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Nature, ISSN 0028-0836, 07/2016, Volume 535, Issue 7610, pp. 111 - 116
Journal Article
Nature Medicine, ISSN 1078-8956, 01/2007, Volume 13, Issue 1, pp. 54 - 61
Anthracyclin-treated tumor cells are particularly effective in eliciting an anticancer immune response, whereas other DNA-damaging agents such as etoposide and... 
MEDICINE, RESEARCH & EXPERIMENTAL | CLEARANCE | DENDRITIC CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | TUMOR | CHAPERONE | CELL BIOLOGY | DYING CELLS | APOPTOTIC CELLS | SURFACE CALRETICULIN | ENDOPLASMIC-RETICULUM | ENCODING CALRETICULIN | ANTIGEN | Apoptosis - drug effects | Colonic Neoplasms - drug therapy | Dendritic Cells - immunology | Electrophoresis, Gel, Two-Dimensional | Immunoblotting | Antineoplastic Agents - therapeutic use | Protein Transport - drug effects | Calreticulin - genetics | Colonic Neoplasms - metabolism | Cell Cycle Proteins - antagonists & inhibitors | RNA Interference | Anthracyclines - pharmacology | Neoplasms, Experimental - immunology | Calreticulin - metabolism | Antigens, Differentiation - metabolism | Antineoplastic Agents - pharmacology | Cell Membrane - metabolism | Protein Phosphatase 1 | Cell Membrane - drug effects | Mitomycin - therapeutic use | Cell Cycle Proteins - metabolism | Phagocytosis - immunology | Etoposide - pharmacology | Etoposide - therapeutic use | Recombinant Proteins - pharmacology | Mitomycin - pharmacology | Animals | Apoptosis - immunology | Mice, Nude | Colonic Neoplasms - pathology | Cell Line, Tumor | Cell Membrane - immunology | Mice | Mice, Inbred BALB C | Anthracyclines - therapeutic use | Calreticulin - immunology | Neoplasms, Experimental - metabolism | Neoplasms, Experimental - drug therapy | Chemotherapy | Immunology | DNA damage | Rodents | Cancer | Apoptosis | Tumors | Antigens, Differentiation | Cell Membrane | Anthracyclines | Dendritic Cells | Recombinant Proteins | Life Sciences | Calreticulin | Neoplasms, Experimental | Mitomycin | Etoposide | Antineoplastic Agents | Protein Transport | Phagocytosis | Cell Cycle Proteins | Colonic Neoplasms
Journal Article
Nature Chemical Biology, ISSN 1552-4450, 2014, Volume 10, Issue 4, pp. 305 - 312
Journal Article
Nature, ISSN 0028-0836, 07/2016, Volume 535, Issue 7610, pp. 153 - 158
Inflammatory caspases (caspases 1, 4, 5 and 11) are activated in response to microbial infection and danger signals. When activated, they cleave mouse and... 
LISTERIA-MONOCYTOGENES | INTERLEUKIN-1-BETA | MULTIDISCIPLINARY SCIENCES | MIXED LINEAGE KINASE | PERFORIN | NLRP3 INFLAMMASOME | INTRACELLULAR BACTERIA | GRANZYMES | CASPASE-1 ACTIVATION | GRANULYSIN | CELL-DEATH | Conserved Sequence - genetics | Inflammasomes - metabolism | Phosphatidylinositol Phosphates - metabolism | Pyroptosis - drug effects | Escherichia coli - drug effects | Humans | Molecular Sequence Data | Neoplasm Proteins - pharmacology | Escherichia coli - cytology | Neoplasm Proteins - metabolism | Escherichia coli - metabolism | Protein Multimerization - genetics | Listeria monocytogenes - metabolism | Cell Membrane - metabolism | Membrane Proteins - metabolism | Listeria monocytogenes - cytology | Porosity - drug effects | Neoplasm Proteins - genetics | Cell Membrane - drug effects | Staphylococcus aureus - metabolism | Amino Acid Sequence | Cell Line | Microbial Viability - drug effects | Membrane Proteins - genetics | Mice, Inbred C57BL | Phosphatidylserines - metabolism | Neoplasm Proteins - chemistry | Cardiolipins - metabolism | Cell Membrane - ultrastructure | Protein Structure, Tertiary - genetics | Microscopy, Electron | Pyroptosis - genetics | Protein Transport | Liposomes - chemistry | Animals | Membrane Proteins - chemistry | Cell Membrane Permeability - drug effects | Staphylococcus aureus - cytology | Liposomes - metabolism | Mice | Mutation | Staphylococcus aureus - drug effects | Listeria monocytogenes - drug effects | Observations | Apoptosis | Proteins | Membranes | Bacterial infections | Immunology | Plasmids | Bacteria | Infections | Cells
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 12/2008, Volume 118, Issue 12, pp. 3917 - 3929
The role of autophagy in oncogenesis remains ambiguous, and mechanisms that induce autophagy and regulate its outcome in human cancers are poorly understood.... 
BREAST-CANCER | SURVIVAL | MEDICINE, RESEARCH & EXPERIMENTAL | APOPTOSIS | THERAPY | RELEVANCE | MECHANISMS | OPPORTUNITIES | TUMORIGENESIS | EXPRESSION | PROGRESSION | Protein Kinases - metabolism | Neoplasm Transplantation | Protein Kinases - genetics | Antibiotics, Antineoplastic - pharmacology | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Humans | Ovarian Neoplasms - pathology | Cell Survival - genetics | Transplantation, Heterologous | Phosphatidylinositol 3-Kinases - metabolism | Autophagy - drug effects | Ovarian Neoplasms - genetics | Chloroquine - pharmacology | Cysteine Endopeptidases - metabolism | Tumor Suppressor Proteins - genetics | Female | Ovarian Neoplasms - metabolism | Antirheumatic Agents - pharmacology | Autophagy - genetics | Cell Survival - drug effects | Tumor Suppressor Proteins - metabolism | rho GTP-Binding Proteins - genetics | Phagosomes - metabolism | Sirolimus - pharmacology | Genomic Imprinting - drug effects | Genomic Imprinting - genetics | Phosphatidylinositol 3-Kinases - genetics | Animals | Intercellular Signaling Peptides and Proteins - pharmacology | Mice, Nude | Cysteine Endopeptidases - genetics | rho GTP-Binding Proteins - metabolism | Cell Line, Tumor | Mice | Mice, Inbred BALB C | TOR Serine-Threonine Kinases | Phagosomes - genetics | Care and treatment | Causes of | Physiological aspects | Tumor suppressor genes | Genetic aspects | Research | Health aspects | Apoptosis | Ovarian cancer
Journal Article
Nature, ISSN 0028-0836, 10/2015, Volume 526, Issue 7572, pp. 218 - 223
HIV-1 Nef and the unrelated mouse leukaemia virus glycosylated Gag (glycoGag) strongly enhance the infectivity of HIV-1 virions produced in certain cell types... 
CYTOPLASMIC DOMAIN | CELL-SURFACE CD4 | GLYCOSYLATED-GAG | VIRION FUSION | REPLICATION | PRIMARY T-LYMPHOCYTES | MULTIDISCIPLINARY SCIENCES | IMMUNODEFICIENCY-VIRUS TYPE-1 | CD4 DOWN-REGULATION | MURINE LEUKEMIA-VIRUS | OPTIMAL VIRAL INFECTIVITY | Humans | Neoplasm Proteins - antagonists & inhibitors | Neoplasm Proteins - pharmacology | Virion - chemistry | Host-Pathogen Interactions - drug effects | Membrane Proteins - pharmacology | Neoplasm Proteins - metabolism | Receptors, Cell Surface - antagonists & inhibitors | Membrane Proteins - deficiency | HIV-1 - growth & development | HIV-1 - physiology | HIV-1 - chemistry | Gene Deletion | nef Gene Products, Human Immunodeficiency Virus - metabolism | Membrane Proteins - metabolism | Cell Line | Virus Replication - drug effects | nef Gene Products, Human Immunodeficiency Virus - deficiency | HIV-1 - drug effects | Down-Regulation | HIV Infections - virology | Virion - physiology | CD4-Positive T-Lymphocytes - metabolism | Receptors, Cell Surface - metabolism | Gene Products, gag - metabolism | Protein Transport | Virion - drug effects | Membrane Proteins - antagonists & inhibitors | Receptors, Cell Surface - deficiency | HIV Infections - drug therapy | Neoplasm Proteins - deficiency | Virion - growth & development | Leukemia Virus, Murine - chemistry | Development and progression | Genetic aspects | Virulence (Microbiology) | Viral proteins | Properties | HIV infection | Proteins | Genomes | Immunology | Mutation | Human immunodeficiency virus--HIV | Cells
Journal Article
Cancer Cell, ISSN 1535-6108, 2011, Volume 19, Issue 1, pp. 31 - 44
Polarization of tumor-associated macrophages (TAMs) to a proangiogenic/immune-suppressive (M2-like) phenotype and abnormal, hypoperfused vessels are hallmarks... 
Clodronic Acid - pharmacology | Gene Expression - genetics | Dendritic Cells - immunology | Humans | Pregnancy Proteins - genetics | Microvessels - pathology | Pregnancy Proteins - metabolism | Chemotactic Factors - metabolism | Neoplasm Metastasis - immunology | Antibodies - immunology | Neovascularization, Pathologic - immunology | Macrophages, Peritoneal - drug effects | Macrophages - pathology | Neoplasms - blood supply | Down-Regulation - genetics | Mice, Knockout | Macrophages - metabolism | Neoplasms - immunology | Cell Line, Tumor | Placenta Growth Factor | Mice | Mice, Inbred BALB C | CD8-Positive T-Lymphocytes - immunology | Macrophages, Peritoneal - metabolism | Neoplasms - metabolism | CD8-Positive T-Lymphocytes - pathology | Gene Expression - drug effects | Regional Blood Flow - genetics | Dendritic Cells - pathology | Culture Media, Conditioned - pharmacology | Lung Neoplasms - pathology | Hypoxia - metabolism | Neovascularization, Pathologic - pathology | Regional Blood Flow - drug effects | Transfection | Lung Neoplasms - secondary | Neoplasms - genetics | Dendritic Cells - metabolism | Macrophages - immunology | Lung Neoplasms - genetics | Microvessels - ultrastructure | Cytokines - metabolism | Mice, Inbred C57BL | Microvessels - drug effects | Pregnancy Proteins - immunology | Antibodies - pharmacology | Proteins - genetics | Neoplasm Metastasis - genetics | Hypoxia - genetics | Lung Neoplasms - immunology | Animals | Proteins - metabolism | Endothelial Cells - cytology | Neoplasm Metastasis - pathology | Macrophages - drug effects | Neovascularization, Pathologic - genetics | Cell Proliferation - drug effects | Proteins - pharmacology | Neoplasms - pathology | Endothelial Cells - drug effects
Journal Article
Cancer Letters, ISSN 0304-3835, 2017, Volume 403, pp. 48 - 58
Abstract Mesenchymal-type cancers after epithelial mesenchymal transition (EMT) were recently shown to acquire chemoresistance through expressing EMT specific... 
Hematology, Oncology and Palliative Medicine | BCL2 | Druggable target | Chemoradioresistance | Mesenchymal cancer cells | LAMTOR3 | ERK | SURVIVAL | METASTASIS | CELL INVASION | DEATH | TRANSITION | ONCOLOGY | RESISTANCE | INHIBITORS | PROMOTES | EXPRESSION | CONTRIBUTES | Up-Regulation | Adenocarcinoma - pathology | Diphenylamine - pharmacology | Adenocarcinoma of Lung | Humans | Radiation Tolerance | Gene Expression Regulation, Neoplastic | Drug Resistance, Neoplasm | Lung Neoplasms - pathology | Peptide Fragments - pharmacology | Chemoradiotherapy | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Dose-Response Relationship, Drug | Diphenylamine - analogs & derivatives | Proto-Oncogene Proteins c-bcl-2 - metabolism | Molecular Mimicry | Transfection | Biphenyl Compounds - pharmacology | Nitrophenols - pharmacology | RNA Interference | Adenocarcinoma - genetics | Benzamides - pharmacology | Signal Transduction - radiation effects | Lung Neoplasms - genetics | Proto-Oncogene Proteins - pharmacology | A549 Cells | Cell Survival - drug effects | MAP Kinase Kinase 1 - antagonists & inhibitors | Aniline Compounds - pharmacology | Lung Neoplasms - enzymology | Mitogen-Activated Protein Kinase 3 - genetics | Adenocarcinoma - enzymology | Etoposide - pharmacology | MAP Kinase Kinase 1 - metabolism | Lung Neoplasms - therapy | Sulfonamides - pharmacology | Piperazines - pharmacology | Adenocarcinoma - therapy | Mitogen-Activated Protein Kinase 3 - metabolism | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Signal Transduction - drug effects | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Adaptor Proteins, Signal Transducing - metabolism | Proto-Oncogene Proteins c-bcl-2 - genetics | Mitogen-Activated Protein Kinases - metabolism | Medical research | Care and treatment | Lung cancer | Analysis | Stem cells | Medicine, Experimental | DNA binding proteins | Drug approval | Cancer | Adenocarcinoma | Drugs | Transcription factors | Immunoglobulins | Mesenchyme | Manufacturers | Chemoresistance | Extracellular signal-regulated kinase | MAP kinase | Breast cancer | Metastasis | Kinases | Gene expression | Drug resistance | Cancer therapies | Patients | Proteins | Cell growth | Pancreatic cancer | Trends | Apoptosis
Journal Article
Brain Research, ISSN 0006-8993, 05/2006, Volume 1089, Issue 1, pp. 67 - 78
Small heat shock proteins Hsp20 and HspB2/B3 co-localize with Aβ deposition in senile plaques and cerebral amyloid angiopathy in Alzheimer's disease brains,... 
Cerebrovascular amyloid | Amyloid-β protein | Small heat shock protein | Alzheimer's disease | Fibrillization | HSPB8 | ALPHA-B-CRYSTALLIN | ALZHEIMERS-DISEASE BRAINS | CHAPERONE | NEUROSCIENCES | VESSEL WALL | HUMAN BRAIN PERICYTES | fibrillization | IN-VITRO | small heat shock protein | A-BETA | amyloid-beta protein | SMOOTH-MUSCLE-CELLS | cerebrovascular amyloid | EXPRESSION | Protein Binding - genetics | Humans | Neoplasm Proteins - pharmacology | Cerebral Amyloid Angiopathy - metabolism | Neoplasm Proteins - metabolism | alpha-Crystallins - metabolism | HSP20 Heat-Shock Proteins - metabolism | Neuroprotective Agents - metabolism | HSP20 Heat-Shock Proteins - pharmacology | Neuroprotective Agents - pharmacology | Amyloid beta-Peptides - genetics | Amyloid beta-Peptides - metabolism | Peptide Fragments - genetics | Alzheimer Disease - physiopathology | Peptide Fragments - metabolism | Plaque, Amyloid - pathology | Cerebral Amyloid Angiopathy - physiopathology | Heat-Shock Proteins - metabolism | Cells, Cultured | Cerebral Arteries - physiopathology | Heat-Shock Proteins - pharmacology | Mutation - genetics | Amyloid beta-Peptides - antagonists & inhibitors | alpha-Crystallins - pharmacology | Cerebral Arteries - metabolism | Peptide Fragments - antagonists & inhibitors | Alzheimer Disease - metabolism | Plaque, Amyloid - metabolism | Amyloid beta-Peptides - chemistry | HSP27 Heat-Shock Proteins
Journal Article