | Mice, Transgenic | Proto-Oncogene Proteins - genetics | Melanoma - pathology | Melanoma - secondary | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | Melanoma, Experimental - genetics | GTP Phosphohydrolases - genetics | Keratinocytes - metabolism | Mice, Nude | Nuclear Proteins - antagonists & inhibitors | Proto-Oncogene Proteins - physiology | Signal Transduction - physiology | Mice | Nuclear Proteins - physiology | Drug Resistance, Neoplasm - physiology | Drug Resistance, Neoplasm - drug effects | Care and treatment | Gene mutations | Melanoma | Diagnosis | Research | Gene expression | Identification and classification | Skin cancer | Proteins | Cell growth | Mutation | Cell cycle | Index Medicus
Journal Article
Gastroenterology, ISSN 0016-5085, 2013, Volume 144, Issue 7, pp. 1530 - 1542.e12
Journal Article
Nature Structural & Molecular Biology, ISSN 1545-9993, 10/2010, Volume 17, Issue 10, pp. 1247 - 1254
Inherited mutations in human PALB2 are associated with a predisposition to breast and pancreatic cancers. PALB2's tumor-suppressing effect is thought to be... 
POLY(ADP-RIBOSE) POLYMERASE | COMPLEX | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOUBLE-STRAND BREAKS | HISTONE H2AX | FANCONI-ANEMIA | CELL BIOLOGY | RAD51 | BIOPHYSICS | IN-VIVO | SUSCEPTIBILITY GENE | D-LOOP FORMATION | DNA-REPAIR | Recombination, Genetic - physiology | DNA, Neoplasm - metabolism | Humans | Neoplasm Proteins - physiology | DNA Repair - physiology | Molecular Sequence Data | Structure-Activity Relationship | DNA Breaks, Double-Stranded | BRCA2 Protein - physiology | Breast Neoplasms - metabolism | Base Sequence | Tumor Suppressor Proteins - chemistry | Tumor Suppressor Proteins - genetics | Female | Protein Interaction Domains and Motifs | Nuclear Proteins - genetics | Nucleic Acid Conformation | Fanconi Anemia Complementation Group N Protein | Peptide Fragments - metabolism | Neoplasm Proteins - chemistry | Nuclear Proteins - chemistry | Poly(ADP-ribose) Polymerase Inhibitors | Protein Interaction Mapping | Tumor Suppressor Proteins - physiology | Peptide Fragments - chemistry | Apoptosis Regulatory Proteins | Models, Biological | Rad51 Recombinase - chemistry | Rad51 Recombinase - physiology | BRCA2 Protein - chemistry | Nuclear Proteins - physiology | Poly (ADP-Ribose) Polymerase-1 | Breast cancer | Genetic aspects | Research | BRCA mutations | Ovarian cancer | Proteins | Mutation | Molecular biology | Prostate cancer | Index Medicus | homologous recombination | BRCA2 | PALB2
Journal Article
Nature Cell Biology, ISSN 1465-7392, 08/2010, Volume 12, Issue 8, pp. 781 - 790
In eukaryotic cells, autophagy is a highly conserved self-digestion process to promote cell survival in response to nutrient starvation and other metabolic... 
UBIQUITINATION | ACTIVATION | INHIBITION | GENE | CATENIN PATHWAY | TUMOR-SUPPRESSOR PROTEIN | BETA-CATENIN | TUMORIGENESIS | REQUIRES DIRECT BINDING | LIGASE | CELL BIOLOGY | Immunohistochemistry | Colonic Neoplasms - genetics | Protein Binding - genetics | Immunoprecipitation | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Sequestosome-1 Protein | Humans | Immunoblotting | Autophagy - physiology | Phosphoproteins - metabolism | Wnt Proteins - metabolism | Colonic Neoplasms - metabolism | Microscopy, Immunoelectron | Ubiquitination | Membrane Proteins - physiology | Apoptosis Regulatory Proteins - genetics | Autophagy - genetics | Dishevelled Proteins | Beclin-1 | Cell Line | Membrane Proteins - genetics | Signal Transduction - genetics | Reverse Transcriptase Polymerase Chain Reaction | Microtubule-Associated Proteins - physiology | Adaptor Proteins, Signal Transducing - physiology | Models, Biological | Adaptor Proteins, Signal Transducing - genetics | Fluorescent Antibody Technique | Cell Line, Tumor | Apoptosis Regulatory Proteins - physiology | Signal Transduction - physiology | Wnt3 Protein | HeLa Cells | Adaptor Proteins, Signal Transducing - metabolism | Protein Binding - physiology | Autophagy (Cytology) | Cellular signal transduction | Research | Ubiquitin-proteasome system | Index Medicus
Journal Article
Cell, ISSN 0092-8674, 2007, Volume 131, Issue 2, pp. 271 - 285
The chromosomal passenger complex (CPC) is a key regulator of chromosome segregation and cytokinesis. CPC functions are connected to its localization. The... 
CELLBIO | PROTEINS | CELLCYCLE | MITOSIS | AURORA-B KINASE | CYTOKINESIS | PROTEIN | HELA-CELLS | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOTIC SPINDLE | CLEAVAGE FURROW | CENTROMERE | SPLICE VARIANTS | CELL BIOLOGY | Microtubule-Associated Proteins - chemistry | Microtubule-Associated Proteins - genetics | Humans | Neoplasm Proteins - physiology | Molecular Sequence Data | Cell Cycle Proteins - chemistry | Aurora Kinase B | Spindle Apparatus - genetics | Cell Cycle Proteins - genetics | Chromosome Segregation - physiology | Chromosomal Proteins, Non-Histone - physiology | Neoplasm Proteins - genetics | Spindle Apparatus - physiology | Dimerization | Recombinant Proteins - metabolism | Amino Acid Sequence | Inhibitor of Apoptosis Proteins | Protein-Serine-Threonine Kinases - physiology | Protein-Serine-Threonine Kinases - genetics | Models, Molecular | Recombinant Proteins - chemistry | Centromere - physiology | Neoplasm Proteins - chemistry | Recombinant Proteins - genetics | Aurora Kinases | Cytokinesis | Chromosomal Proteins, Non-Histone - genetics | Microtubule-Associated Proteins - physiology | Centromere - genetics | Protein Binding | Protein-Serine-Threonine Kinases - chemistry | HeLa Cells | Mutation | Cell Cycle Proteins - physiology | Chromosomal Proteins, Non-Histone - chemistry | Chromosome Segregation - genetics | Index Medicus
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 05/2015, Volume 125, Issue 5, pp. 2123 - 2135
The G protein coupled estrogen receptor (GPER) mediates both the genomic and nongenomic effects of estrogen and has been implicated in breast cancer... 
MIGRATION | MEDICINE, RESEARCH & EXPERIMENTAL | DRUG-THERAPY | ACTIVATION | PATHWAY | GROWTH | GPR30 | PROTEIN-COUPLED RECEPTORS | SIZE-CONTROL | TAZ | 17-BETA-ESTRADIOL | Carcinoma, Ductal, Breast - genetics | Neoplasms, Hormone-Dependent - metabolism | Protein-Serine-Threonine Kinases - analysis | Phosphorylation | Estrogens - pharmacology | Humans | Neoplasm Proteins - physiology | Gene Expression Regulation, Neoplastic | Neoplasms, Hormone-Dependent - physiopathology | Breast Neoplasms - physiopathology | Breast Neoplasms - metabolism | Neoplasms, Hormone-Dependent - genetics | RNA Interference | Phospholipase C beta - physiology | Cell Division | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Female | Transcription, Genetic | Phosphoproteins - physiology | Receptors, G-Protein-Coupled - drug effects | Carcinoma, Ductal, Breast - metabolism | Protein-Serine-Threonine Kinases - metabolism | Receptors, G-Protein-Coupled - physiology | Estrogens - physiology | GTP-Binding Protein alpha Subunits, Gq-G11 - genetics | rho-Associated Kinases - physiology | Transcription Factors - physiology | Protein Kinase C - physiology | Carcinoma, Ductal, Breast - physiopathology | Protein-Serine-Threonine Kinases - physiology | GTP-Binding Protein alpha Subunits, Gq-G11 - antagonists & inhibitors | GTP-Binding Protein alpha Subunits, Gq-G11 - physiology | Tumor Suppressor Proteins - physiology | Adaptor Proteins, Signal Transducing - physiology | Receptors, Estrogen - drug effects | Animals | Breast Neoplasms - genetics | Cell Transformation, Neoplastic | Signal Transduction - physiology | Mice | Mice, Inbred BALB C | Protein Processing, Post-Translational | Cell Movement | Receptors, Estrogen - physiology | Tumor Suppressor Proteins - analysis | Cell receptors | Estrogen | Physiological aspects | Development and progression | Breast cancer | Cellular signal transduction | Research | Studies | Kinases | Rodents | Index Medicus | Abridged Index Medicus | Oncology
Journal Article
The Journal of Cell Biology, ISSN 0021-9525, 1/2005, Volume 168, Issue 3, pp. 441 - 452
Invadopodia are actin-rich membrane protrusions with a matrix degradation activity formed by invasive cancer cells. We have studied the molecular mechanisms of... 
Receptors | Microfilaments | Actin depolymerizing factors | Small interfering RNA | Actins | Antibodies | Polymerization | Cultured cells | Cell membranes | Cells | CARCINOMA-CELLS | GROWTH-FACTOR RECEPTOR | MAMMARY ADENOCARCINOMA | ACTIN POLYMERIZATION | LAMELLIPOD EXTENSION | N-WASP | EXTRACELLULAR-MATRIX | SPECIALIZED SURFACE PROTRUSIONS | ALDRICH-SYNDROME PROTEIN | INVASIVE CELLS | CELL BIOLOGY | Oncogene Proteins - genetics | RNA, Small Interfering - genetics | Epidermal Growth Factor - physiology | Cytoskeletal Proteins - genetics | Actins - metabolism | Microfilament Proteins - physiology | Extracellular Matrix - metabolism | cdc42 GTP-Binding Protein - metabolism | Quinazolines | Oncogene Proteins - physiology | Cell Movement - physiology | Transfection | Cytoskeletal Proteins - metabolism | Microfilament Proteins - metabolism | Cytoskeletal Proteins - physiology | Wiskott-Aldrich Syndrome Protein Family | Microfilament Proteins - genetics | Carrier Proteins - physiology | Nerve Tissue Proteins - physiology | Wiskott-Aldrich Syndrome Protein, Neuronal | Cell Surface Extensions - metabolism | Neoplasm Invasiveness | RNA, Small Interfering - pharmacology | Enzyme Inhibitors - pharmacology | Oncogene Proteins - metabolism | Rats | Tyrphostins - pharmacology | Actin Depolymerizing Factors | cdc42 GTP-Binding Protein - physiology | Nerve Tissue Proteins - genetics | Fibronectins - metabolism | Nerve Tissue Proteins - metabolism | Carrier Proteins - genetics | Adaptor Proteins, Signal Transducing - physiology | Animals | Carrier Proteins - metabolism | GRB2 Adaptor Protein | Models, Biological | cdc42 GTP-Binding Protein - genetics | Cell Surface Extensions - drug effects | Adaptor Proteins, Signal Transducing - genetics | Actin-Related Protein 2 | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Actin-Related Protein 3 | Adaptor Proteins, Signal Transducing - metabolism | Microscopy, Fluorescence | Cell Surface Extensions - physiology | Epidermal growth factor | Metastasis | Cancer invasiveness | Cancer cells | Cellular biology | Cancer | Index Medicus
Journal Article
Cancer Research, ISSN 0008-5472, 08/2011, Volume 71, Issue 15, pp. 5296 - 5306
The switch of tumor cells from an epithelial to a mesenchymal-like phenotype [designated as epithelial-to-mesenchymal transition (EMT)] is known to induce... 
BREAST-CARCINOMA | STEM-CELLS | IN-VITRO | ONCOLOGY | SERUM INTERLEUKIN-8 | PROSTATE-CANCER | METASTATIC PHENOTYPE | MALIGNANT-MELANOMA | TUMOR-GROWTH | EXPRESSION | PROGRESSION | Receptors, Interleukin-8 - genetics | T-Box Domain Proteins - physiology | Breast Neoplasms - secretion | Fibronectins - biosynthesis | Carcinoma - secretion | T-Box Domain Proteins - antagonists & inhibitors | Epithelial-Mesenchymal Transition - physiology | Humans | Neoplasm Proteins - physiology | T-Box Domain Proteins - biosynthesis | Culture Media, Conditioned - pharmacology | Culture Media, Serum-Free | Interleukin-8 - physiology | Neoplasm Proteins - antagonists & inhibitors | Bystander Effect | Tumor Microenvironment - physiology | Recombinant Fusion Proteins - antagonists & inhibitors | Cell Line, Tumor - pathology | Receptors, Interleukin-8 - biosynthesis | Cell Line, Tumor - secretion | Gene Expression Regulation, Neoplastic - drug effects | Intercellular Signaling Peptides and Proteins - secretion | Carcinoma - pathology | Neoplasm Proteins - genetics | Pancreatic Neoplasms - secretion | Promoter Regions, Genetic | Chemokines - secretion | Neoplasm Invasiveness | Neoplasm Proteins - biosynthesis | Pancreatic Neoplasms - pathology | RNA, Small Interfering - pharmacology | Cytokines - secretion | Fetal Proteins - physiology | Fetal Proteins - antagonists & inhibitors | Fetal Proteins - biosynthesis | T-Box Domain Proteins - genetics | Breast Neoplasms - pathology | Fetal Proteins - genetics | Fibronectins - genetics | Cell Movement | Index Medicus | Brachyury | tumor microenvironment | IL-8 | metastasis | EMT
Journal Article