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MOLECULAR CELL, ISSN 1097-2765, 05/2016, Volume 62, Issue 4, pp. 507 - 519
UV-induced DNA damage, a major risk factor for skin cancers, is primarily repaired by nucleotide excision repair (NER). UV radiation resistance-associated gene... 
COMPLEX | PROTEIN | INDUCED UBIQUITYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | CUTANEOUS MELANOMA | RISK | XPC | MUTATIONS | CANCER | NUCLEOTIDE EXCISION-REPAIR | CELL BIOLOGY | Autophagy - radiation effects | Humans | DNA Repair - radiation effects | Drosophila Proteins - metabolism | Drosophila melanogaster - genetics | DNA-Binding Proteins - metabolism | Ubiquitination | Skin Neoplasms - enzymology | Transfection | Ultraviolet Rays | RNA Interference | Time Factors | Proteolysis | Retina - enzymology | Tumor Suppressor Proteins - genetics | HEK293 Cells | Cullin Proteins - metabolism | Signal Transduction - radiation effects | Drosophila melanogaster - radiation effects | Retina - radiation effects | Skin Neoplasms - pathology | Melanoma, Experimental - enzymology | Tumor Suppressor Proteins - metabolism | Ubiquitin-Protein Ligases - metabolism | Melanoma, Experimental - pathology | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Cullin Proteins - genetics | Transcription Factors - metabolism | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Melanoma, Experimental - genetics | Skin Neoplasms - genetics | Drosophila melanogaster - enzymology | DNA Damage | Drosophila Proteins - genetics | Enzyme Activation | HeLa Cells | Ubiquitin-Protein Ligases - genetics
Journal Article
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 04/2016, Volume 126, Issue 4, pp. 1367 - 1382
Most skin cancers develop as the result of UV light-induced DNA damage; however, a substantial number of cases appear to occur independently of UV damage. A... 
P53 MUTATIONS | MEDICINE, RESEARCH & EXPERIMENTAL | CLASS SWITCH RECOMBINATION | SOMATIC HYPERMUTATION | DNA-DAMAGE | SQUAMOUS-CELL CARCINOMA | ORAL-CAVITY | TP53 MUTATIONS | AID | ULTRAVIOLET-LIGHT | MOUSE SKIN | Proto-Oncogene Proteins p21(ras) - genetics | Carcinoma, Squamous Cell - genetics | Carcinoma, Squamous Cell - pathology | Humans | Neoplasms, Experimental - enzymology | Male | Tumor Suppressor Protein p53 - genetics | Neoplasms, Experimental - pathology | Skin Neoplasms - enzymology | Neoplasms, Experimental - genetics | Female | Skin - pathology | Proto-Oncogene Proteins p21(ras) - metabolism | Carcinoma, Squamous Cell - enzymology | Cytidine Deaminase - genetics | Tumor Suppressor Protein p53 - metabolism | Organ Specificity | Skin - enzymology | Ultraviolet Rays - adverse effects | Mice, Knockout | Animals | Mice, Nude | Cytidine Deaminase - metabolism | Skin Neoplasms - genetics | Mice | Mice, Inbred BALB C | Mutation | Development and progression | Ionizing radiation | Squamous cell carcinoma | Genetic aspects | B cells | Analysis | Enzymes | Molecular targeted therapy | Innovations | Hydrolases | Properties | Skin cancer | Medical research | Psoriasis | Dermatology | Colleges & universities | Environmental health | Melanoma | Gene expression | Experiments | Cancer therapies | Keratin | Cell growth | Rodents | Tumors | Index Medicus | Abridged Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2014, Volume 9, Issue 4, p. e95893
Although it is well-established that the macrophage M1 to M2 transition plays a role in tumor progression, the molecular basis for this process remains... 
Macrophages - physiology | Neoplasm Transplantation | Melanoma, Experimental - enzymology | Integrin alpha4beta1 - metabolism | Lung Neoplasms - enzymology | Melanoma, Experimental - blood supply | Signal Transduction | Neoplasm Invasiveness | Mice, Inbred C57BL | Melanoma, Experimental - pathology | Tumor Burden | Receptor, Macrophage Colony-Stimulating Factor - metabolism | Mice, Knockout | Neovascularization, Pathologic - enzymology | Animals | Lung Neoplasms - secondary | Platelet Endothelial Cell Adhesion Molecule-1 - metabolism | Cell Line, Tumor | Cell Differentiation | Enzyme Activation | rac GTP-Binding Proteins - physiology | Lung Neoplasms - blood supply | ACTIVATION | INTEGRIN | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | CSF | GTPASE RAC2 | CELL | POLARIZATION | EXPRESSION | RHO FAMILY | PROGRESSION | Development and progression | Metastasis | Gene expression | Guanosine triphosphatase | Analysis | Pediatrics | Animal models | Laboratories | Genomes | Neuroblastoma | Kinases | Macrophages | Experiments | Defects | Metastases | Cell adhesion & migration | Proteins | Angiogenesis | Cell activation | Rodents | Bone marrow | Extracellular matrix | Iterative methods | Wound healing | Inflammation | Rac2 protein | Polymerase chain reaction | DNA microarrays | Mice | Protein interaction | Differentiation | Bayesian analysis | Cancer | Guanosinetriphosphatase | Tumors
Journal Article
Journal Article
Oncogene, ISSN 0950-9232, 05/2008, Volume 27, Issue 20, pp. 2851 - 2857
Journal Article
Cancer Letters, ISSN 0304-3835, 2016, Volume 383, Issue 2, pp. 161 - 170
Abstract Lgr4 is a member of the leucine-rich, G protein–coupled receptor family of proteins, and has recently been shown to augment Wnt/β-catenin signaling... 
Hematology, Oncology and Palliative Medicine | Lgr4 | β-Catenin | Squamous cell carcinoma | ERK1/2 | TPA | ACTIVATION | GPR48 | PROLIFERATION | GENE | ONCOLOGY | beta-Catenin | RECEPTORS | UP-REGULATION | EXPRESSION | MOUSE SKIN | Cyclin D1 - metabolism | Tetradecanoylphorbol Acetate | Cell Proliferation | Receptors, G-Protein-Coupled - metabolism | Papilloma - enzymology | Humans | Neoplasms, Experimental - enzymology | Cell Transformation, Neoplastic - chemically induced | Neoplasms, Experimental - chemically induced | Extracellular Signal-Regulated MAP Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - genetics | Transcription Factor AP-1 - metabolism | Neoplasms, Experimental - pathology | Skin Neoplasms - enzymology | Transfection | RNA Interference | Time Factors | Cell Transformation, Neoplastic - genetics | Neoplasms, Experimental - genetics | Papilloma - pathology | Keratinocytes - enzymology | Papilloma - chemically induced | Wnt Signaling Pathway | Skin Neoplasms - pathology | Papilloma - genetics | Genetic Predisposition to Disease | MAP Kinase Kinase 1 - metabolism | Skin Neoplasms - chemically induced | Cell Transformation, Neoplastic - metabolism | Mice, Knockout | Keratinocytes - pathology | Phenotype | Animals | Receptors, G-Protein-Coupled - deficiency | Cyclin D1 - genetics | Skin Neoplasms - genetics | Cell Line, Tumor | Receptors, G-Protein-Coupled - genetics | Cell Transformation, Neoplastic - pathology | Transcription factors | Phosphorylation | Wnt protein | Colorectal cancer | Activation | Metastasis | Leucine | Cyclin D1 | Kinases | Cancer therapies | Carcinogenesis | Experiments | Skin cancer | Proteins | β-catenin | Signal transduction | Carcinogens | Pathways | Rodents | Conflicts of interest | Tumorigenesis | Cloning | Melanoma | Extracellular signal-regulated kinase | Gene expression | Signaling | Papilloma | Skin | Mice | Acetic acid | Tumors | Index Medicus
Journal Article
Cancer Letters, ISSN 0304-3835, 12/2017, Volume 410, pp. 1 - 11
Although glucocorticoids (GCs) regulate proliferation, differentiation and apoptosis of tumor cells, their influence on metastasis of tumor cells is poorly... 
AKT | Metastasis | Glucocorticoid | Migration | Rho-associated kinase | Melanoma | SURVIVAL | PREDNISOLONE PHOSPHATE | RECEPTOR | CELL-PROLIFERATION | CHRONIC STRESS | CANCER | CHEMOTHERAPY | B16 MELANOMA | ONCOLOGY | GROWTH | RESISTANCE | Up-Regulation | Humans | Melanoma - enzymology | Dexamethasone - toxicity | Receptors, Glucocorticoid - metabolism | Receptors, Glucocorticoid - agonists | Skin Neoplasms - enzymology | Lung Neoplasms - secondary | Time Factors | rho-Associated Kinases - metabolism | Melanoma, Experimental - secondary | Female | Glucocorticoids - toxicity | Protein Stability | Proto-Oncogene Proteins c-akt - metabolism | Skin Neoplasms - pathology | Melanoma, Experimental - enzymology | Lung Neoplasms - enzymology | Neoplasm Invasiveness | Mice, Inbred C57BL | Phosphatidylinositol 3-Kinase | Cell Adhesion - drug effects | Melanoma - secondary | Cell Movement - drug effects | Animals | Signal Transduction - drug effects | Cell Line, Tumor | Mice, Inbred BALB C | Corticosteroids | Skin cancer | Steroids | Cell proliferation | Drinking water | Motility | Glucocorticoids | Leukocyte migration | AKT protein | Matrix metalloproteinase | Kinases | Cancer therapies | Metastases | Cell adhesion & migration | Angiogenesis | Metalloproteinase | Dexamethasone | Tumor cells | RhoA protein | Breast cancer | Stress | 1-Phosphatidylinositol 3-kinase | Studies | Chemotherapy | Lungs | Skin | Laboratory animals | Cell migration | Apoptosis | Tumors | Index Medicus
Journal Article
Biochemical Pharmacology, ISSN 0006-2952, 2012, Volume 83, Issue 3, pp. 385 - 394
Journal Article
ONCOGENE, ISSN 0950-9232, 08/2014, Volume 33, Issue 34, pp. 4330 - 4339
Journal Article
Journal of the National Cancer Institute, ISSN 0027-8874, 08/2004, Volume 96, Issue 16, pp. 1219 - 1230
Journal Article
Journal Article