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Journal of Clinical Investigation, ISSN 0021-9738, 11/2016, Volume 126, Issue 11, pp. 4076 - 4087
Radiotherapy causes dose-limiting toxicity and long-term complications in rapidly renewing tissues, including the gastrointestinal tract. Currently, there is... 
MEDICINE, RESEARCH & EXPERIMENTAL | GASTROINTESTINAL-SYNDROME | APOPTOSIS | STEM-CELLS | REPAIR | DEPENDENT KINASE 4/6 | PUMA | DAMAGE | P21 | DNA-REPLICATION | P53 | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Intestinal Diseases - prevention & control | Cell Cycle - genetics | Stem Cells - immunology | Apoptosis - drug effects | Radiation Injuries, Experimental - immunology | Cyclin-Dependent Kinase 4 - genetics | Apoptosis - genetics | Intestinal Diseases - immunology | Cyclin-Dependent Kinase 6 - immunology | Tumor Suppressor Protein p53 - genetics | Receptors, G-Protein-Coupled - immunology | Radiation Injuries, Experimental - prevention & control | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cell Cycle - immunology | Tumor Suppressor Proteins - genetics | Apoptosis Regulatory Proteins - genetics | DNA Damage - genetics | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Radiation Injuries, Experimental - genetics | Apoptosis Regulatory Proteins - immunology | Cyclin-Dependent Kinase 6 - genetics | Intestinal Diseases - genetics | DNA Damage - immunology | Tumor Suppressor Protein p53 - immunology | Radiation Injuries, Experimental - pathology | Piperazines - pharmacology | Tumor Suppressor Proteins - immunology | Mice, Knockout | Cyclin-Dependent Kinase 4 - immunology | Animals | Apoptosis - immunology | Cyclin-Dependent Kinase Inhibitor p21 - immunology | Stem Cells - pathology | Mice | Pyridines - pharmacology | Receptors, G-Protein-Coupled - genetics | Cell Cycle - drug effects | Usage | Radiotherapy | DNA damage | Analysis | Gastrointestinal system | Colleges & universities | Cell division | FDA approval | Kinases | Gene expression | Experiments | Phase transitions | DNA repair | Proteins | Rodents | Cell cycle | Stem cells | Deoxyribonucleic acid--DNA | Methods | Cancer | Apoptosis | Index Medicus | Abridged Index Medicus
Journal Article
2003, 2 ed., ISBN 9781402075919, xvi, 557
Edward B. Lewis' science is the bridge linking experimental genetics as conducted in the first half of the twentieth century, and the powerful molecular... 
Nobel Prizes | Radiation carcinogenesis | Developmental genetics | Genes | Genetic aspects | Geneticists | Lewis, Edward B., 1918- Awards | Biology, life sciences | Awards | United States | Lewis, Edward B | Biography | Miscellanea | 1918-2004 | Human Genetics | Cancer Research | Oncology | Biomedicine | Life Sciences, general
Book
Human Gene Therapy, ISSN 1043-0342, 06/2017, Volume 28, Issue 6, pp. 523 - 532
Radiation-induced lung injury (RILI) is a major clinical complication for radiotherapy in thoracic tumors. An immediate effect of lung irradiation is the... 
Research Articles | manganese superoxide dismutase | radiation-induced lung injury | cell therapy | mesenchymal stem cells | FIBROSIS | MEDICINE, RESEARCH & EXPERIMENTAL | MNSOD | RISK | MECHANISMS | MODEL | PROTECTS | THERAPY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | INFLAMMATION | GENETICS & HEREDITY | PNEUMONITIS | STROMAL CELLS | Bronchoalveolar Lavage Fluid | Tumor Necrosis Factor-alpha - metabolism | Interleukin-1 - genetics | Lung Injury - pathology | Superoxide Dismutase - genetics | Gamma Rays - adverse effects | Humans | Tumor Necrosis Factor-alpha - genetics | Apoptosis - genetics | Male | Transplantation, Heterologous | Green Fluorescent Proteins - genetics | Lung Injury - etiology | Mesenchymal Stromal Cells - immunology | Lentivirus - metabolism | Lung Injury - therapy | Mesenchymal Stromal Cells - cytology | Lung Injury - metabolism | Interleukin-10 - metabolism | Lentivirus - genetics | Lung - radiation effects | Lung - metabolism | Transgenes | Interleukin-6 - metabolism | Genes, Reporter | Superoxide Dismutase - metabolism | Green Fluorescent Proteins - metabolism | Interleukin-1 - metabolism | Gene Expression | Lung - pathology | Genetic Vectors - chemistry | Interleukin-6 - genetics | Genetic Vectors - metabolism | Mesenchymal Stromal Cells - metabolism | Mice, SCID | Administration, Intravenous | Animals | Interleukin-10 - genetics | Mice | Mesenchymal Stem Cell Transplantation | Oxidative stress | Severe combined immunodeficiency | Mesenchyme | Hydroxyproline | DNA damage | Interleukin | Radiation | Stem cell transplantation | Lipids | Superoxide dismutase | Interleukin 6 | Proteins | Rodents | Radiation injuries | Oxidation | Growth factors | Deoxyribonucleic acid--DNA | Radiation effects | Cytokines | Diabetes mellitus | Thorax | Superoxide | Inflammation | Radiation therapy | Radiation dosage | DNA nucleotidylexotransferase | Cell injury | Lungs | Cell death | Stem cells | Interleukin 10 | Irradiation | Plasma levels | Immunofluorescence | Colonization | Apoptosis | Manganese | Tumors
Journal Article
Science, ISSN 0036-8075, 11/2016, Volume 354, Issue 6313, pp. 765 - 768
Journal Article
Journal of Clinical Oncology, ISSN 0732-183X, 05/2008, Volume 26, Issue 13, pp. 2192 - 2197
Purpose Standard therapy for glioblastoma (GBM) is temozolomide (TMZ) administration, initially concurrent with radiotherapy (RT), and subsequently as... 
NECROSIS | THERAPY | ONCOLOGY | PHASE-II | DIFFUSION | RADIOTHERAPY | MULTIFORME | CANCER | BRAIN | CONCURRENT | TEMOZOLOMIDE | Dacarbazine - adverse effects | Glioblastoma - enzymology | Humans | Middle Aged | Male | Glioblastoma - radiotherapy | Glioblastoma - genetics | Time Factors | Chemotherapy, Adjuvant - adverse effects | Radiotherapy, Adjuvant - adverse effects | Brain Diseases - etiology | Genetic Predisposition to Disease | Tumor Suppressor Proteins - metabolism | DNA Modification Methylases - metabolism | Brain Neoplasms - genetics | Brain Diseases - enzymology | Brain Neoplasms - drug therapy | Radiation Injuries - enzymology | Disease Progression | Radiation Injuries - etiology | Magnetic Resonance Imaging | Glioblastoma - pathology | Radiation Injuries - pathology | Antineoplastic Agents, Alkylating - adverse effects | Glioblastoma - drug therapy | Brain Diseases - genetics | Brain Neoplasms - pathology | DNA Repair Enzymes - genetics | Gene Expression Regulation, Neoplastic | Necrosis | Patient Selection | DNA Methylation | Radiation Injuries - genetics | Tumor Suppressor Proteins - genetics | DNA Repair Enzymes - metabolism | Dacarbazine - analogs & derivatives | Adult | Female | Retrospective Studies | Brain Neoplasms - radiotherapy | Promoter Regions, Genetic | Brain Neoplasms - enzymology | Kaplan-Meier Estimate | Proportional Hazards Models | Treatment Outcome | Gene Expression Regulation, Enzymologic | DNA Modification Methylases - genetics | Brain Diseases - pathology | Aged | Index Medicus
Journal Article
Free Radical Biology and Medicine, ISSN 0891-5849, 10/2016, Volume 99, pp. 463 - 471
We have reported that hematopoietic system injury induced by total body irradiation (TBI) leads to generation of intracellular reactive oxygen species (ROS)... 
Hematopoietic stem/progenitor cells | Oxidative stress | 3,3′-diindolylmethane | Radioprotection | APOPTOSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | INDUCTION | 3,3 '-diindolylmethane | BAX/BCL-2 | PREMATURE SENESCENCE | PHARMACOKINETICS | ENDOCRINOLOGY & METABOLISM | GENE-EXPRESSION | STEM-CELL INJURY | INDOLE-3-CARBINOL | IONIZING-RADIATION | Whole-Body Irradiation | Heme Oxygenase-1 - metabolism | Phosphorylation | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Proto-Oncogene Proteins c-bcl-2 - agonists | Male | NF-E2-Related Factor 2 - agonists | Bone Marrow - radiation effects | Heme Oxygenase-1 - genetics | Proto-Oncogene Proteins c-bcl-2 - metabolism | Radiation Injuries, Experimental - prevention & control | Bone Marrow - metabolism | NADPH Oxidase 4 - antagonists & inhibitors | Indoles - pharmacology | NF-E2-Related Factor 2 - genetics | Membrane Proteins - metabolism | bcl-2-Associated X Protein - genetics | Bone Marrow - drug effects | Radiation Injuries, Experimental - genetics | Radiation Injuries, Experimental - metabolism | NADPH Oxidase 4 - genetics | Signal Transduction | Membrane Proteins - genetics | Mice, Inbred C57BL | bcl-2-Associated X Protein - metabolism | Hematopoietic Stem Cell Transplantation | Hematopoietic Stem Cells - metabolism | Antioxidants - pharmacology | Radiation Injuries, Experimental - pathology | bcl-2-Associated X Protein - antagonists & inhibitors | Membrane Proteins - agonists | Gene Expression Regulation - drug effects | NADPH Oxidase 4 - metabolism | Reactive Oxygen Species - antagonists & inhibitors | Animals | Histones - genetics | Bone Marrow - pathology | Hematopoietic Stem Cells - cytology | NF-E2-Related Factor 2 - metabolism | Gene Expression Regulation - radiation effects | Mice | Histones - metabolism | Oxidative Stress - drug effects | Graft Survival - drug effects | Proto-Oncogene Proteins c-bcl-2 - genetics | Oxidases | Antioxidants | Ionizing radiation | Hematopoietic stem cells | Heme
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 04/2015, Volume 125, Issue 4, pp. 1620 - 1636
Kidney injury molecule 1 (KIM-1, also known as TIM-1) is markedly upregulated in the proximal tubule after injury and is maladaptive when chronically... 
ISCHEMIA-REPERFUSION INJURY | B-CELLS | MEDICINE, RESEARCH & EXPERIMENTAL | ISCHEMIA/REPERFUSION INJURY | MOLECULE-1 KIM-1 | EPITHELIAL-CELLS | APOPTOTIC CELLS | INNATE IMMUNE-RESPONSE | T-CELL IG | ACUTE-RENAL-FAILURE | URINARY BIOMARKER | Epithelial Cells - metabolism | Kidney - blood supply | Macrophage Activation - genetics | Apoptosis - drug effects | Intercellular Signaling Peptides and Proteins - biosynthesis | Male | NF-kappa B - metabolism | LLC-PK1 Cells | Epithelial Cells - secretion | Cisplatin - toxicity | Extracellular Matrix Proteins | Membrane Proteins - physiology | Swine | Kidney Tubules, Proximal - secretion | Acute Kidney Injury - chemically induced | Intercellular Signaling Peptides and Proteins - secretion | Acute Kidney Injury - etiology | Macrophage Activation - physiology | Protein Structure, Tertiary | Membrane Proteins - genetics | Mice, Inbred C57BL | Cytokines - secretion | Gene Expression Regulation | Phagocytosis - physiology | Inflammation | Radiation Chimera | Hepatitis A Virus Cellular Receptor 1 | Immunity, Innate | Acute Kidney Injury - prevention & control | Homeodomain Proteins - genetics | Mice, Knockout | Animals | Reperfusion Injury - prevention & control | Membrane Proteins - chemistry | Kidney Tubules, Proximal - metabolism | Phosphatidylinositol 3-Kinases - physiology | Mice | Apoptosis - physiology | Cytokines - biosynthesis | Kidneys | Immune response | Genetic research | Genetic aspects | Research | Gene expression | Injuries | Proteins | Phosphorylation | Hospitals | Laboratories | Mortality | Rodents | Acidification | Kinases | Apoptosis | Nephrology | Cell Biology
Journal Article
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 12/2017, Volume 21, Issue 12, pp. 3264 - 3276
Radiation‐induced lung injury (RILI) is one of the most common and fatal complications of thoracic radiotherapy. It is characterized with two main features... 
radiation‐induced lung injury | free radicals | epithelial–mesenchymal transition (EMT) | polydatin (PD) | radiation-induced lung injury | MEDICINE, RESEARCH & EXPERIMENTAL | APOPTOSIS | SMAD3 | INDUCED FIBROSIS | CANCER CELLS | IRRADIATED MICE | DAMAGE | IMPAIRMENT | CELL BIOLOGY | epithelial-mesenchymal transition (EMT) | TH2-LIKE IMMUNE-RESPONSE | GROWTH | EXPRESSION | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics | Epithelial Cells - metabolism | Epithelial-Mesenchymal Transition - radiation effects | Radiation Pneumonitis - pathology | Epithelial Cells - drug effects | Humans | Acute Lung Injury - genetics | Epithelial-Mesenchymal Transition - drug effects | Smad3 Protein - immunology | Stilbenes - pharmacology | Radiation Pneumonitis - prevention & control | NF-E2-Related Factor 2 - immunology | Smad3 Protein - genetics | Transforming Growth Factor beta1 - immunology | Acute Lung Injury - prevention & control | Radiation-Protective Agents - pharmacology | Female | Lung - radiation effects | NF-E2-Related Factor 2 - genetics | Lung - metabolism | Th1-Th2 Balance - drug effects | Disease Models, Animal | Cell Line | Epithelial Cells - radiation effects | Glucosides - pharmacology | Lung - pathology | Sirtuin 3 - genetics | Signal Transduction | Mice, Inbred C57BL | Gene Expression Regulation | Epithelial Cells - pathology | Transforming Growth Factor beta1 - genetics | Acute Lung Injury - pathology | Radiation Pneumonitis - immunology | Sirtuin 3 - immunology | Animals | Th1-Th2 Balance - radiation effects | Lung - drug effects | Radiation Pneumonitis - genetics | Acute Lung Injury - immunology | Mice | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - immunology | Transforming growth factors | Lung diseases | Stem cells | Radiation | Cell culture | Radiation effects | Mesenchyme | Complications | Lymphocytes T | Smad3 protein | Thorax | Radiation therapy | Tissues | Signaling | Signal transduction | Pneumonitis | Beta irradiation | Lungs | Fibrosis | Radiation injuries | Irradiation | Inhibition | Injuries | Original
Journal Article
International Journal of Radiation Oncology, Biology, Physics, ISSN 0360-3016, 2011, Volume 81, Issue 1, pp. 52 - 58
Purpose Clinical radiosensitivity varies considerably among patients, and radiation-induced side effects developing in normal tissue can be therapy limiting.... 
Radiology | Hematology, Oncology and Palliative Medicine | Breast cancer | Radiosensitivity | Radiotherapy | Single-nucleotide polymorphism (SNP) | CELLS | ONCOLOGY | DNA-REPAIR GENES | RISK | IONIZING-RADIATION | RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING | DAMAGE | Radiotherapy Dosage | Breast Neoplasms - surgery | MutL Protein Homolog 1 | Prospective Studies | Xeroderma Pigmentosum Group D Protein - genetics | Humans | DNA Repair Enzymes - genetics | Radiation Tolerance - genetics | MutS Homolog 2 Protein - genetics | Radiodermatitis - genetics | DNA Repair - genetics | DNA-Binding Proteins - genetics | Breast Neoplasms - radiotherapy | DNA Modification Methylases - genetics | Breast Neoplasms - genetics | Glutathione Transferase - genetics | Gene Deletion | Tumor Suppressor Proteins - genetics | Adaptor Proteins, Signal Transducing - genetics | Polymorphism, Single Nucleotide - genetics | Female | MutS Homolog 3 Protein | Nuclear Proteins - genetics | X-ray Repair Cross Complementing Protein 1 | Index Medicus | SURGERY | X-RAY DIFFRACTION | RADIATION EFFECTS | SENSITIVITY | MEDICINE | BIOLOGICAL RECOVERY | PHOTOELECTRON SPECTROSCOPY | REPAIR | POLYMERASE CHAIN REACTION | THERAPY | GLANDS | BIOLOGICAL EFFECTS | GENES | RADIOLOGY AND NUCLEAR MEDICINE | BIOLOGICAL RADIATION EFFECTS | DIFFRACTION | GENE AMPLIFICATION | RADIOTHERAPY | SKIN | RADIOLOGY | SCATTERING | INJURIES | MAMMARY GLANDS | NEOPLASMS | ORGANIC COMPOUNDS | COHERENT SCATTERING | RADIATION INJURIES | NUCLEAR MEDICINE | NUCLEOTIDES | ORGANS | DISEASES | SPECTROSCOPY | ELECTRON SPECTROSCOPY | DNA REPAIR | BIOLOGICAL REPAIR | X-RAY PHOTOELECTRON SPECTROSCOPY | RADIOSENSITIVITY | BODY | HAZARDS
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 02/2019, Volume 129, Issue 2, pp. 786 - 801
Tumor cure with conventional fractionated radiotherapy is 65%, dependent on tumor cell-autonomous gradual buildup of DNA double-strand break (DSB) misrepair.... 
STROMAL SENSITIVITY | MEDICINE, RESEARCH & EXPERIMENTAL | GAMMA-H2AX FOCI | EXTRACRANIAL OLIGOMETASTASES | OXYGEN-TENSION | INTENSITY-MODULATED RADIOTHERAPY | DOUBLE-STRAND BREAKS | BODY RADIATION-THERAPY | PHASE I/II TRIAL | CERAMIDE | STRESS | Neoplasms - metabolism | Chromatin - metabolism | Reperfusion Injury | Small Ubiquitin-Related Modifier Proteins - metabolism | Ubiquitins - genetics | Humans | Homologous Recombination | Signal Transduction - genetics | Neoplasm Proteins - metabolism | Small Ubiquitin-Related Modifier Proteins - genetics | Animals | Neoplasms - genetics | Cell Line, Tumor | Neoplasms - radiotherapy | Mice | Signal Transduction - radiation effects | Neoplasm Proteins - genetics | Neoplasms - pathology | Chromatin - genetics | Ubiquitins - metabolism | Care and treatment | Usage | Radiotherapy | Reperfusion injury | Peroxiredoxin | Chromatin | Endothelin | DNA damage | Homologous recombination | Tempol | Homology | Lethality | Metastasis | Cancer therapies | DNA repair | Reperfusion | Radiosensitization | Ischemia | Cell cycle | Stress response | Deoxyribonucleic acid--DNA | Tumor cells | Vasoconstriction | Endothelin 1 | Radiation therapy | Double-strand break repair | Sphingomyelin phosphodiesterase | Perfusion | Stem cells | Microvasculature | Chromosome aberrations | Cellular stress response | Apoptosis | Cancer | Tumors
Journal Article
Journal Article