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PLoS ONE, ISSN 1932-6203, 05/2014, Volume 9, Issue 5, p. e92596
Background: Large-scale genomic analyses of patient cohorts have revealed extensive heterogeneity between individual tumors, contributing to treatment failure... 
CANCER-CELLS | METASTATIC MELANOMA | FACTOR-BETA | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | EPIGENETIC REGULATION | NEURAL CREST | SOX10 | PROMOTES | TUMOR MICROENVIRONMENT | CD133 | Meta-Analysis as Topic | Antigens, CD - biosynthesis | Humans | Peptides - genetics | Male | Antigens, CD - genetics | Gene Knockdown Techniques | Neoplastic Stem Cells - metabolism | Melanoma - genetics | Nerve Tissue Proteins - biosynthesis | Neoplastic Stem Cells - pathology | Female | Neoplasm Proteins - genetics | SOXE Transcription Factors - biosynthesis | Glycoproteins - genetics | Melanoma - metabolism | Receptors, Nerve Growth Factor - biosynthesis | Neoplasm Proteins - biosynthesis | Melanoma - pathology | AC133 Antigen | Nerve Tissue Proteins - genetics | Receptors, Nerve Growth Factor - genetics | Glycoproteins - biosynthesis | Animals | Cell Line, Tumor | Mice, Inbred NOD | Biomarkers, Tumor - genetics | Mice | Biomarkers, Tumor - biosynthesis | SOXE Transcription Factors - genetics | Nerve growth factor | Drug resistance | Analysis | Genomics | Stem cells | Transcription factors | Laboratories | Genes | Genomes | Metastasis | Cell surface | Metastases | Genotype & phenotype | Heterogeneity | Rodents | Fibroblasts | Growth factors | Antigens | Colonies | Markers | Melanoma | Cell division | Tumorigenicity | Gene expression | Neural crest | Sox10 protein | Pathology | Properties (attributes) | Cell lines | Epigenetics | Neural stem cells | Surface markers | Cancer | Tumors
Journal Article
PLoS Genetics, ISSN 1553-7390, 12/2010, Volume 6, Issue 12, pp. 1 - 19
Journal Article
Molecular Systems Biology, ISSN 1744-4292, 07/2013, Volume 9, Issue 1, pp. 673 - n/a
The epidermal growth factor receptor (EGFR) signaling network is activated in most solid tumors, and small‐molecule drugs targeting this network are... 
mathematical modeling | modular response analysis | EGFR signaling | cancer | signal transduction | PATHWAYS | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACQUIRED-RESISTANCE | ERK ACTIVATION | CELL-DEATH | REGULATED KINASE | COLON-CANCER | GROWTH | KRAS | NEGATIVE FEEDBACK | AZD6244 ARRY-142886 | Receptor, Epidermal Growth Factor - genetics | ras Proteins - genetics | Protein Interaction Maps - drug effects | Colorectal Neoplasms - genetics | Humans | ras Proteins - metabolism | Transplantation, Heterologous | Phosphatidylinositol 3-Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - genetics | Proto-Oncogene Proteins c-akt - genetics | Receptor, Epidermal Growth Factor - metabolism | Colorectal Neoplasms - drug therapy | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Drug Therapy, Combination | Proto-Oncogene Proteins c-akt - metabolism | Colorectal Neoplasms - metabolism | Proto-Oncogene Proteins B-raf - metabolism | Phosphatidylinositol 3-Kinases - genetics | Animals | Signal Transduction - drug effects | Tumor Burden - drug effects | Mice, Nude | Proto-Oncogene Proteins B-raf - genetics | Cell Line, Tumor | Mice | Models, Genetic | Protein Kinase Inhibitors - pharmacology | Colorectal Neoplasms - pathology | Drug Screening Assays, Antitumor | Therapy | Phosphorylation | Xenotransplantation | Crosstalk | Colorectal carcinoma | Colorectal cancer | AKT protein | Genomes | Drug delivery | Kinases | Inactivation | Cancer therapies | Signal transduction | Negative feedback | Epidermal growth factor | Feedback | Xenografts | Mathematical models | Inhibition | Growth factors | Deoxyribonucleic acid--DNA | Deactivation | Epidermal growth factor receptors | Tumor cells | Extracellular signal-regulated kinase | MAP kinase | Perturbation | Tumor cell lines | 1-Phosphatidylinositol 3-kinase | Studies | Signaling | Cell lines | Ordinary differential equations | Mutation | Solid tumors | Combinatorial analysis | Tumors | Cancer
Journal Article
Molecular Systems Biology, ISSN 1744-4292, 2012, Volume 8, Issue 1, pp. 601 - n/a
RAS mutations are highly relevant for progression and therapy response of human tumours, but the genetic network that ultimately executes the oncogenic effects... 
oncogenes | modular response analysis | cancer systems biology | signal transduction | ovarian carcinoma model | PROMOTES GROWTH | KLF6 TUMOR-SUPPRESSOR | BIOCHEMISTRY & MOLECULAR BIOLOGY | THYROID-CELLS | EPITHELIAL-CELLS | FEEDBACK-REGULATION | PROSTATE-CANCER | IN-VIVO | GENE-EXPRESSION | NF-KAPPA-B | CELLULAR-TRANSFORMATION | ras Proteins - genetics | Kruppel-Like Factor 6 | Proto-Oncogene Proteins p21(ras) | Epithelial Cells - metabolism | Epithelial Cells - drug effects | Humans | ras Proteins - metabolism | Gene Regulatory Networks - physiology | HMGA2 Protein - antagonists & inhibitors | Ovarian Neoplasms - genetics | HMGA2 Protein - metabolism | Cell Transformation, Neoplastic - genetics | Kruppel-Like Transcription Factors - metabolism | Microarray Analysis | HMGA2 Protein - genetics | Female | Ovary - drug effects | Ovarian Neoplasms - metabolism | Gene Expression Regulation, Neoplastic - physiology | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins c-fos - antagonists & inhibitors | Proto-Oncogene Proteins - antagonists & inhibitors | Ovary - pathology | Signal Transduction | RNA, Small Interfering - pharmacology | Proto-Oncogene Proteins c-fos - metabolism | Rats | Epithelial Cells - pathology | Proto-Oncogene Proteins - genetics | Transcription Factors - antagonists & inhibitors | Transcription Factors - genetics | Reverse Transcriptase Polymerase Chain Reaction | Cell Transformation, Neoplastic - metabolism | Transcription Factors - metabolism | Animals | Analysis of Variance | Models, Biological | Cell Line, Tumor | Proto-Oncogene Proteins c-fos - genetics | Cell Proliferation - drug effects | Genes, ras | Kruppel-Like Transcription Factors - antagonists & inhibitors | Kruppel-Like Transcription Factors - genetics | RNA, Small Interfering - metabolism | Phenotypes | Deregulation | Transcription factors | Ovarian carcinoma | Reverse engineering | Epithelial cells | Gene regulation | Perturbation | Kinases | Gene expression | K-Ras protein | Ovarian cancer | Gene silencing | Engineering | Signal transduction | Algorithms | DNA microarrays | Predictions | Ordinary differential equations | Mutation | Human behavior | Growth factors | Functional groups | Tumors
Journal Article