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Molecular Cell, ISSN 1097-2765, 08/2016, Volume 63, Issue 3, pp. 514 - 525
An emerging therapeutic strategy for cancer is to induce selective lethality in a tumor by exploiting interactions between its driving mutations and specific... 
COMBINED INHIBITION | FISSION YEAST | REPAIR | TUMOR MUTATIONS | STRATEGY | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENETIC INTERACTION MAP | DNA-DAMAGE | SACCHAROMYCES-CEREVISIAE | DRUGGABLE GENOME | CHK1 INHIBITION | CELL BIOLOGY | Protein Interaction Maps - drug effects | RecQ Helicases - metabolism | Saccharomyces cerevisiae - genetics | Humans | RecQ Helicases - genetics | Saccharomyces cerevisiae - drug effects | Antineoplastic Agents - therapeutic use | Synthetic Lethal Mutations | Gene Regulatory Networks - drug effects | Molecular Targeted Therapy | Dose-Response Relationship, Drug | Saccharomyces cerevisiae - metabolism | Gene Expression Regulation, Fungal - drug effects | Transfection | RNA Interference | Time Factors | Uterine Cervical Neoplasms - metabolism | Cell Cycle Proteins - genetics | Female | Gene Expression Regulation, Neoplastic - drug effects | Genes, Tumor Suppressor | Uterine Cervical Neoplasms - mortality | Cell Survival - drug effects | Genetic Predisposition to Disease | Cell Cycle Proteins - metabolism | Kaplan-Meier Estimate | Uterine Cervical Neoplasms - drug therapy | Saccharomyces cerevisiae Proteins - genetics | Uterine Cervical Neoplasms - genetics | Phenotype | Signal Transduction - drug effects | Saccharomyces cerevisiae Proteins - metabolism | Biomarkers, Tumor - genetics | Cell Proliferation - drug effects | HeLa Cells | Mutation | Precision Medicine - methods | Antimitotic agents | Care and treatment | Analysis | Drug therapy, Combination | Antineoplastic agents | Health aspects | Phosphotransferases | Cancer | Index Medicus
Journal Article
Cell Host & Microbe, ISSN 1931-3128, 12/2014, Volume 16, Issue 6, pp. 795 - 805
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2017, Volume 12, Issue 7, pp. e0180616 - e0180616
Background Acquired drug resistance to the chemotherapeutic drug irinotecan (the active metabolite of which is SN-38) is one of the significant obstacles in... 
LIVER METASTASES | PROTEIN-INTERACTION NETWORKS | DIFFERENTIAL EXPRESSION | BINDING PEPTIDE | MULTIDISCIPLINARY SCIENCES | ADJUVANT TREATMENT | TUMOR-CELLS | OVARIAN-CANCER | CLINICAL-PRACTICE | MOLECULAR-BASIS | THYMIDYLATE-SYNTHASE | Protein Interaction Maps - drug effects | Colorectal Neoplasms - genetics | Genes, Neoplasm | HCT116 Cells | Humans | Kaplan-Meier Estimate | Gene Expression Profiling | Signal Transduction - genetics | Down-Regulation - drug effects | Up-Regulation - drug effects | Drug Resistance, Neoplasm - genetics | MAP Kinase Signaling System - drug effects | MAP Kinase Signaling System - genetics | Protein Interaction Maps - genetics | Signal Transduction - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Camptothecin - pharmacology | Gene Ontology | Camptothecin - analogs & derivatives | Drug Resistance, Neoplasm - drug effects | Colorectal cancer | Cellular signal transduction | Genetic aspects | Research | Biological markers | Drug therapy | Drug resistance | Correlation | Fibroblast growth factor receptor 9 | Colorectal carcinoma | Genes | Metastasis | Kinases | Autophagy | Cancer therapies | Data bases | Proteins | Disease resistance | Pathways | Surgery | Bioindicators | Deoxyribonucleic acid--DNA | Fibroblast growth factor 2 | Bone morphogenetic protein 6 | Medical research | MAP kinase | RNA polymerase | Gene expression | Patients | Survival | Medicine | Irinotecan | Chemotherapy | Hospitals | Brain-derived neurotrophic factor | Medical prognosis | Cell lines | Biomarkers | Transduction | Clinical medicine | Gene mapping | Protein interaction | Binding sites | Tumors | Cancer | Apoptosis | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article
Journal Article
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 | Index Medicus
Journal Article