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Nature, ISSN 0028-0836, 11/2017, Volume 551, Issue 7681, pp. 517 - 520
Checkpoint blockade immunotherapies enable the host immune system to recognize and destroy tumour cells(1). Their clinical activity has been correlated with... 
CELL LUNG-CANCER | CTLA-4 BLOCKADE | MELANOMA | THERAPY | LANDSCAPE | PD-1 BLOCKADE | MULTIDISCIPLINARY SCIENCES | SENSITIVITY | RESISTANCE | CLINICAL-RESPONSE | REPERTOIRES | Humans | Lung Neoplasms - pathology | Programmed Cell Death 1 Receptor - antagonists & inhibitors | Antigen Presentation | Melanoma - genetics | Immunotherapy | Cell Cycle Checkpoints - genetics | Cell Cycle Checkpoints - immunology | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Antigens, Neoplasm - genetics | Antigens, Neoplasm - immunology | Carcinoma, Non-Small-Cell Lung - genetics | Lymphocyte Activation | CTLA-4 Antigen - genetics | Lung Neoplasms - therapy | Melanoma - pathology | CTLA-4 Antigen - immunology | Carcinoma, Non-Small-Cell Lung - immunology | Carcinoma, Non-Small-Cell Lung - therapy | Lung Neoplasms - immunology | Models, Immunological | Melanoma - immunology | Survival Analysis | T-Lymphocytes - immunology | Programmed Cell Death 1 Receptor - immunology | CTLA-4 Antigen - antagonists & inhibitors | Melanoma - therapy | Programmed Cell Death 1 Receptor - genetics | Cohort Studies | Evolution, Molecular | Antigens | Care and treatment | Patient outcomes | Models | Health aspects | Tumors | Medical research | Peptides | PD-1 protein | Lung cancer | Melanoma | Cytotoxicity | Lymphocytes T | Patients | Proteins | Cell recognition | CTLA-4 protein | Major histocompatibility complex | Immune checkpoint | Lymphocytes | Evolution | Mutation | Histocompatibility | Cancer | Immune system | Fitness | Index Medicus
Journal Article
Nature Cell Biology, ISSN 1465-7392, 11/2014, Volume 16, Issue 12, pp. 1257 - 1264
Journal Article
Journal Article
Nature Cell Biology, ISSN 1465-7392, 07/2015, Volume 17, Issue 7, pp. 868 - 879
The spindle assembly checkpoint (SAC) is a unique signalling mechanism that responds to the state of attachment of the kinetochore to spindle microtubules. SAC... 
NDC80 COMPLEX | RECRUITMENT | BUDDING YEAST | MPS1 | PHOSPHORYLATION | CHROMOSOME CONGRESSION | KINASE | MICROTUBULE ATTACHMENT | MITOTIC SPINDLE | PROTEIN ARCHITECTURE | CELL BIOLOGY | Phosphorylation | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Saccharomyces cerevisiae - genetics | Tubulin Modulators - pharmacology | Nocodazole - pharmacology | Saccharomyces cerevisiae - drug effects | Saccharomyces cerevisiae - metabolism | Microtubules - metabolism | Spindle Apparatus - metabolism | Cell Cycle Proteins - genetics | Cell Cycle Checkpoints - genetics | Time-Lapse Imaging - methods | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Aurora Kinases - metabolism | Kinetochores - metabolism | Aurora Kinases - genetics | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Cell Cycle Checkpoints - physiology | Nuclear Proteins - metabolism | Signal Transduction - genetics | Saccharomyces cerevisiae Proteins - genetics | Sirolimus - pharmacology | Signal Transduction - drug effects | Cell Cycle Checkpoints - drug effects | Saccharomyces cerevisiae Proteins - metabolism | Protein Binding | Luminescent Proteins - genetics | Signal Transduction - physiology | Microscopy, Fluorescence | Luminescent Proteins - metabolism | Spindle (Cell division) | Cellular signal transduction | Genetic aspects | Properties | Kinetochores | Index Medicus
Journal Article
Science, ISSN 0036-8075, 10/2015, Volume 350, Issue 6257, pp. 207 - 211
Journal Article
Genes and Development, ISSN 0890-9369, 01/2014, Volume 28, Issue 2, pp. 140 - 152
Journal Article
Cancer Cell, ISSN 1535-6108, 11/2015, Volume 28, Issue 5, pp. 623 - 637
In normal cells, p53 is activated by DNA damage checkpoint kinases to simultaneously control the G1/S and G2/M cell cycle checkpoints through transcriptional... 
ADJUVANT CHEMOTHERAPY | LUNG-CANCER | MESSENGER-RNAS | ONCOLOGY | PHOSPHORYLATION | DNA-DAMAGE RESPONSE | STABILIZATION | KINASE | IDENTIFICATION | INHIBITOR | P53 | CELL BIOLOGY | Neoplasms - metabolism | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Male | Antineoplastic Agents - therapeutic use | Tumor Suppressor Protein p53 - genetics | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Neoplasms - genetics | RNA Interference | HEK293 Cells | Cell Cycle Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Cell Cycle Checkpoints - genetics | Female | Nuclear Proteins - genetics | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Heterogeneous-Nuclear Ribonucleoproteins - metabolism | Nuclear Proteins - metabolism | Genetic Pleiotropy | Reverse Transcriptase Polymerase Chain Reaction | Neoplasms - drug therapy | Heterogeneous-Nuclear Ribonucleoproteins - genetics | Drug Resistance, Neoplasm - genetics | Animals | Cisplatin - therapeutic use | Survival Analysis | Cell Line, Tumor | Aged | Mutation | Cyclin-Dependent Kinase Inhibitor p27 - genetics | Chemotherapy | RNA | Lung cancer | Cell cycle | Tumor proteins | Phosphotransferases | Cancer | Protein binding | Tumors | Messenger RNA | Research institutes | Genetic transcription | Binding proteins | DNA repair | Index Medicus
Journal Article
Journal Article
Molecular Cancer Research, ISSN 1541-7786, 01/2015, Volume 13, Issue 1, pp. 16 - 28
Journal Article