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Oncotarget, ISSN 1949-2553, 02/2016, Volume 7, Issue 7, pp. 7610 - 7628
Radiotherapy represents an important therapeutic strategy in the treatment of cancer cells. However, it often fails to eliminate all tumor cells because of the... 
Notch inhibitor | Treatment resistance | Radiotherapy | Notch | Personalized treatment | Radiation Tolerance - drug effects | Radiation-Sensitizing Agents - therapeutic use | Neoplasms - prevention & control | Receptors, Notch - antagonists & inhibitors | Animals | Humans
Journal Article
Cancer Cell, ISSN 1535-6108, 2008, Volume 13, Issue 3, pp. 261 - 271
Malignant mesothelioma is a devastating disease that has been associated with loss of Neurofibromatosis type 2 ( ) and genetic lesions affecting and pathways.... 
CELLCYCLE | SITE-SPECIFIC RECOMBINATION | ONCOLOGY | DEFICIENCY COOPERATE | CRE RECOMBINASE | NEUROFIBROMATOSIS TYPE-2 GENE | TUMOR-SUPPRESSOR PROTEIN | LARGE-T-ANTIGEN | CROCIDOLITE ASBESTOS | SARCOMATOID MESOTHELIOMA | SPINDLE-CELL NEOPLASMS | MUTANT NF2 PROTEIN | CELL BIOLOGY | Immunohistochemistry | Thoracic Cavity - pathology | Epithelial Cells - metabolism | Mesothelioma - pathology | Luminescent Measurements | Loss of Heterozygosity | Tumor Suppressor Protein p53 - genetics | Neoplasms, Experimental - pathology | Mixed Tumor, Malignant - pathology | Time Factors | Cell Transformation, Neoplastic - genetics | Recombination, Genetic | Neoplasms, Experimental - genetics | Adenoviridae - genetics | Integrases - metabolism | Neurofibromatosis 2 - metabolism | Mixed Tumor, Malignant - metabolism | Epithelioid Cells - pathology | Neoplasm Invasiveness | Thoracic Neoplasms - pathology | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Epithelial Cells - pathology | Genotype | Mesothelioma - genetics | Neurofibromatosis 2 - genetics | Sarcoma - pathology | Cell Transformation, Neoplastic - metabolism | Thoracic Neoplasms - metabolism | Epithelioid Cells - metabolism | Mice, Knockout | Sarcoma - metabolism | Phenotype | Animals | Mesothelioma - metabolism | Thoracic Neoplasms - genetics | Cell Line, Tumor | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Mice | Neoplasms, Experimental - metabolism | Cell Transformation, Neoplastic - pathology | Genetic Vectors | Integrases - genetics | Thoracic Cavity - metabolism | Tumor proteins | Mesothelioma
Journal Article
Nature, ISSN 0028-0836, 06/2018, Volume 558, Issue 7711, pp. 605 - 609
Reprogramming of mRNA translation has a key role in cancer development and drug resistance(1). However, the molecular mechanisms that are involved in this... 
CELLS | MELANOMA | INHIBITION | TRANSFER-RNAS | MULTIDISCIPLINARY SCIENCES | KINASE | IMPROVED SURVIVAL | MUTATIONS | HUMAN CANCER | VEMURAFENIB | RIBOSOME | Phosphorylation | Humans | Melanoma, Experimental - drug therapy | Male | Uridine - genetics | RNA, Messenger - metabolism | Vemurafenib - therapeutic use | Melanoma - genetics | RNA, Transfer - genetics | Carrier Proteins - chemistry | Female | Codon - genetics | Codon - drug effects | RNA, Transfer - chemistry | Uridine - chemistry | Signal Transduction | RNA, Transfer - metabolism | RNA, Messenger - genetics | Melanoma, Experimental - pathology | Melanoma - pathology | Mice, SCID | Vemurafenib - pharmacology | Zebrafish - genetics | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Mechanistic Target of Rapamycin Complex 2 - metabolism | Drug Resistance, Neoplasm - genetics | Animals | Carrier Proteins - metabolism | Melanoma, Experimental - genetics | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Line, Tumor | Mice, Inbred NOD | Protein Biosynthesis - drug effects | Uridine - metabolism | Mice | Drug Resistance, Neoplasm - drug effects | Care and treatment | Codon | Oncology, Experimental | Melanoma | Research | Genetic translation | Cancer | Enzymes | Physiological aspects | Development and progression | Protein biosynthesis | Transfer RNA | Short term | Therapy | Transformation | Genomes | mRNA | Kinases | Proteins | Signal transduction | Translation | Cell survival | tRNA | MAP kinase | Pharmacology | Decoding | Metabolism | Gene expression | Chemical compounds | Survival | Molecular chains | 1-Phosphatidylinositol 3-kinase | Signaling | Molecular modelling | Protein synthesis | Uridine | Glycolysis | Mutation
Journal Article
ONCOGENE, ISSN 0950-9232, 07/2019, Volume 38, Issue 27, pp. 5457 - 5468
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive cancer arising from T-cell progenitors. Although current treatments, including chemotherapy and... 
ACTIVATION | PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | AUTOPHAGY | CANCER | CELL-DEATH | CELL BIOLOGY | REGULATOR | ONCOLOGY | GENETICS & HEREDITY | GENE-EXPRESSION | RESISTANCE | MUTATIONS | CYTOTOXICITY | Acute lymphatic leukemia | Glucocorticoids | Chloroquine | DNA damage | Lymphocytes T | Lymphatic leukemia | Autophagy | Synergism | Chemotherapy | Cell lines | Phagocytosis | Secretase | Deoxyribonucleic acid--DNA
Journal Article