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Cancer Cell, ISSN 1535-6108, 02/2014, Volume 25, Issue 2, pp. 243 - 256
Mutations in are prevalent in human cancers and universally predictive of resistance to anticancer therapeutics. Although it is widely accepted that... 
ACTIVATION | INHIBITION | ONCOGENIC RAS | TUMOR PROGRESSION | CHK1 | ONCOLOGY | INITIATION | COMBINATION | SUPPRESSION | ATR | KINASES | CELL BIOLOGY | Neoplasms - metabolism | Protein Kinases - metabolism | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) - genetics | Humans | ras Proteins - metabolism | Drug Resistance, Neoplasm | Phosphatidylinositol 3-Kinases - metabolism | GTP Phosphohydrolases - antagonists & inhibitors | Ribosomal Protein S6 Kinases, 90-kDa - metabolism | Flow Cytometry | Neoplasms - genetics | DNA Damage - genetics | Female | Antineoplastic Agents - pharmacology | Membrane Proteins - metabolism | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | DNA Damage - drug effects | Proto-Oncogene Proteins - metabolism | Cell Survival - drug effects | Membrane Proteins - genetics | Proto-Oncogene Proteins - genetics | Mutation - genetics | Animals | GTP Phosphohydrolases - metabolism | Membrane Proteins - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - metabolism | GTP Phosphohydrolases - genetics | Mice, Nude | Proto-Oncogene Proteins p21(ras) - antagonists & inhibitors | Checkpoint Kinase 1 | Mice | Cell Transformation, Neoplastic - pathology | Neoplasms - pathology | Mitogen-Activated Protein Kinase 1 - metabolism | Chemotherapy | DNA damage | DNA | Genetic research | DNA repair | Cancer | Tumors | Index Medicus
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 09/2013, Volume 20, Issue 9, pp. 1241 - 1249
When the cell cycle becomes arrested, MTOR (mechanistic Target of Rapamycin) converts reversible arrest into senescence (geroconversion). Hyperexpression of... 
senescence | MEK | cancer | aging | cell cycle | rapamycin | PHOSPHATIDYLINOSITOL 3-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | C-MYC | PROLIFERATION | CELLULAR SENESCENCE | REPLICATIVE SENESCENCE | CELL BIOLOGY | ONCOGENIC RAS | GROWTH ARREST | EXPRESSION | HUMAN TUMOR-CELLS | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Cyclin D1 - metabolism | Antibiotics, Antineoplastic - pharmacology | Nitriles - pharmacology | TOR Serine-Threonine Kinases - metabolism | Humans | Cellular Senescence - drug effects | Neoplasm Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p16 | MAP Kinase Kinase 1 - genetics | Cyclin D1 - antagonists & inhibitors | TOR Serine-Threonine Kinases - genetics | RNA Interference | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Cell Cycle Checkpoints - genetics | Benzamides - pharmacology | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | TOR Serine-Threonine Kinases - drug effects | Cellular Senescence - genetics | MAP Kinase Kinase 1 - antagonists & inhibitors | Butadienes - pharmacology | Enzyme Inhibitors - pharmacology | MAP Kinase Kinase 1 - metabolism | Cyclin D1 - biosynthesis | Piperazines - pharmacology | Sirolimus - pharmacology | Cell Division - drug effects | Cyclin D1 - genetics | Cell Cycle Checkpoints - drug effects | Cell Line, Tumor | Pyridines - pharmacology | RNA, Small Interfering | Index Medicus | Original Paper
Journal Article
Nature, ISSN 0028-0836, 08/2017, Volume 548, Issue 7669, pp. 537 - 542
Somatic gene mutations can alter the vulnerability of cancer cells to T-cell-based immunotherapies. Here we perturbed genes in human melanoma cells to mimic... 
CELL LUNG-CANCER | METASTATIC MELANOMA | DIFFERENTIAL GENE | CTLA-4 BLOCKADE | PD-1 BLOCKADE | MULTIDISCIPLINARY SCIENCES | ENDOTHELIAL-CELLS | RECEPTOR | T-CELLS | GENOME | LYMPHOCYTES | Neoplasms - metabolism | Humans | Genome - genetics | Adoptive Transfer | Janus Kinase 1 - metabolism | T-Lymphocytes, Cytotoxic - drug effects | Apelin - metabolism | Neoplasms - therapy | Apelin Receptors - genetics | Neoplasms - genetics | Melanoma - genetics | Immunotherapy | Female | Genes, Essential - genetics | Melanoma - metabolism | T-Lymphocytes, Cytotoxic - immunology | Knowledge Bases | Reproducibility of Results | Histocompatibility Antigens Class I - immunology | Antigen Presentation - genetics | CRISPR-Cas Systems - genetics | Apelin Receptors - metabolism | Animals | T-Lymphocytes, Cytotoxic - metabolism | Melanoma - immunology | Neoplasms - immunology | Interferon-gamma - immunology | Cell Line, Tumor | Mice | Mutation | Melanoma - therapy | Care and treatment | Genetic aspects | Nucleotide sequencing | Methods | DNA sequencing | Cancer | Cytolytic activity | Animal models | CD8 antigen | Genes | Genomics | Effector cells | Genomes | Lymphocytes T | Kinases | Cancer therapies | Lymphocytes | Janus kinase | Antigen presentation | Antigens | CRISPR | Melanoma | T cell receptors | Tumor cell lines | Signaling | Immune checkpoint | γ-Interferon | Interferon | Tumors | Index Medicus
Journal Article
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 764 - 17
Checkpoint kinases sense replicative stress to prevent DNA damage. Here we show that the histone deacetylases HDAC1/HDAC2 sustain the phosphorylation of the... 
CANCER-CELLS | RIBONUCLEOTIDE REDUCTASE | CHK1 | TUMOR SUPPRESSION | DNA-DAMAGE RESPONSE | MULTIDISCIPLINARY SCIENCES | GENOME INTEGRITY | DOUBLE-STRAND BREAKS | HISTONE DEACETYLASE INHIBITORS | REPLICATION FORK COLLAPSE | ATR | Phosphorylation | Ataxia Telangiectasia Mutated Proteins - metabolism | Protein-Tyrosine Kinases - metabolism | Humans | Tumor Suppressor Protein p53 - genetics | CDC2 Protein Kinase - metabolism | Checkpoint Kinase 2 - metabolism | Checkpoint Kinase 2 - genetics | Protein-Tyrosine Kinases - genetics | Cell Cycle Proteins - genetics | Nuclear Proteins - genetics | Histone Deacetylase 1 - genetics | Histone Deacetylase 2 - genetics | CDC2 Protein Kinase - genetics | Cell Cycle Proteins - metabolism | Gene Expression Regulation | Protein Phosphatase 2 - genetics | Tumor Suppressor Protein p53 - metabolism | Nuclear Proteins - metabolism | Checkpoint Kinase 1 - metabolism | Cell Cycle | Protein Phosphatase 2 - metabolism | Histone Deacetylase 2 - metabolism | Ataxia Telangiectasia Mutated Proteins - genetics | Checkpoint Kinase 1 - genetics | Histone Deacetylase 1 - metabolism | Histone deacetylase | p53 Protein | DNA damage | Serine | Homologous recombination | Homology | Dephosphorylation | Kinases | Phosphatase | Damage prevention | Cell fate | Cell cycle | Inhibition | HDAC2 protein | Null cells | Deoxyribonucleic acid--DNA | Stresses | CHK2 protein | Threonine | Phase transformations | CHK1 protein | Protein-serine/threonine phosphatase | Replication protein A | Protein A | Ablation | Stress | DNA biosynthesis | S phase | Replication | Threonine phosphatase | Phase transition | Tumors | Apoptosis | Index Medicus
Journal Article
Cellular Signalling, ISSN 0898-6568, 01/2018, Volume 42, pp. 11 - 20
Journal Article
by Liu, D and Huang, Y and Bu, D and Liu, A.D and Holmberg, L and Jia, Y and Tang, C and Du, J and Jin, H
Cell death & disease, ISSN 2041-4889, 2014, Volume 5, Issue 5, pp. e1251 - e1251
Journal Article
PLoS ONE, ISSN 1932-6203, 10/2014, Volume 9, Issue 10, pp. e109630 - e109630
Background: In this study we investigated the in vitro and in vivo anticancer effect of carnosol, a naturally occurring polyphenol, in triple negative breast... 
CROSS-TALK | RESVERATROL | ACTIVATION | HISTONE H3 | MULTIDISCIPLINARY SCIENCES | P62/SQSTM1 | DOWN-REGULATION | LEUKEMIA-CELLS | MECHANISMS | INDUCTION | CELL-DEATH | Free Radical Scavengers - pharmacology | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Humans | 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt - pharmacology | Membrane Potential, Mitochondrial - drug effects | Autophagy - drug effects | Antineoplastic Agents, Phytogenic - antagonists & inhibitors | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | G2 Phase Cell Cycle Checkpoints - drug effects | Mitogen-Activated Protein Kinase 1 - genetics | Triple Negative Breast Neoplasms - pathology | Apoptosis Regulatory Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Diterpenes, Abietane - antagonists & inhibitors | Female | Membrane Proteins - metabolism | Phosphorylation - drug effects | Beclin-1 | Mitogen-Activated Protein Kinase 3 - genetics | Membrane Proteins - genetics | Apoptosis Regulatory Proteins - metabolism | Diterpenes, Abietane - pharmacology | Triple Negative Breast Neoplasms - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Triple Negative Breast Neoplasms - metabolism | Cell Line, Tumor | Cell Proliferation - drug effects | DNA Damage | Antineoplastic Agents, Phytogenic - pharmacology | Cyclin-Dependent Kinase Inhibitor p27 - genetics | Mitogen-Activated Protein Kinase 1 - metabolism | Breast cancer | Apoptosis | Drugs | Health sciences | Reactive oxygen species | Leukemia | DNA damage | Homeostasis | Cytotoxicity | Biology | Mitochondrial DNA | Coexistence | Autophagy | Cancer therapies | Anticancer properties | Cell cycle | Inhibition | Deoxyribonucleic acid--DNA | Extracellular signal-regulated kinase | Exploration | Gene expression | Cyclin-dependent kinase inhibitor p21 | Phytochemicals | Damage detection | Medical prognosis | Breast | In vivo methods and tests | Viability | Phagocytosis | Cancer | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2017, Volume 12, Issue 7, pp. e0181183 - e0181183
Introduction The regulation of reactive oxygen species (ROS) exists as a therapeutic target for cancer treatments. Previous studies have shown that... 
DEOXYCHOLIC-ACID | APOPTOSIS | INFLAMMATORY-BOWEL-DISEASE | MULTIDISCIPLINARY SCIENCES | ULCERATIVE-COLITIS | CHEMOPREVENTIVE AGENT | RISK | CYCLE PROGRESSION | NF-KAPPA-B | PRIMARY SCLEROSING CHOLANGITIS | SUSTAINED ERK PHOSPHORYLATION | Neoplastic Stem Cells - cytology | Cyclin-Dependent Kinases - metabolism | Reactive Oxygen Species - metabolism | Neoplastic Stem Cells - drug effects | HCT116 Cells | Humans | RNA, Messenger - metabolism | Colonic Neoplasms - metabolism | HT29 Cells | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Ursodeoxycholic Acid - pharmacology | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Neoplastic Stem Cells - metabolism | Cell Cycle Checkpoints - drug effects | Colonic Neoplasms - pathology | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Cell Proliferation - drug effects | p38 Mitogen-Activated Protein Kinases - metabolism | Oxidative Stress - drug effects | Cyclin-Dependent Kinases - genetics | Real-Time Polymerase Chain Reaction | Cyclin-Dependent Kinase Inhibitor p27 - genetics | Mitogen-Activated Protein Kinase 1 - metabolism | Cell proliferation | Oxidative stress | Reactive oxygen species | Colon cancer | Growth | Analysis | Cancer cells | Ursodiol | Research | Fluorescein isothiocyanate | Cell culture | Flow cytometry | Regulations | Biotechnology | GTP-binding protein | Phosphorylation | Colorectal cancer | Fluorescence | Staining | Bromodeoxyuridine | mRNA | Cancer therapies | Phase transitions | Cyclin-dependent kinase 4 | Western blotting | Ursodeoxycholic acid | Cell growth | Rodents | Gastroenterology | Cell cycle | Colon | Inhibition | Immunoglobulins | Internal medicine | Extracellular signal-regulated kinase | Isothiocyanate | Tumor cell lines | Cell counters | Cyclin-dependent kinase 2 | Polymerase chain reaction | Medicine | Inhibitors | Microscopy | Fluorescein | Intracellular | Cancer | Index Medicus
Journal Article
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 12/2017, Volume 494, Issue 1-2, pp. 325 - 331
Alpha lipoic acid (α -LA) is a naturally occurring antioxidant and metabolic enzyme co-factor. Recently, α -LA has been reported to inhibit the growth of... 
Cell proliferation | α-lipoic acid | Grb2 | NSCLC | EGFR | ACTIVATION | alpha-lipoic acid | METASTASIS | STATISTICS | NODE | BIOCHEMISTRY & MOLECULAR BIOLOGY | BIOPHYSICS | POOR-PROGNOSIS | GROWTH | Oncogene Proteins - genetics | RNA, Small Interfering - genetics | Receptor, Epidermal Growth Factor - genetics | ras Proteins - genetics | Cyclin-Dependent Kinase 4 - genetics | Humans | Gene Expression Regulation, Neoplastic | ras Proteins - metabolism | Cyclin E - genetics | Receptor, Epidermal Growth Factor - metabolism | Cyclin D3 - genetics | GRB2 Adaptor Protein - genetics | Mitogen-Activated Protein Kinase 1 - genetics | Antineoplastic Agents - pharmacology | Phosphorylation - drug effects | Cyclin D3 - metabolism | A549 Cells | Cyclin-Dependent Kinase 2 - metabolism | Mitogen-Activated Protein Kinase 3 - genetics | Proto-Oncogene Proteins c-raf - genetics | Signal Transduction | Cyclin-Dependent Kinase 6 - genetics | Oncogene Proteins - metabolism | Cyclin-Dependent Kinase 2 - genetics | Thioctic Acid - pharmacology | Cyclin-Dependent Kinase 6 - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Proto-Oncogene Proteins c-raf - metabolism | GRB2 Adaptor Protein - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - metabolism | Cell Proliferation - drug effects | Cyclin E - metabolism | G1 Phase Cell Cycle Checkpoints - drug effects | GRB2 Adaptor Protein - metabolism | Mitogen-Activated Protein Kinase 1 - metabolism | RNA, Small Interfering - metabolism | Index Medicus
Journal Article