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Journal Article
JOURNAL OF CELLULAR BIOCHEMISTRY, ISSN 0730-2312, 08/2017, Volume 118, Issue 8, pp. 1979 - 1983
Journal Article
CURRENT PHARMACEUTICAL DESIGN, ISSN 1381-6128, 2018, Volume 24, Issue 39, pp. 4599 - 4600
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 01/2018, Volume 233, Issue 1, pp. 378 - 386
The DNA repair protein O6‐Methylguanine‐DNA methyltransferase (MGMT) is suggested to be associated with resistance to alkylating agents such as Temozolomide... 
overall survival | glioblastoma | MGMT methylation | progression‐free survival | progression-free survival | PHYSIOLOGY | NEWLY-DIAGNOSED GLIOBLASTOMA | MULTIFORME | ADJUVANT TEMOZOLOMIDE | CELL BIOLOGY | GENE | RANDOMIZED PHASE-III | PROTEIN EXPRESSION | DOSE-DENSE | CENTRAL-NERVOUS-SYSTEM | RADIOTHERAPY | O-6-METHYLGUANINE-DNA METHYLTRANSFERASE | Glioblastoma - enzymology | Humans | Brain Neoplasms - pathology | DNA Repair Enzymes - genetics | DNA Methylation | Glioblastoma - genetics | Time Factors | Tumor Suppressor Proteins - genetics | Biomarkers, Tumor - metabolism | Brain Neoplasms - mortality | Promoter Regions, Genetic | Brain Neoplasms - enzymology | Genetic Predisposition to Disease | Risk Factors | Brain Neoplasms - genetics | Treatment Outcome | Clinical Trials as Topic | Brain Neoplasms - drug therapy | Disease Progression | Antineoplastic Agents, Alkylating - therapeutic use | Disease-Free Survival | DNA Modification Methylases - genetics | Drug Resistance, Neoplasm - genetics | Phenotype | Glioblastoma - pathology | Glioblastoma - drug therapy | Glioblastoma - mortality | Medicine, Experimental | Medical research | Prognosis | Methylation | Glioblastoma multiforme | Methylguanine | Alkylating agents | Glioblastoma | Clinical trials | DNA repair | Patients | Survival | Alkylation | O6-methylguanine-DNA methyltransferase | Medical prognosis | DNA methylation | Biomarkers | DNA methyltransferase | Libraries | Temozolomide | Repair | Risk management | Deoxyribonucleic acid--DNA | Index Medicus
Journal Article
Journal Article
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 03/2018, Volume 233, Issue 3, pp. 2058 - 2066
The V‐Ki‐ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) is frequently dysregulated in colorectal cancer (CRC). It is involved in the modulation of... 
novel anticancer agent | cetuximab | KRAS | colorectal cancer | 1ST-LINE TREATMENT | PHYSIOLOGY | COMBINATION THERAPY | KRAS-MUTANT LUNG | WILD-TYPE KRAS | CHEMOTHERAPY | CELL BIOLOGY | MEK INHIBITION | RESISTANCE | IRINOTECAN | MUTATIONS | Receptor, Epidermal Growth Factor - genetics | Membrane Proteins - genetics | Proto-Oncogene Proteins p21(ras) - genetics | Colorectal Neoplasms - genetics | Humans | Phenylurea Compounds - therapeutic use | Antibodies, Monoclonal - therapeutic use | GTP Phosphohydrolases - antagonists & inhibitors | Cetuximab - therapeutic use | Membrane Proteins - antagonists & inhibitors | Antineoplastic Agents, Immunological - therapeutic use | Cell Transformation, Neoplastic | GTP Phosphohydrolases - genetics | Proto-Oncogene Proteins p21(ras) - antagonists & inhibitors | Colorectal Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Colorectal Neoplasms - pathology | Proto-Oncogene Proteins p21(ras) - metabolism | Pyridines - therapeutic use | Care and treatment | Sarcoma | Colorectal cancer | Drug therapy | Health aspects | Drug approval | Cancer | Drugs | Therapy | Colorectal carcinoma | Raf protein | Homology | AKT protein | Metastasis | Drug development | Cancer therapies | K-Ras protein | Metastases | Signal transduction | Pathways | Modulation | Tumorigenesis | Epidermal growth factor receptors | Invasiveness | Extracellular signal-regulated kinase | Patients | 1-Phosphatidylinositol 3-kinase | Signaling | Effectors | Mutation | Index Medicus
Journal Article
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 03/2018, Volume 233, Issue 3, pp. 2162 - 2169
Colorectal cancer is among the most lethal malignancies globally. BRAF is a member of the RAS/RAF/MEK/ERK signaling pathway. Its constitutive activation can... 
colorectal cancer | RAS/RAF/MEK/ERK pathway | BRAF mutation | target therapy | RAF INHIBITION | PHYSIOLOGY | KINASE | ACQUIRED-RESISTANCE | DOSE-ESCALATION TRIAL | V600E MUTATION | BRAF(V600E) | CELL BIOLOGY | ISLAND METHYLATOR PHENOTYPE | COLON-CANCER | MELANOMA | VEMURAFENIB | ErbB Receptors - antagonists & inhibitors | Colorectal Neoplasms - genetics | Humans | Oximes - therapeutic use | Piperazines - therapeutic use | Extracellular Signal-Regulated MAP Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Vemurafenib | Drug Resistance, Neoplasm - genetics | Sulfonamides - therapeutic use | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Colorectal Neoplasms - drug therapy | Amino Acid Substitution - genetics | Indoles - therapeutic use | Imidazoles - therapeutic use | Carbamates - therapeutic use | Colorectal Neoplasms - pathology | MAP Kinase Kinase Kinases - antagonists & inhibitors | Cinnamates - therapeutic use | Cancer patients | Care and treatment | Gene mutations | Colorectal cancer | Genetic aspects | Metastasis | Health aspects | Medical research | Therapy | Epidermal growth factor receptors | Colorectal carcinoma | MEK inhibitors | Clinical trials | Extracellular signal-regulated kinase | Raf protein | 1-Phosphatidylinositol 3-kinase | Metastases | Signal transduction | Signaling | Inhibitors | Mutation | Cancer
Journal Article