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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
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 8/2010, Volume 107, Issue 31, pp. 13836 - 13841
Journal Article
Current Cancer Drug Targets, ISSN 1568-0096, 05/2017, Volume 17, Issue 4, pp. 304 - 310
Background: Silencing of two or more complementary signaling pathways can lead to cell death, while loss of any single genetic function does not show a severe... 
Signaling pathways | Synthetic lethality | Drug resistance | Targeted therapy | Cancer therapy | PARP inhibitors | TARGET | targeted therapy | CELLS | INHIBITOR DINACICLIB MK-7965 | DNA-DAMAGE RESPONSE | REPAIR PATHWAYS | GENOME | PARP INHIBITOR | cancer therapy | signaling pathways | RANDOMIZED PHASE-2 | ONCOLOGY | IN-VIVO | TUMOR-SUPPRESSOR | drug resistance
Journal Article
Cell Reports, ISSN 2211-1247, 10/2019, Volume 29, Issue 1, pp. 118 - 134.e8
The mitogen-activated protein kinase (MAPK) pathway is a critical effector of oncogenic RAS signaling, and MAPK pathway inhibition may be an effective... 
synthetic lethal | KRAS | MEK inhibitor | SHOC2 | Ras | CRISPR-Cas9 screen | DRUG | FEEDBACK ACTIVATION | MELANOMA | STRATEGY | ACQUIRED-RESISTANCE | KRAS-MUTANT LUNG | BRAF | MAPK PATHWAY | PROMOTES | REVEALS | CELL BIOLOGY
Journal Article
细胞研究:英文版, ISSN 1001-0602, 2012, Volume 22, Issue 8, pp. 1227 - 1245
Oncogenic mutations in RAS genes are very common in human cancer, resulting in cells with well-characterized selective advantages, but also less... 
显示 | 合成 | 测定 | 致死作用 | 靶向治疗 | RAS基因 | 突变基因 | 肿瘤细胞 | oncogene addiction | proteasome | synthetic lethal | topoisomerase | KRAS | ONCOLOGY-GROUP | RNAI SCREENS | CDC6 | ADDICTION | GENOME | CELL BIOLOGY | PHASE | RAS ONCOGENE | K-RAS | LUNG ADENOCARCINOMA | HUMAN TUMOR-CELLS | RNA, Small Interfering - genetics | ras Proteins - genetics | Colonic Neoplasms - genetics | Proto-Oncogene Proteins p21(ras) | Humans | Transcriptional Activation | Gene Expression Regulation, Neoplastic | ras Proteins - metabolism | Deoxycytidine - pharmacology | Colonic Neoplasms - metabolism | Gene Knockdown Techniques | Topoisomerase I Inhibitors - pharmacology | RNA Interference | Cell Transformation, Neoplastic - genetics | Cell Cycle Proteins - genetics | Antineoplastic Agents - pharmacology | Nuclear Proteins - genetics | GATA2 Transcription Factor - genetics | Proto-Oncogene Proteins - metabolism | Bortezomib | Topotecan - pharmacology | DNA Topoisomerases, Type I - metabolism | Proteasome Inhibitors - pharmacology | Cell Survival | Cell Cycle Proteins - metabolism | Nuclear Proteins - metabolism | Proto-Oncogene Proteins - genetics | Cell Transformation, Neoplastic - metabolism | Proteasome Endopeptidase Complex - genetics | Colonic Neoplasms - pathology | Alleles | GATA2 Transcription Factor - metabolism | Cell Line, Tumor | Mutation | Proteasome Endopeptidase Complex - metabolism | Pyrazines - pharmacology | Deoxycytidine - analogs & derivatives | Apoptosis | Boronic Acids - pharmacology | RNA, Small Interfering - metabolism | Original
Journal Article
BMC MEDICAL GENOMICS, ISSN 1755-8794, 07/2019, Volume 12, Issue 1, pp. 112 - 112
BackgroundSynthetic lethal interactions (SLIs) that occur between gene pairs are exploited for cancer therapeutics. Studies in the model eukaryote yeast have... 
CELLS | APOPTOSIS | ACTIVATION | RIBOSE | Breast cancer | NETWORKS | Synthetic lethality | Gene expression | IDENTIFICATION | DISCOVERY | GROWTH | GENETICS & HEREDITY | Genetic interaction network | TUMOR-SUPPRESSOR | METABOLIC CONTROL ANALYSIS | Care and treatment | Genetic aspects | Research | Cancer | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2017, Volume 114, Issue 50, pp. E10755 - E10762
Synthetic sick or synthetic lethal (SS/L) screens are a powerful way to identify candidate drug targets to specifically kill tumor cells, but this approach... 
High-throughput screening | RNAi | Drug target discovery | Synthetic lethality | Drosophila | drug target discovery | MULTIDISCIPLINARY SCIENCES | synthetic lethality | high-throughput screening | NETWORKS | DEATH | IDENTIFICATION | INHIBITION | DATABASE | TRANSGENIC RNAI PROJECT | SCREENS | GENETIC INTERACTIONS | LITHIUM | PROGRESSION | Biological Sciences | PNAS Plus
Journal Article