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Nature communications, ISSN 2041-1723, 2019, Volume 10, Issue 1, pp. 1897 - 17
The cellular decision regarding whether to undergo proliferation or death is made at the restriction (R)-point, which is disrupted in nearly all tumors. The... 
UBIQUITINATION | AML1-ETO | ACETYLATION | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | PROTEINS | QUANTITATIVE-ANALYSIS | POLYCOMB | CANCER | KINASES | FAMILY | Chromatin - metabolism | RNA, Small Interfering - genetics | Myeloid-Lymphoid Leukemia Protein - metabolism | TOR Serine-Threonine Kinases - metabolism | Core Binding Factor Alpha 3 Subunit - antagonists & inhibitors | Humans | Polycomb-Group Proteins - metabolism | TOR Serine-Threonine Kinases - genetics | Cell Cycle Checkpoints - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Chromatin - chemistry | MAP Kinase Kinase 1 - antagonists & inhibitors | Butadienes - pharmacology | Signal Transduction | Epithelial Cells - pathology | MAP Kinase Kinase 1 - metabolism | Imidazoles - pharmacology | Cyclin-Dependent Kinase 4 - metabolism | Piperazines - pharmacology | Cell Cycle Checkpoints - drug effects | Polycomb-Group Proteins - genetics | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cell Line, Tumor | MAP Kinase Kinase 4 - genetics | RNA, Small Interfering - metabolism | ras Proteins - genetics | Core Binding Factor Alpha 3 Subunit - metabolism | Epithelial Cells - metabolism | Nitriles - pharmacology | Cyclin-Dependent Kinase 4 - genetics | Epithelial Cells - drug effects | ras Proteins - metabolism | Drosophila melanogaster - genetics | Chromatin Assembly and Disassembly - drug effects | Drosophila melanogaster - metabolism | MAP Kinase Kinase 1 - genetics | TOR Serine-Threonine Kinases - antagonists & inhibitors | MAP Kinase Kinase 4 - metabolism | HEK293 Cells | MAP Kinase Kinase 4 - antagonists & inhibitors | Chromatin - drug effects | Histone-Lysine N-Methyltransferase - genetics | Drosophila melanogaster - cytology | Gene Expression Regulation | p38 Mitogen-Activated Protein Kinases - genetics | Sirolimus - pharmacology | Animals | Histone-Lysine N-Methyltransferase - metabolism | Myeloid-Lymphoid Leukemia Protein - genetics | Core Binding Factor Alpha 3 Subunit - genetics | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Pyridines - pharmacology | Polycomb group proteins | Regulators | Molecular modelling | S phase | Genes | Cell cycle | Loci | Runx3 protein | Recruitment | Tumors | Chromatin remodeling
Journal Article
Cancer discovery, ISSN 2159-8274, 04/2016, Volume 6, Issue 4, pp. 353 - 367
Journal Article
Molecular cell, ISSN 1097-2765, 2014, Volume 53, Issue 2, pp. 193 - 208
Journal Article
The Journal of experimental medicine, ISSN 0022-1007, 2014, Volume 211, Issue 7, pp. 1379 - 1391
Journal Article
The lancet oncology, ISSN 1470-2045, 2015, Volume 16, Issue 1, pp. 25 - 35
Summary Background Palbociclib (PD-0332991) is an oral, small-molecule inhibitor of cyclin-dependent kinases (CDKs... 
Hematology, Oncology and Palliative Medicine | SURVIVAL | EXEMESTANE | ONCOLOGY | CELL-CYCLE | POSTMENOPAUSAL WOMEN | HER2 | PLUS | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Piperazines - administration & dosage | Triazoles - administration & dosage | Receptor, ErbB-2 - genetics | Humans | Middle Aged | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Receptors, Estrogen - analysis | Molecular Targeted Therapy | North America | Nitriles - administration & dosage | Breast Neoplasms - enzymology | Time Factors | Postmenopause | Female | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Republic of Korea | Aromatase Inhibitors - administration & dosage | Pyridines - administration & dosage | Drug Administration Schedule | Administration, Oral | Biomarkers, Tumor - analysis | Europe | Proportional Hazards Models | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Treatment Outcome | Cyclin-Dependent Kinase 6 - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Breast Neoplasms - drug therapy | Disease-Free Survival | Protein Kinase Inhibitors - administration & dosage | Breast Neoplasms - genetics | Cyclin D1 - genetics | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Breast Neoplasms - pathology | Intention to Treat Analysis | South Africa | Aged | Biomarkers, Tumor - genetics | Receptor, ErbB-2 - analysis | Antimitotic agents | Care and treatment | Oncology, Experimental | Estrogen | Breast cancer | Research | Antineoplastic agents | Phosphotransferases | Cancer
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... 
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
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2019, Volume 116, Issue 36, pp. 17990 - 18000
Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors are an established treatment in estrogen receptor-positive breast cancer and are currently in clinical development in melanoma, a tumor that exhibits high rates of CDK4 activation... 
PRMT5 | METHYLATION | MULTIDISCIPLINARY SCIENCES | VULNERABILITY | COMBINATION | acquired resistance | p53 | BREAST-CANCER | PALBOCICLIB | CDK4 | THERAPEUTIC TARGET | ARGININE METHYLTRANSFERASE | GROWTH | RESISTANCE | MDM4 | METHYLOSOME | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Cyclin-Dependent Kinase 4 - genetics | Humans | Protein-Arginine N-Methyltransferases - antagonists & inhibitors | Drug Resistance, Neoplasm | Tumor Suppressor Protein p53 - genetics | MCF-7 Cells | Melanoma - genetics | HEK293 Cells | Cell Cycle Proteins - genetics | Protein-Arginine N-Methyltransferases - genetics | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Melanoma - metabolism | Proto-Oncogene Proteins - metabolism | Cyclin-Dependent Kinase 2 - metabolism | Cell Cycle Proteins - metabolism | Cyclin-Dependent Kinase 6 - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase 2 - genetics | Proto-Oncogene Proteins - genetics | Cyclin-Dependent Kinase 6 - metabolism | Melanoma - pathology | Cyclin-Dependent Kinase 4 - metabolism | Piperazines - pharmacology | Protein-Arginine N-Methyltransferases - metabolism | Melanoma - drug therapy | Protein Kinase Inhibitors - pharmacology | Pyridines - pharmacology | RNA | Tumor proteins | Analysis | Melanoma | GTP-binding protein | p53 Protein | Estrogens | Menopause | mRNA | Kinases | Cyclin-dependent kinase 4 | Proteins | Cell activation | Pancreatic carcinoma | Arginine | Inhibition | Pancreas | Esophageal carcinoma | Splicing | Cyclin-dependent kinases | Protein arginine methyltransferase | Breast cancer | Esophagus | Cyclin-dependent kinase 2 | Sensitivity | Inhibitors | Tumor suppressor genes | Tumors | Biological Sciences | PNAS Plus
Journal Article
Epigenetics, ISSN 1559-2294, 11/2010, Volume 5, Issue 8, pp. 685 - 690
The INK4b-ARF-INK4a locus encodes for two cyclin-dependent kinase inhibitors, p15 INK4b and p16 INK4a and a regulator of the p53 pathway, ARF... 
Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | ANRIL | DNA methylation | Polycomb | Histone demethylases | Senescence | ARF | INK4A-ARF LOCUS | EMBRYONIC FIBROBLASTS | histone demethylases | BIOCHEMISTRY & MOLECULAR BIOLOGY | METHYLATED HISTONE H3 | METHYLTRANSFERASE ACTIVITY | CELL-PROLIFERATION | senescence | polycomb | GENETICS & HEREDITY | TUMOR-SUPPRESSOR | p16(INK4a) | p15(INK4b) | TARGETED DELETION | DEMETHYLASE JMJD3 CONTRIBUTES | POLYCOMB-GROUP | GENOME-WIDE ASSOCIATION | Chromatin - metabolism | Proto-Oncogene Proteins c-mdm2 - genetics | Cyclin-Dependent Kinase 4 - genetics | Diabetes Mellitus, Type 2 - genetics | Epigenesis, Genetic | Humans | Diabetes Mellitus, Type 2 - metabolism | Genetic Loci | Cardiovascular Diseases - genetics | Cyclin-Dependent Kinase Inhibitor p15 - biosynthesis | RNA, Untranslated - genetics | Tumor Suppressor Protein p53 - genetics | Cyclin-Dependent Kinase Inhibitor p15 - genetics | ADP-Ribosylation Factors - biosynthesis | DNA Modification Methylases | Cyclin-Dependent Kinase Inhibitor p16 - biosynthesis | G1 Phase - genetics | ADP-Ribosylation Factors - genetics | Proto-Oncogene Proteins c-mdm2 - metabolism | Repressor Proteins - metabolism | Cardiovascular Diseases - metabolism | Cyclin-Dependent Kinase 6 - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Repressor Proteins - genetics | Cyclin-Dependent Kinase 6 - metabolism | Signal Transduction - genetics | Polycomb-Group Proteins | Cyclin-Dependent Kinase 4 - metabolism | Animals | Histone Demethylases | RNA, Untranslated - biosynthesis | Alzheimer Disease - metabolism | Transcription, Genetic - genetics | Alzheimer Disease - genetics | Chromatin - genetics | p16INK4a | Point-of-View | p15INK4b
Journal Article
Nature (London), ISSN 1476-4687, 2016, Volume 534, Issue 7605, pp. 55 - 62
Somatic mutations have been extensively characterized in breast cancer, but the effects of these genetic alterations on the proteomic landscape remain poorly understood... 
PATHWAYS | HETEROGENEITY | PIK3CA MUTATIONS | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | GENES | BIOLOGY | RECEPTOR | EXPRESSION | SIGNATURE | REVEALS | Protein Kinases - metabolism | Focal Adhesion Kinase 1 - genetics | Receptor, Epidermal Growth Factor - genetics | Protein Kinases - genetics | Cyclin-Dependent Kinases - metabolism | Receptor, ErbB-2 - genetics | Receptors, G-Protein-Coupled - metabolism | Genomics | Humans | Gene Expression Regulation, Neoplastic | Receptor, ErbB-2 - metabolism | Phosphoproteins - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - genetics | Tumor Suppressor Protein p53 - genetics | Breast Neoplasms - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - metabolism | Breast Neoplasms - enzymology | Receptor, Epidermal Growth Factor - metabolism | Phosphoproteins - analysis | Mass Spectrometry | src-Family Kinases - metabolism | Female | Cyclin-Dependent Kinases - genetics | Focal Adhesion Kinase 1 - metabolism | Chromosomes, Human, Pair 5 - genetics | Breast Neoplasms - classification | Chromosome Deletion | p21-Activated Kinases - genetics | Signal Transduction | Molecular Sequence Annotation | Calcium-Binding Proteins - deficiency | Phosphoproteins - genetics | Mutation - genetics | S-Phase Kinase-Associated Proteins - metabolism | p21-Activated Kinases - metabolism | Phosphatidylinositol 3-Kinases - genetics | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Proteomics | S-Phase Kinase-Associated Proteins - genetics | Receptors, G-Protein-Coupled - genetics | src-Family Kinases - genetics | Calcium-Binding Proteins - genetics | Breast cancer | Genetic aspects | Research | Oncology, Experimental | Cancer | Physiological aspects | Methods | Mutation (Biology) | Proteins | Gene amplification | Peptides | Protein expression | Genomes | Mutation | Kinases | Deoxyribonucleic acid--DNA | Tumors
Journal Article