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Journal of the National Cancer Institute, ISSN 0027-8874, 04/2011, Volume 103, Issue 8, pp. 645 - 661
Background Ionizing radiation (IR) is effectively used in cancer therapy. However, in subsets of patients, a few radioresistant cancer cells survive and cause... 
STEM-CELLS | IN-VITRO | ONCOLOGY | TYROSINE KINASE | HGF | CELL INVASION | RECEPTOR | EPITHELIAL-MESENCHYMAL TRANSITIONS | NF-KAPPA-B | SCATTER-FACTOR | PROTOONCOGENE | Humans | Neoplasm Invasiveness - prevention & control | Radiation Tolerance | Receptors, Growth Factor - antagonists & inhibitors | NF-kappa B - metabolism | RNA, Messenger - metabolism | NF-kappa B - radiation effects | Receptors, Growth Factor - genetics | Proto-Oncogene Proteins c-met - radiation effects | Signal Transduction - radiation effects | Protein-Serine-Threonine Kinases - metabolism | Radiation, Ionizing | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - radiation effects | Proto-Oncogene Proteins c-met - antagonists & inhibitors | Cell Cycle Proteins - metabolism | Cell Cycle Proteins - radiation effects | Receptors, Growth Factor - radiation effects | Proto-Oncogene Proteins c-met - drug effects | Ataxia Telangiectasia Mutated Proteins | Phosphorylation - radiation effects | Cell Line, Tumor | Mice | RNA, Small Interfering | Tumor Suppressor Proteins - radiation effects | Receptors, Growth Factor - metabolism | Neoplasms - metabolism | Proto-Oncogene Proteins c-met - metabolism | Apoptosis - radiation effects | Up-Regulation - radiation effects | Transcription, Genetic - radiation effects | Transplantation, Heterologous | Sulfones - pharmacology | DNA-Binding Proteins - metabolism | Chromatin Immunoprecipitation | Protein-Serine-Threonine Kinases - radiation effects | Tumor Suppressor Proteins - genetics | Polymerase Chain Reaction | Cell Cycle Proteins - genetics | Indoles - pharmacology | Neoplasms - radiotherapy | Gene Expression Regulation, Neoplastic - drug effects | In Situ Nick-End Labeling | Enzyme-Linked Immunosorbent Assay | Radiation-Sensitizing Agents - pharmacology | Gene Silencing | Protein-Serine-Threonine Kinases - genetics | DNA-Binding Proteins - genetics | Cell Survival - radiation effects | Cell Movement - radiation effects | Proto-Oncogene Proteins c-met - genetics | Blotting, Northern | Animals | NF-kappa B - genetics | Protein Kinase Inhibitors - pharmacology | Neoplasms - pathology | Receptors, Growth Factor - drug effects | DNA Damage - radiation effects | Mitogen-Activated Protein Kinases - metabolism | Ionizing radiation | Physiological aspects | Genetic aspects | Cancer invasiveness | Research | Gene expression | Radiotherapy | Health aspects
Journal Article
Cancer Cell, ISSN 1535-6108, 05/2012, Volume 21, Issue 5, pp. 668 - 679
DNA damage induced by ionizing radiation activates the ATM kinase, which subsequently stabilizes and activates the p53 tumor suppressor protein. Although... 
INDUCED TUMORIGENESIS | PATHWAYS | APOPTOSIS | DEPENDENT PHOSPHORYLATION | MDM2-DEFICIENT MICE | P53-DEFICIENT MICE | ONCOLOGY | P53 ACTIVATION | IN-VIVO | TUMOR-SUPPRESSOR | EMBRYONIC LETHALITY | CELL BIOLOGY | Phosphorylation | Proto-Oncogene Proteins c-mdm2 - genetics | Intestine, Small - pathology | Apoptosis - radiation effects | Radiation Tolerance | Serine | Mice, 129 Strain | Mutation, Missense | Thymus Gland - enzymology | Intestine, Small - enzymology | DNA-Binding Proteins - metabolism | Spleen - enzymology | Thymus Gland - radiation effects | Time Factors | Protein-Serine-Threonine Kinases - radiation effects | Thymus Gland - pathology | Intestine, Small - radiation effects | Protein Stability | Spleen - pathology | Proto-Oncogene Proteins c-mdm2 - metabolism | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - radiation effects | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Cell Cycle Proteins - radiation effects | Tumor Suppressor Protein p53 - metabolism | Ataxia Telangiectasia Mutated Proteins | Animals | Spleen - radiation effects | Mice | DNA Damage | Enzyme Activation | Tumor Suppressor Proteins - radiation effects | Automated teller machines | Tumor proteins | Nuclear radiation | DNA repair | DNA | DNA damage | mouse models | Mdm2 | ATM | tumorigenesis | DNA damage response | p53
Journal Article
Oncogene, ISSN 0950-9232, 03/2007, Volume 26, Issue 10, pp. 1449 - 1458
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 8/2010, Volume 107, Issue 32, pp. 14205 - 14210
Journal Article
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 03/2013, Volume 433, Issue 1, pp. 36 - 39
► Protein microarray shows the differential expression of 27 proteins induced by RFR. ► RPA32 related to DNA repair is down-regulated in Western blot. ► p73... 
Protein microarray | Replication Protein A | DNA repair | p73 | Radiofrequency radiation | Apoptosis | P73 | SYSTEM | ACTIVATION | INDUCED APOPTOSIS | CASPASE-1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | ELECTROMAGNETIC-FIELDS | CANCER | MOBILE PHONE | REPAIR | REPLICATION | BIOPHYSICS | Cell Transformation, Neoplastic - radiation effects | Apoptosis - radiation effects | Humans | Precursor Cells, B-Lymphoid - metabolism | Precursor Cells, B-Lymphoid - radiation effects | Up-Regulation - radiation effects | DNA Repair - radiation effects | Down-Regulation - radiation effects | DNA-Binding Proteins - metabolism | Radio Waves - adverse effects | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Replication Protein A - radiation effects | Cell Line | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - radiation effects | Cell Cycle - radiation effects | Nuclear Proteins - metabolism | Replication Protein A - metabolism | Nuclear Proteins - radiation effects | Tumor Protein p73 | Proteins - metabolism | Proteins - radiation effects | Protein Array Analysis | Hypoxia-Inducible Factor 1, alpha Subunit - radiation effects | Tumor Suppressor Proteins - radiation effects | Cell Proliferation - radiation effects | Proteins | Mobile communication systems | Wireless communication systems | Nuclear radiation | GSM (Global System for Mobile Communications) | Genomics | Genetic research | Telecommunications services industry | Communications industry | APOPTOSIS | BIOLOGICAL EFFECTS | DNA REPAIR | CELL PROLIFERATION | CELL CYCLE | ABSORPTION | PROTEINS | 60 APPLIED LIFE SCIENCES | RADIOWAVE RADIATION | DNA DAMAGES
Journal Article
Mutagenesis, ISSN 0267-8357, 2015, Volume 30, Issue 2, pp. 287 - 296
To investigate polypeptide from Chlamy Farreri (PCF)'s protective effect against skin cancer, we used a cellular model of ultraviolet B (UVB)-induced malignant... 
CARCINOGENESIS | DNA METHYLATION | EPITHELIAL-CELLS | INDUCED SKIN TUMORS | INDUCED APOPTOSIS | GADD45A | GENETICS & HEREDITY | KERATINOCYTES | TOXICOLOGY | ULTRAVIOLET-RADIATION | CANCER | CELLULAR-TRANSFORMATION | Cell Cycle Proteins - drug effects | Gene Expression - drug effects | Keratinocytes - radiation effects | Humans | Cyclin-Dependent Kinase Inhibitor p16 | Neoplasm Proteins - drug effects | Neoplasms, Radiation-Induced - genetics | Skin Neoplasms - prevention & control | Ultraviolet Rays | DNA Methylation - radiation effects | Cell Transformation, Neoplastic - genetics | Protective Agents - pharmacology | Tumor Suppressor Proteins - genetics | DNA (Cytosine-5-)-Methyltransferases - radiation effects | Cell Cycle Proteins - genetics | DNA (Cytosine-5-)-Methyltransferases - drug effects | Neoplasms, Radiation-Induced - prevention & control | Nuclear Proteins - drug effects | Neoplasm Proteins - genetics | Nuclear Proteins - genetics | Cell Line | Cell Cycle Proteins - radiation effects | Nuclear Proteins - radiation effects | Pectinidae | Gene Expression - radiation effects | Peptides - pharmacology | DNA (Cytosine-5-)-Methyltransferases - genetics | Neoplasm Proteins - radiation effects | Animals | Keratinocytes - drug effects | Skin Neoplasms - genetics | Tumor Suppressor Proteins - drug effects | Cell Transformation, Neoplastic - drug effects | DNA Methylation - drug effects | Tumor Suppressor Proteins - radiation effects | Index Medicus
Journal Article
Radiation Research, ISSN 0033-7587, 2006, Volume 165, Issue 5, pp. 505 - 515
Abstract Costes, S. V., Boissière, A., Ravani, S., Romano, R., Parvin, B. and Barcellos-Hoff, M. H. Imaging Features that Discriminate between Foci Induced by... 
Dose response relationship | DNA damage | Cell nucleus | Cell cycle | Cell lines | Irradiation | Solar X rays | Nitrogen | Radiation dosage | Radiation damage | LOCALIZATION | CHROMATIN | DNA-DAMAGE | DOUBLE-STRAND BREAKS | PHOSPHORYLATED HISTONE H2AX | GAMMA-H2AX FOCI | BIOPHYSICS | BIOLOGY | NUCLEAR FOCI | CELL-CYCLE | ATM | EXPRESSION | RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING | Humans | Image Interpretation, Computer-Assisted - methods | DNA - ultrastructure | DNA - radiation effects | Histones - radiation effects | Protein-Serine-Threonine Kinases - radiation effects | Sensitivity and Specificity | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | DNA Damage - genetics | Fibroblasts - metabolism | Radiation, Ionizing | Reproducibility of Results | DNA-Binding Proteins - radiation effects | Micronucleus Tests - methods | Cell Cycle Proteins - radiation effects | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Ataxia Telangiectasia Mutated Proteins | Radiation Dosage | DNA-Binding Proteins - genetics | Phosphorylation - radiation effects | Histones - genetics | Fibroblasts - radiation effects | Microscopy, Fluorescence - methods | Fibroblasts - cytology | Linear Energy Transfer | Dose-Response Relationship, Radiation | Tumor Suppressor Proteins - radiation effects | Index Medicus | Space life sciences
Journal Article
International Journal of Radiation Oncology, Biology, Physics, ISSN 0360-3016, 2013, Volume 86, Issue 5, pp. 969 - 977
Purpose Ataxia telangiectasia mutated (ATM) is a serine/threonine kinase critical to the cellular DNA-damage response, including from DNA double-strand breaks.... 
Radiology | Hematology, Oncology and Palliative Medicine | CHK2 | ONCOLOGY | ATAXIA-TELANGIECTASIA | RADIATION | CANCER | RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING | Phosphorylation | Luciferases - metabolism | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | DNA, Complementary - genetics | DNA Primers - genetics | Thiourea - pharmacology | Cell Nucleus - enzymology | Luciferases - genetics | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Dose-Response Relationship, Drug | Protein-Serine-Threonine Kinases - radiation effects | Sensitivity and Specificity | Tumor Suppressor Proteins - genetics | HEK293 Cells | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Caffeine - pharmacology | Cell Cycle Proteins - genetics | DNA Primers - metabolism | Female | Benzeneacetamides - pharmacology | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | DNA-Binding Proteins - radiation effects | RNA, Small Interfering - pharmacology | Cell Cycle Proteins - metabolism | Cell Cycle Proteins - radiation effects | Protein-Serine-Threonine Kinases - genetics | Genes, Reporter - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Enzyme Activation - radiation effects | Luminescent Measurements - methods | Animals | Mice, Nude | DNA Repair | Checkpoint Kinase 2 | Mice | Protein Kinase Inhibitors - pharmacology | Tumor Suppressor Proteins - radiation effects | Thiourea - analogs & derivatives | Sects | Nuclear radiation | DNA damage | NEOPLASMS | RNA | PHOSPHORYLATION | VALIDATION | IN VIVO | 60 APPLIED LIFE SCIENCES | LUCIFERASE | STRAND BREAKS | SERINE | DNA | IN VITRO | RADIOLOGY AND NUCLEAR MEDICINE | CELL CYCLE | MICE | TIME DEPENDENCE | BIOLUMINESCENCE | THREONINE
Journal Article
Radiotherapy and Oncology, ISSN 0167-8140, 2011, Volume 101, Issue 1, pp. 13 - 17
Abstract Radiation and other types of DNA damaging agents induce a plethora of signaling events simultaneously originating from the nucleus, cytoplasm, and... 
Hematology, Oncology and Palliative Medicine | ROS | MAP kinase | ATM | AKT | Phosphatase | DNA repair | EGFR | ERK | INDUCED ACTIVATION | PROTEIN-KINASE | HUMAN GLIOMA-CELLS | MAMMALIAN-CELLS | GROWTH-FACTOR RECEPTOR | DAMAGE RESPONSE | ONCOLOGY | HOMOLOGOUS RECOMBINATION | ATM ACTIVATION | IONIZING-RADIATION | ATAXIA-TELANGIECTASIA | RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING | MAP Kinase Signaling System - radiation effects | MAP Kinase Signaling System - physiology | Phosphorylation | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - radiation effects | Cell Survival | Humans | Cell Cycle Proteins - metabolism | Cell Cycle Proteins - radiation effects | DNA Repair - physiology | Signal Transduction - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | DNA Breaks, Double-Stranded | DNA-Binding Proteins - metabolism | Proto-Oncogene Proteins c-akt - radiation effects | Protein-Serine-Threonine Kinases - radiation effects | Cell Cycle Proteins - genetics | DNA Damage - genetics | Signal Transduction - radiation effects | Proto-Oncogene Proteins c-akt - metabolism | Tumor Suppressor Proteins - radiation effects | DNA Damage - radiation effects | Protein-Serine-Threonine Kinases - metabolism | Automated teller machines | Phosphatases | DNA | Radiation | Tumors | phosphatase
Journal Article
Journal of the National Cancer Institute, ISSN 0027-8874, 04/2011, Volume 103, Issue 8, pp. 617 - 619
Journal Article