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Molecular Oncology, ISSN 1574-7891, 08/2016, Volume 10, Issue 7, pp. 949 - 965
Development of therapeutic resistance is responsible for most prostate cancer (PCa) related mortality. Resistance has been attributed to an acquired or... 
Anticancer drugs | Mitochondria | Combination therapy | Prostate cancer | Unfolded protein response | Apoptosis | STEM-CELLS | STRESS-RESPONSE | DNA-DAMAGE | ESTRAMUSTINE PHOSPHATE | CELL-CYCLE ARREST | TUMOR-CELLS | PACLITAXEL | EPITHELIAL-MESENCHYMAL TRANSITION | LUNG-CANCER | ONCOLOGY | ENDOPLASMIC-RETICULUM | Cell Death - radiation effects | Prostatic Neoplasms - radiotherapy | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Membrane Potential, Mitochondrial - radiation effects | Neoplastic Stem Cells - drug effects | Humans | Unfolded Protein Response - radiation effects | Male | Interferon-gamma - metabolism | Neoplastic Stem Cells - metabolism | Neoplastic Stem Cells - pathology | Interleukin-8 - metabolism | Phosphorylation - drug effects | Prostatic Neoplasms - drug therapy | G2 Phase - radiation effects | Cytoskeleton - radiation effects | beta Catenin - metabolism | Cell Cycle Checkpoints - radiation effects | G1 Phase - radiation effects | Cell Cycle Checkpoints - drug effects | X-Rays | Cell Line, Tumor | Cytoskeleton - metabolism | Peptides, Cyclic - therapeutic use | Thapsigargin - pharmacology | Thapsigargin - therapeutic use | Prostatic Neoplasms - metabolism | Apoptosis - radiation effects | Peptides, Cyclic - pharmacology | G1 Phase - drug effects | Membrane Potential, Mitochondrial - drug effects | G2 Phase - drug effects | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Caspases - metabolism | Paclitaxel | Mitochondria - radiation effects | Cell Death - drug effects | Neoplastic Stem Cells - radiation effects | Prostatic Neoplasms - pathology | Unfolded Protein Response - drug effects | Mitochondria - metabolism | Mitochondria - drug effects | Enzyme Activation - drug effects | HSP70 Heat-Shock Proteins - metabolism | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Matrix Metalloproteinases - metabolism | Transforming Growth Factor beta - metabolism | Cytoskeleton - drug effects | Care and treatment | Mortality | Oncology, Experimental | Mitochondrial DNA | Research | Drug resistance | Transforming growth factors | Nuclear radiation | Stem cells | Bone morphogenetic proteins | Germany | Cancer | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2013, Volume 8, Issue 4, pp. e62082 - e62082
Some potent chemotherapy drugs including tubulin-binding agents had been developed from nature plants, such as podophyllotoxin and paclitaxel. However, poor... 
MITOSIS | ANTIMITOTIC ACTIVITY | MICROTUBULES | NATURAL-PRODUCTS | MULTIDISCIPLINARY SCIENCES | DRUG DISCOVERY | RESISTANCE | TUBULIN | BINDING AGENTS | EXPRESSION | KINASES | Lung Neoplasms - drug therapy | Podophyllotoxin - pharmacology | Apoptosis - drug effects | Humans | Lung Neoplasms - metabolism | Apoptosis - genetics | Endoplasmic Reticulum Stress - genetics | Microtubules - metabolism | Podophyllotoxin - toxicity | Drug Evaluation, Preclinical | Disease Models, Animal | DNA Damage - drug effects | Lung Neoplasms - genetics | M Phase Cell Cycle Checkpoints - drug effects | Endoplasmic Reticulum Stress - drug effects | Antineoplastic Agents, Phytogenic - toxicity | Xenograft Model Antitumor Assays | Animals | Mitosis - drug effects | Signal Transduction - drug effects | Tumor Burden - drug effects | Cell Cycle Checkpoints - drug effects | Models, Biological | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Antineoplastic Agents, Phytogenic - pharmacology | Protein Multimerization - drug effects | Podophyllotoxin - analogs & derivatives | Chemotherapy | Podophyllotoxin | Analysis | Lung cancer | Polymerization | Stress (Physiology) | Tubulins | Health aspects | Apoptosis | Cancer | Drugs | Flow cytometry | Toxicity | Mitosis | Leukemia | Lung | DNA damage | Cytotoxicity | Selectivity | Drug development | Kinases | Cancer therapies | Anticancer properties | Metastases | Proteins | Signal transduction | Tubulin | Paclitaxel | Xenografts | Cell cycle | Inhibition | Stains | Deoxyribonucleic acid--DNA | Stresses | Plants (botany) | Hematology | Injection | Survivin | Tumor cell lines | Gene expression | Stress | Aurora B protein | Signaling | Side effects | Cell lines | Colonization | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article
Molecular Cancer Therapeutics, ISSN 1535-7163, 07/2008, Volume 7, Issue 7, pp. 1772 - 1781
We have already reported that epidermal growth factor receptor/phosphatidylinositol 3-kinase/AKT signaling is an important pathway in regulating radiation... 
Radiosensitization | NSCLC | DNA repair | PI3K/AKT targeting | CATALYTIC SUBUNIT | IN-VITRO | ONCOLOGY | INDUCED APOPTOSIS | ANTICANCER AGENTS | PROTEIN-KINASE-B/AKT | CERVICAL-CANCER | LUNG-CANCER CELLS | IONIZING-RADIATION | PRECLINICAL EVALUATION | ATAXIA-TELANGIECTASIA | DNA-Activated Protein Kinase - antagonists & inhibitors | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Apoptosis - drug effects | Apoptosis - radiation effects | Humans | DNA Repair - radiation effects | Lung Neoplasms - pathology | DNA Breaks, Double-Stranded - radiation effects | Radiation Tolerance - radiation effects | Caspases - metabolism | DNA Breaks, Double-Stranded - drug effects | DNA-Activated Protein Kinase - metabolism | Protein Binding - drug effects | Protein Binding - radiation effects | Phosphorylation - drug effects | Radiation, Ionizing | Carcinoma, Non-Small-Cell Lung - pathology | DNA Repair - drug effects | Lung Neoplasms - enzymology | Proto-Oncogene Proteins - genetics | Mutation - genetics | Radiation Tolerance - drug effects | Phosphorylation - radiation effects | Poly(ADP-ribose) Polymerases - metabolism | Cell Line, Tumor | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - enzymology | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Cell Proliferation - radiation effects | Index Medicus
Journal Article
Science, ISSN 0036-8075, 11/2013, Volume 342, Issue 6161, pp. 971 - 976
Journal Article
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 06/2018, Volume 233, Issue 6, pp. 4666 - 4676
This study evaluated the efficacy of a novel small‐molecule benzoxazole derivative (AU14022) for targeting p53‐related pathways for the attenuation... 
benzoxazole derivative | apoptosis | cell cycle arrest | mitochondria | p53 | ACTIVATION | PHYSIOLOGY | DNA-DAMAGE | RADIATION | CELL BIOLOGY | CHK1 | IN-VIVO | MDM2 | GENE-THERAPY | ANTAGONISTS | CHECKPOINTS | Benzoxazoles - pharmacology | Transcription, Genetic - drug effects | Apoptosis - drug effects | Apoptosis - radiation effects | Colorectal Neoplasms - genetics | Humans | Radiation Tolerance | Transcription, Genetic - radiation effects | Chemoradiotherapy | Tumor Suppressor Protein p53 - genetics | Dose-Response Relationship, Drug | G2 Phase Cell Cycle Checkpoints - radiation effects | Colorectal Neoplasms - therapy | G2 Phase Cell Cycle Checkpoints - drug effects | Mitochondria - radiation effects | Female | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Signal Transduction - radiation effects | Colorectal Neoplasms - metabolism | HCT116 Cells | Radiation-Sensitizing Agents - pharmacology | Tumor Suppressor Protein p53 - metabolism | Mitochondria - metabolism | Mitochondria - drug effects | Mitochondria - pathology | HT29 Cells | Xenograft Model Antitumor Assays | Animals | Signal Transduction - drug effects | Mice, Nude | Cell Proliferation - drug effects | Gene Expression Regulation, Neoplastic - radiation effects | Mice, Inbred BALB C | HeLa Cells | Colorectal Neoplasms - pathology | Cell Proliferation - radiation effects | Cytochrome c | Ionizing radiation | Chemotherapy | Analysis | Colorectal cancer | Lymphomas | Biochemistry | Tumor proteins | Radiotherapy | Apoptosis | Cancer | Cytochrome | Phosphorylation | Radiosensitivity | Transcription | p53 Protein | Xenotransplantation | Colorectal carcinoma | Cancer therapies | Anticancer properties | Proteins | Mitochondria | Cell activation | Colon cancer | Cell cycle | Xenografts | Colon | Sensitizing | I.R. radiation | Radiation therapy | Gene expression | Lymphoma | Lymphocytes B | Cell death | Tumor suppressor genes | Combined treatment | Index Medicus
Journal Article
Annals of Oncology, ISSN 0923-7534, 2013, Volume 24, Issue 2, pp. 398 - 405
Journal Article