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BMC Cancer, ISSN 1471-2407, 01/2014, Volume 14, Issue 1, p. 32
Background: Although MYC is an attractive therapeutic target for breast cancer treatment, it has proven challenging to inhibit MYC directly, and clinically... 
Cyclin-dependent kinase | Breast cancer | Synthetic lethality | MYC | SYNTHETIC LETHAL | C-MYC | TUMOR-CELLS | PROLIFERATION | INHIBITION | GENE | ONCOLOGY | PATHWAY | ESTROGEN | THERAPEUTIC TARGETS | EXPRESSION | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Phosphorylation | Cyclin-Dependent Kinase 4 - genetics | Humans | Molecular Targeted Therapy | CDC2 Protein Kinase - metabolism | Dose-Response Relationship, Drug | Breast Neoplasms - enzymology | Transfection | Bcl-2-Like Protein 11 | RNA Interference | Female | Antineoplastic Agents - pharmacology | Membrane Proteins - metabolism | Cell Death - drug effects | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Proto-Oncogene Proteins - metabolism | Cyclin-Dependent Kinase 2 - metabolism | CDC2 Protein Kinase - genetics | CDC2 Protein Kinase - antagonists & inhibitors | Cyclin-Dependent Kinase 6 - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase 2 - genetics | Cyclin-Dependent Kinase 6 - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Proto-Oncogene Proteins c-myc - metabolism | Apoptosis Regulatory Proteins - metabolism | Breast Neoplasms - genetics | Signal Transduction - drug effects | Breast Neoplasms - pathology | Cell Cycle Checkpoints - drug effects | Cell Line, Tumor | Cyclin-Dependent Kinase 2 - antagonists & inhibitors | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Proto-Oncogene Proteins c-myc - genetics | Care and treatment | Patient outcomes | Cancer cells | Physiological aspects | Genetic aspects | Research | Risk factors | Cyclins
Journal Article
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 04/2017, Volume 486, Issue 2, pp. 385 - 390
TEA domain transcription factor 4 (TEAD4), which has critical functions in the process of embryonic development, is expressed in various cancers. However, the... 
TEA domain transcription factor 4 | Human oral squamous cell carcinoma | Yes-associated protein (YAP) | TARGET | BIOMARKER | BIOCHEMISTRY & MOLECULAR BIOLOGY | HIPPO PATHWAY | YAP | FAMILY | BIOPHYSICS | DNA | PROGNOSTIC MARKER | EXPRESSION | RNA, Small Interfering - genetics | Cell Proliferation | Carcinoma, Squamous Cell - pathology | Humans | Middle Aged | Male | Cyclin E - genetics | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Cell Nucleus - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Muscle Proteins - antagonists & inhibitors | Transcription, Genetic | Mouth Neoplasms - genetics | Cyclin-Dependent Kinase 2 - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction | Cyclin-Dependent Kinase 2 - genetics | Cyclin-Dependent Kinase 6 - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Muscle Proteins - genetics | Cell Nucleus - genetics | Cyclin D1 - genetics | Mouth Neoplasms - surgery | Cell Line, Tumor | RNA, Small Interfering - metabolism | Cyclin D1 - metabolism | Carcinoma, Squamous Cell - genetics | Carcinoma, Squamous Cell - metabolism | Cyclin-Dependent Kinase 4 - genetics | Gene Expression Regulation, Neoplastic | Carcinoma, Squamous Cell - surgery | Mouth Neoplasms - metabolism | Phosphoproteins - metabolism | DNA-Binding Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Muscle Proteins - metabolism | G1 Phase Cell Cycle Checkpoints | Female | Cyclin-Dependent Kinase 6 - genetics | Transcription Factors - antagonists & inhibitors | Phosphoproteins - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Transcription Factors - metabolism | Adaptor Proteins, Signal Transducing - genetics | Mouth Neoplasms - pathology | Aged | Cyclin E - metabolism | Adaptor Proteins, Signal Transducing - metabolism | Cyclin-Dependent Kinase Inhibitor p27 - genetics | Immunohistochemistry | Medical colleges | Embryonic development | Squamous cell carcinoma | Growth | Analysis | DNA polymerases | Genetic transcription | Health aspects | Development and progression | TRANSCRIPTION FACTORS | CHAIN REACTIONS | BIOLOGICAL MARKERS | CELL PROLIFERATION | CELL CYCLE | INTERACTIONS | 60 APPLIED LIFE SCIENCES | PLANT GROWTH
Journal Article
Cell Metabolism, ISSN 1550-4131, 06/2013, Volume 17, Issue 6, pp. 954 - 964
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 02/2017, Volume 376, Issue 6, pp. 536 - 547
Journal Article
Cancer Discovery, ISSN 2159-8274, 03/2017, Volume 7, Issue 3, pp. 264 - 276
Immune checkpoint inhibitors have shown significant therapeutic responses against tumors containing increased mutation-associated neoantigen load. We have... 
METASTATIC MELANOMA | CTLA-4 BLOCKADE | ONCOLOGY | PD-1 BLOCKADE | COLORECTAL-CANCER | PANCREATIC-CANCER | COPY NUMBER | RESISTANCE | MUTATIONS | SEQUENCING DATA | TUMOR PURITY | Humans | Middle Aged | Antibodies, Monoclonal - therapeutic use | Lung Neoplasms - pathology | Male | Programmed Cell Death 1 Receptor - antagonists & inhibitors | Ipilimumab - pharmacology | Immunotherapy | Ipilimumab - therapeutic use | Janus Kinase 1 - genetics | Adult | Female | Receptors, Antigen, T-Cell - immunology | Cell Cycle Checkpoints - immunology | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Receptors, Antigen, T-Cell - metabolism | Antigens, Neoplasm - immunology | Carcinoma, Non-Small-Cell Lung - genetics | Antibodies, Monoclonal - pharmacology | Janus Kinase 2 - genetics | CTLA-4 Antigen - genetics | Drug Resistance, Neoplasm - immunology | Lung Neoplasms - therapy | CTLA-4 Antigen - immunology | Antineoplastic Agents, Immunological - pharmacology | Carcinoma, Non-Small-Cell Lung - immunology | Carcinoma, Non-Small-Cell Lung - therapy | Drug Resistance, Neoplasm - genetics | Lung Neoplasms - immunology | Antineoplastic Agents, Immunological - therapeutic use | Cell Cycle Checkpoints - drug effects | Receptors, Antigen, T-Cell - genetics | Mutation | Programmed Cell Death 1 Receptor - immunology | Programmed Cell Death 1 Receptor - genetics | Cohort Studies
Journal Article
Cancer, ISSN 0008-543X, 05/2017, Volume 123, Issue 10, pp. 1721 - 1730
BACKGROUND As panel testing becomes more common in clinical practice, it is important to understand the prevalence and trends associated with the pathogenic... 
breast cancer type 1 (BRCA1) | panel testing | hereditary breast and ovarian cancer | BRCA2 | triple‐negative breast cancer | triple-negative breast cancer | POPULATION | BRCA2 MUTATIONS | METAANALYSIS | VARIANTS | RISK | PREVALENCE | FAMILY-HISTORY | SUSCEPTIBILITY GENES | COWDEN-SYNDROME | ONCOLOGY | DIFFUSE GASTRIC-CANCER | Genetic Testing | Age Factors | Humans | Middle Aged | Young Adult | Checkpoint Kinase 2 - genetics | Tumor Suppressor Proteins - genetics | Aged, 80 and over | Genes, BRCA2 | Adult | Female | RNA Helicases - genetics | Lynch Syndrome II - genetics | Neoplastic Syndromes, Hereditary - genetics | Genes, BRCA1 | Nuclear Proteins - genetics | Fanconi Anemia Complementation Group N Protein | Hereditary Breast and Ovarian Cancer Syndrome - genetics | DNA-Binding Proteins - genetics | Fanconi Anemia Complementation Group Proteins | Breast Neoplasms - genetics | Triple Negative Breast Neoplasms - genetics | Aged | Ataxia Telangiectasia Mutated Proteins - genetics | Ubiquitin-Protein Ligases - genetics | Women | Breast cancer | Genetic aspects | Diagnosis | Research | Health aspects | Oncogenes | BRCA2 protein | CHK2 protein | Threonine | BRCA1 protein | Genes | Health risks | Protein C | Genetic screening | DNA helicase | Men | Breast | Ataxia | Ataxia telangiectasia mutated protein | Protein-serine/threonine kinase | Mutation | Health risk assessment | Age | Cancer
Journal Article
Journal of Clinical Oncology, ISSN 0732-183X, 04/2017, Volume 35, Issue 10, pp. 1086 - 1095
Journal Article
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 764 - 17
Checkpoint kinases sense replicative stress to prevent DNA damage. Here we show that the histone deacetylases HDAC1/HDAC2 sustain the phosphorylation of the... 
CANCER-CELLS | RIBONUCLEOTIDE REDUCTASE | CHK1 | TUMOR SUPPRESSION | DNA-DAMAGE RESPONSE | MULTIDISCIPLINARY SCIENCES | GENOME INTEGRITY | DOUBLE-STRAND BREAKS | HISTONE DEACETYLASE INHIBITORS | REPLICATION FORK COLLAPSE | ATR | Phosphorylation | Ataxia Telangiectasia Mutated Proteins - metabolism | Protein-Tyrosine Kinases - metabolism | Humans | Tumor Suppressor Protein p53 - genetics | CDC2 Protein Kinase - metabolism | Checkpoint Kinase 2 - metabolism | Checkpoint Kinase 2 - genetics | Protein-Tyrosine Kinases - genetics | Cell Cycle Proteins - genetics | Nuclear Proteins - genetics | Histone Deacetylase 1 - genetics | Histone Deacetylase 2 - genetics | CDC2 Protein Kinase - genetics | Cell Cycle Proteins - metabolism | Gene Expression Regulation | Protein Phosphatase 2 - genetics | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | Checkpoint Kinase 1 - metabolism | Cell Cycle | Protein Phosphatase 2 - metabolism | Histone Deacetylase 2 - metabolism | Ataxia Telangiectasia Mutated Proteins - genetics | Checkpoint Kinase 1 - genetics | Histone Deacetylase 1 - metabolism | Histone deacetylase | p53 Protein | DNA damage | Serine | Homologous recombination | Homology | Dephosphorylation | Kinases | Phosphatase | Damage prevention | Cell fate | Cell cycle | Inhibition | HDAC2 protein | Null cells | Deoxyribonucleic acid--DNA | Stresses | CHK2 protein | Threonine | Phase transformations | CHK1 protein | Protein-serine/threonine phosphatase | Replication protein A | Protein A | Ablation | Stress | DNA biosynthesis | S phase | Replication | Threonine phosphatase | Phase transition | Tumors | Apoptosis
Journal Article
Journal Article
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 1876 - 15
Journal Article