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Nature, ISSN 0028-0836, 11/2006, Volume 444, Issue 7115, pp. 61 - 66
Journal Article
Nature, ISSN 0028-0836, 01/2012, Volume 481, Issue 7381, pp. 329 - 334
Retinoblastoma is an aggressive childhood cancer of the developing retina that is initiated by the biallelic loss of RB1. Tumours progress very quickly... 
ANEUPLOIDY | CELLS | GENE | TYROSINE KINASE | MCL-1 | MULTIDISCIPLINARY SCIENCES | GROWTH | TUMOR | SYK INHIBITOR | CANCER | Retinoblastoma - genetics | Protein-Tyrosine Kinases - metabolism | Genomics | Humans | Retinoblastoma - drug therapy | Gene Expression Regulation, Neoplastic | Aneuploidy | Intracellular Signaling Peptides and Proteins - metabolism | Genes, Retinoblastoma - genetics | Molecular Targeted Therapy | Retinoblastoma - pathology | Protein-Tyrosine Kinases - genetics | Cell Death - drug effects | Intracellular Signaling Peptides and Proteins - genetics | Syk Kinase | Cell Line | Cell Survival - drug effects | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | Retinoblastoma Protein - deficiency | Mutation - genetics | Sequence Analysis, DNA | Xenograft Model Antitumor Assays | Chromosomal Instability - genetics | Animals | Epigenesis, Genetic - genetics | Protein Kinase Inhibitors - therapeutic use | Retinoblastoma Protein - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Protein-Tyrosine Kinases - antagonists & inhibitors | Gene mutations | Development and progression | Genetic aspects | Diagnosis | Research | Retinoblastoma | Gene therapy | Health aspects | Risk factors | Studies | Human subjects | Epigenetics | DNA methylation | Genomes | Mutation | Kinases | Experiments | Chromosomes | Cancer | Children & youth | Apoptosis
Journal Article
Science, ISSN 0036-8075, 01/2017, Volume 355, Issue 6320, pp. 78 - 83
Prostate cancer relapsing from antiandrogen therapies can exhibit variant histology with altered lineage marker expression, suggesting that lineage plasticity... 
PATHWAY | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | SMALL-CELL CARCINOMA | PTEN | GENERATION | TUMORIGENESIS | EXPRESSION | DEFICIENCY | DELETION | EZH2 | Enhancer of Zeste Homolog 2 Protein - antagonists & inhibitors | Epigenesis, Genetic | Humans | SOXB1 Transcription Factors - antagonists & inhibitors | Male | Retinoblastoma-Like Protein p107 - genetics | Tumor Suppressor Protein p53 - genetics | Neoplasms, Experimental - pathology | Neoplasm Metastasis | Prostatic Neoplasms - genetics | SOXB1 Transcription Factors - genetics | Neoplasms, Experimental - genetics | Adenocarcinoma - genetics | Prostatic Neoplasms - drug therapy | Neuroendocrine Tumors - pathology | PTEN Phosphohydrolase - genetics | Prostatic Neoplasms - pathology | Enhancer of Zeste Homolog 2 Protein - genetics | Adenocarcinoma - drug therapy | Adenocarcinoma - secondary | Neuroendocrine Tumors - genetics | Cell Lineage | Drug Resistance, Neoplasm - genetics | Animals | Androgen Antagonists - therapeutic use | Cell Line, Tumor | Neuroendocrine Tumors - drug therapy | Cell Plasticity | Mice | Mutation | Neoplasms, Experimental - drug therapy | Prevention | Antimitotic agents | Epigenetic inheritance | Development and progression | Genetic aspects | Dosage and administration | Metastasis | Gene expression | Antineoplastic agents | Drug resistance | Health aspects | Prostate cancer | Drugs | Therapy | Deprivation | Histology | Hormones | Suppressors | Switching | Signal transduction | Sensitivity | Androgens | Inhibitors | Rodents | Plasticity | Epigenetics | Tumor suppressor genes | Plastic properties | Prostate | Cancer | Tumors | Mutations
Journal Article
Genes and Development, ISSN 0890-9369, 01/2007, Volume 21, Issue 1, pp. 43 - 48
Here we report that RNA interference against ATM inhibited p53 accumulation in cells expressing oncogenic STAT5 and cooperated with Rb inactivation to suppress... 
Senescence | DNA damage | E2F1 | STAT5 | ATM | RasV12 | p53 | ACTIVATION | P19(ARF) | RAS | PHOSPHORYLATION | DEVELOPMENTAL BIOLOGY | CELL BIOLOGY | senescence | PREMATURE SENESCENCE | IN-VIVO | GENETICS & HEREDITY | TUMOR-SUPPRESSOR | HUMAN FIBROBLASTS | CHECKPOINT | Protein Kinases - metabolism | Phosphorylation | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | Oncogenes - physiology | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Genes, ras - physiology | STAT5 Transcription Factor - metabolism | Tumor Suppressor Proteins - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction | RNA, Small Interfering - pharmacology | Retinoblastoma Protein - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cellular Senescence - physiology | Ataxia Telangiectasia Mutated Proteins | E2F1 Transcription Factor - metabolism | DNA-Binding Proteins - genetics | Cell Transformation, Neoplastic | Fluorescent Antibody Technique | Retinoblastoma Protein - antagonists & inhibitors | Checkpoint Kinase 2 | Checkpoint Kinase 1 | Fibroblasts - cytology | DNA Damage | Mutation | Aging | Genetic research | Research | Research Communication
Journal Article
Journal Article
Investigational New Drugs, ISSN 0167-6997, 10/2014, Volume 32, Issue 5, pp. 825 - 837
The G1 restriction point is critical for regulating the cell cycle and is controlled by the Rb pathway (CDK4/6-cyclin D1-Rb-p16/ink4a). This pathway is... 
Medicine & Public Health | Cell cycle | Oncology | In vivo antitumor activity | Pharmacology/Toxicology | Combination therapy | LY2835219 | Kinase inhibitor | CDK4/6 inhibitor | Cdk4/6 inhibitor | LUNG | HUMAN BREAST | PHOSPHORYLATION | CANCER | DEPENDENT KINASE 4/6 | CONSTITUTIVELY ACTIVATED FLT3 | ONCOLOGY | BRAIN METASTASES | RESTRICTION POINT | TUMOR-SUPPRESSOR | PHARMACOLOGY & PHARMACY | EXPRESSION | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Neoplasms - metabolism | Humans | Deoxycytidine - pharmacology | Antineoplastic Agents - therapeutic use | Deoxycytidine - therapeutic use | Aminopyridines - therapeutic use | Female | Antineoplastic Agents - pharmacology | Phosphorylation - drug effects | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Drug Therapy, Combination | Benzimidazoles - therapeutic use | Retinoblastoma Protein - metabolism | Neoplasms - drug therapy | Xenograft Model Antitumor Assays | Animals | Tumor Burden - drug effects | Protein Kinase Inhibitors - therapeutic use | Aminopyridines - pharmacology | Retinoblastoma Protein - antagonists & inhibitors | Cell Line, Tumor | Benzimidazoles - pharmacology | Mice | Protein Kinase Inhibitors - pharmacology | G1 Phase Cell Cycle Checkpoints - drug effects | Neoplasms - pathology | Deoxycytidine - analogs & derivatives | Dosage and administration | Research | Gemcitabine | Studies | Protein expression | Inhibitor drugs | Kinases | Cancer therapies | Analysis | CDK4 | Preclinical Studies | 6 inhibitor
Journal Article
Oncogene, ISSN 0950-9232, 10/2011, Volume 30, Issue 41, pp. 4261 - 4274
In the presence of sustained DNA damage occurring in S-phase or G2, normal cells arrest before mitosis and eventually become senescent. The checkpoint kinases... 
cyclin B1 | ATM | Chk2 | G2-M checkpoint | cell cycle | GENOTOXIC STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOTIC CATASTROPHE | TRANSCRIPTIONAL REPRESSION | G CHECKPOINT | CELL BIOLOGY | GENOMIC INSTABILITY | RETINOBLASTOMA PROTEIN | ONCOLOGY | GENETICS & HEREDITY | P53-DEFICIENT CELLS | CELL-CYCLE EXIT | IONIZING-RADIATION | ATAXIA-TELANGIECTASIA | Protein Kinases - metabolism | G2 Phase Cell Cycle Checkpoints - physiology | Phosphorylation | Protein Kinases - genetics | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | Immunoblotting | Male | Cyclin B1 - metabolism | Pyrones - pharmacology | Tumor Suppressor Protein p53 - genetics | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | G2 Phase Cell Cycle Checkpoints - drug effects | RNA Interference | Tumor Suppressor Proteins - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Antineoplastic Agents - pharmacology | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | HCT116 Cells | Cell Cycle Proteins - metabolism | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin B1 - genetics | Morpholines - pharmacology | Signal Transduction - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Piperazines - pharmacology | G2 Phase Cell Cycle Checkpoints - genetics | Signal Transduction - drug effects | Cell Line, Tumor | Checkpoint Kinase 2 | Bleomycin - pharmacology | Checkpoint Kinase 1 | Signal Transduction - physiology | DNA Damage | HeLa Cells | Cell division | Oxidative stress | Signal transduction | DNA damage | Cyclin-dependent kinases | Cell cycle | CHK2 protein | Epithelial cells | Mitosis | CHK1 protein | G2 phase | Genotoxicity | Osteosarcoma cells | p53 protein | Cyclin-dependent kinase | Chemotherapy | Fibroblasts | Cancer
Journal Article
Journal Article