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Adenosylmethionine --- S--Adenosylmethionine --- Adenosylmethionine. --- S--Adenosylmethionine.
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La S-adénosylméthionine (AdoMet), synthétisée à partir de méthionine (Met) et d’ATP, est le principal donneur de méthyle de la cellule. Son groupement méthyle peut être transféré à une très large variété d’accepteurs : acides nucléiques, protéines, phospholipides, catécholamines, glycine, guanidoacétate, etc.
l’intérêt particulier pour cette molécule et son métabolisme depuis une quinzaine d’années provient du fait que son administration thérapeutique s’est révélée très efficace pour le traitement d’affections hépatiques comme les cirrhoses et cholestases. Le mécanisme d’action de l’AdoMet n’est cependant pas encore bien compris. Il a été proposé que l’administration d’AdoMet permettrait de restaurer un taux normal d’AdoMet intrahépatique, dont la synthèse est en effet déficiente en cas d’atteinte hépatique. Cette théorie implique que l’AdoMet exogène puisse être transportée à travers la membrane plasmique, ce qui est largement controversé.
Il a dès lors été décidé dans notre laboratoire de réinvestiguer en détail le métabolisme de l’AdoMet dans des suspensions d’hépatocytes isolés de rat. Bontemps et Van den Berghe (1997) ont montré que l’AdoMet exogène n’entre pas dans la cellule mais qu’elle est utilisée par les hépatocytes pour méthyler des phospholipides de la face externe de la membrane plasmique.
L’objectif de ce mémoire était de comparer le métabolisme d el’AdoMet exogène dans des hépatocytes intacts et dans des hépatocytes perméabilisés afin de voir si la membrane plasmique constitue bien une barrière pour le passage de l’AdoMet dans les hépatocytes.
en accord avec cette hypothèse, nous avons pu montrer que la vitesse du métabolisme de l’AdoMet est en effet fortement augmentée (7 à 8 fois) dan les hépatocytes perméabilisés. L’augmentation de son métabolisme est principalement due à une augmentation de la méthylation de produits solubles dans l’acide, cette dernière étant quasi indétectable lorsque les hépatocytes sont intacts. Quant à la méthylation de produits insolubles dans l’acide, qui se sont avérés être principalement des phospholipides, elle est augmentée moins de deux fois dans les hépatocytes perméabilisés, ce qui peut s’expliquer par le fait que la méthylation des phospholipides peut se produire en absence de toute pénétration de l’AdoMet. Si les hépatocytes perméabilisés sont lavés avant addition de l’AdoMet, le métabolisme de l’AdoMet est fortement réduit, principalement parce que la méthylation des produits solubles dans l’acide est supprimée ; celle des phospholipides n’est pas modifiée, ce qui confirme que ce sont des transméthylases membranaire qui sont responsables de la méthylation des phospholipides.
Nous avons d’autre part comparé l’effet d’une addition de phospholipase C à des hépatocytes préincubés en présence de [méthyl-14C] et ou en présence de [méthyl-14C]AdoMet, intacts ou perméabilisés. Nous montrons que la phospholipase C agit directement sur les phospholipides méthylés à partir d’AdoMet, mais ne peut agir sur les phospholipides méthylés à partir de Met que si les hépatocytes sont perméabilisés. Ceci confirme que le groupement méthyle de l’AdoMet exogène est transféré sur la face externe de la membrane plasmique, contrairement au groupement méthyle de la Met qui est transféré sur des phospholipides intracellulaires
S-Adenosylmethionine --- Liver --- Liver
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The chemistry of nickel in biological systems has been intensely investigated since the discovery of the essential role played by this transition metal in the enzyme urease, ca. 1975. Since then, several nickel-dependent enzymes have been discovered and characterized at the molecular level using structural, spectroscopic, and kinetic methods, and insight into reaction mechanisms has been elaborated using synthetic and computational models. The dual role of nickel as both an essential nutrient and as a toxin has prompted efforts to understand the molecular mechanisms of nickel toxicology and to uncover the means by which cells select nickel from among a pool of different and more readily available metal ions and thus regulate the intracellular chemistry of nickel. This latter effort highlights the importance of proteins involved in the extra- and intra-cellular sensing of nickel, the roles of nickel-selective proteins for import and export, and nickel-responsive transcription factors, all of which are important for regulating nickel homeostasis. In this Special Issue, the contributing authors have covered recent advances in many of these aspects of nickel biochemistry, including toxicology, bacterial pathogenesis, carcinogenesis, computational and synthetic models, nickel trafficking proteins, and enzymology.
Research & information: general --- InrS --- nickel-dependent transcriptional regulators --- molecular modelling --- nickel --- hydrogenase --- urease --- Ni-enzymes --- pathogens --- ncRNA --- miRNA --- lncRNA --- lung carcinogenesis --- histidine-rich protein --- carbon monoxide dehydrogenase --- nickel chaperone --- nickel-induced oligomerization --- urease maturation --- metallochaperone --- G-protein --- conformational change --- bioavailability --- carcinogenicity --- genotoxicity --- allergy --- reproductive --- asthma --- nanoparticles --- ecotoxicity --- environment --- biological nickel sites --- nickel-thiolates --- dinuclear nickel metallopeptides --- thiolate oxidative damage --- nickel enzymes --- reaction mechanism --- quantum chemical calculations --- glyoxalase --- streptomyces --- mycothiol --- metalloenzyme --- AD11 --- nickel-dependent enzyme --- methionine salvage pathway --- methionine --- S-adenosylmethionine (SAM) --- methylthioadenosine (MTA) --- enolase phosphatase 1 (ENOPH1) --- polyamine --- matrix metalloproteinase MT1 (MT1-MMP) --- metalloregulator --- chaperone --- [NiFe]-hydrogenase --- n/a
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The chemistry of nickel in biological systems has been intensely investigated since the discovery of the essential role played by this transition metal in the enzyme urease, ca. 1975. Since then, several nickel-dependent enzymes have been discovered and characterized at the molecular level using structural, spectroscopic, and kinetic methods, and insight into reaction mechanisms has been elaborated using synthetic and computational models. The dual role of nickel as both an essential nutrient and as a toxin has prompted efforts to understand the molecular mechanisms of nickel toxicology and to uncover the means by which cells select nickel from among a pool of different and more readily available metal ions and thus regulate the intracellular chemistry of nickel. This latter effort highlights the importance of proteins involved in the extra- and intra-cellular sensing of nickel, the roles of nickel-selective proteins for import and export, and nickel-responsive transcription factors, all of which are important for regulating nickel homeostasis. In this Special Issue, the contributing authors have covered recent advances in many of these aspects of nickel biochemistry, including toxicology, bacterial pathogenesis, carcinogenesis, computational and synthetic models, nickel trafficking proteins, and enzymology.
InrS --- nickel-dependent transcriptional regulators --- molecular modelling --- nickel --- hydrogenase --- urease --- Ni-enzymes --- pathogens --- ncRNA --- miRNA --- lncRNA --- lung carcinogenesis --- histidine-rich protein --- carbon monoxide dehydrogenase --- nickel chaperone --- nickel-induced oligomerization --- urease maturation --- metallochaperone --- G-protein --- conformational change --- bioavailability --- carcinogenicity --- genotoxicity --- allergy --- reproductive --- asthma --- nanoparticles --- ecotoxicity --- environment --- biological nickel sites --- nickel-thiolates --- dinuclear nickel metallopeptides --- thiolate oxidative damage --- nickel enzymes --- reaction mechanism --- quantum chemical calculations --- glyoxalase --- streptomyces --- mycothiol --- metalloenzyme --- AD11 --- nickel-dependent enzyme --- methionine salvage pathway --- methionine --- S-adenosylmethionine (SAM) --- methylthioadenosine (MTA) --- enolase phosphatase 1 (ENOPH1) --- polyamine --- matrix metalloproteinase MT1 (MT1-MMP) --- metalloregulator --- chaperone --- [NiFe]-hydrogenase --- n/a
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The chemistry of nickel in biological systems has been intensely investigated since the discovery of the essential role played by this transition metal in the enzyme urease, ca. 1975. Since then, several nickel-dependent enzymes have been discovered and characterized at the molecular level using structural, spectroscopic, and kinetic methods, and insight into reaction mechanisms has been elaborated using synthetic and computational models. The dual role of nickel as both an essential nutrient and as a toxin has prompted efforts to understand the molecular mechanisms of nickel toxicology and to uncover the means by which cells select nickel from among a pool of different and more readily available metal ions and thus regulate the intracellular chemistry of nickel. This latter effort highlights the importance of proteins involved in the extra- and intra-cellular sensing of nickel, the roles of nickel-selective proteins for import and export, and nickel-responsive transcription factors, all of which are important for regulating nickel homeostasis. In this Special Issue, the contributing authors have covered recent advances in many of these aspects of nickel biochemistry, including toxicology, bacterial pathogenesis, carcinogenesis, computational and synthetic models, nickel trafficking proteins, and enzymology.
Research & information: general --- InrS --- nickel-dependent transcriptional regulators --- molecular modelling --- nickel --- hydrogenase --- urease --- Ni-enzymes --- pathogens --- ncRNA --- miRNA --- lncRNA --- lung carcinogenesis --- histidine-rich protein --- carbon monoxide dehydrogenase --- nickel chaperone --- nickel-induced oligomerization --- urease maturation --- metallochaperone --- G-protein --- conformational change --- bioavailability --- carcinogenicity --- genotoxicity --- allergy --- reproductive --- asthma --- nanoparticles --- ecotoxicity --- environment --- biological nickel sites --- nickel-thiolates --- dinuclear nickel metallopeptides --- thiolate oxidative damage --- nickel enzymes --- reaction mechanism --- quantum chemical calculations --- glyoxalase --- streptomyces --- mycothiol --- metalloenzyme --- AD11 --- nickel-dependent enzyme --- methionine salvage pathway --- methionine --- S-adenosylmethionine (SAM) --- methylthioadenosine (MTA) --- enolase phosphatase 1 (ENOPH1) --- polyamine --- matrix metalloproteinase MT1 (MT1-MMP) --- metalloregulator --- chaperone --- [NiFe]-hydrogenase --- InrS --- nickel-dependent transcriptional regulators --- molecular modelling --- nickel --- hydrogenase --- urease --- Ni-enzymes --- pathogens --- ncRNA --- miRNA --- lncRNA --- lung carcinogenesis --- histidine-rich protein --- carbon monoxide dehydrogenase --- nickel chaperone --- nickel-induced oligomerization --- urease maturation --- metallochaperone --- G-protein --- conformational change --- bioavailability --- carcinogenicity --- genotoxicity --- allergy --- reproductive --- asthma --- nanoparticles --- ecotoxicity --- environment --- biological nickel sites --- nickel-thiolates --- dinuclear nickel metallopeptides --- thiolate oxidative damage --- nickel enzymes --- reaction mechanism --- quantum chemical calculations --- glyoxalase --- streptomyces --- mycothiol --- metalloenzyme --- AD11 --- nickel-dependent enzyme --- methionine salvage pathway --- methionine --- S-adenosylmethionine (SAM) --- methylthioadenosine (MTA) --- enolase phosphatase 1 (ENOPH1) --- polyamine --- matrix metalloproteinase MT1 (MT1-MMP) --- metalloregulator --- chaperone --- [NiFe]-hydrogenase
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Alzheimer’s disease (AD) is an age-related neurological disease that affects tens of millions of people, in addition to their carers. Hallmark features of AD include plaques composed of amyloid beta, as well as neurofibrillary tangles of tau protein. However, despite more than a century of study, the cause of Alzheimer’s disease remains unresolved. The roles of amyloid beta and tau are being questioned and other causes of AD are now under consideration. The contributions of researchers, model organisms, and various hypotheses will be examined in this Special Issue.
HOTAIR --- neurosciences --- sleep disturbance --- positron emission tomography (PET) --- vitamin B complex --- neurodegeneration --- Tau --- miR-15/107 --- default-mode network --- complement receptor 1 --- neuronal differentiation --- epigenetics --- brain glucose metabolism --- oligomerization --- genetic risk --- A?O receptors --- prion --- ryanodine receptor --- type 3 diabetes --- complement --- cognitive behavioral therapy for insomnia --- cognitive function --- epigenome-wide association study --- Alzheimer’s disease --- calcium signaling --- ?-secretase --- tau --- Prolyl isomerases --- NEAT1 --- complement C3b/C4b receptor --- proteostasis --- amyloid beta --- yeast --- slow-wave sleep --- amyloid ? --- nutrition --- 4 --- protein aggregation --- apolipoprotein E --- dementia --- MALAT1 --- inositol 1 --- lncRNAs --- molecular biology --- methylenetetrahydrofolate reductase MTHFR gene --- 5-trisphosphate receptor --- CR1 density --- miR-34c --- aggregation --- heat shock protein --- dendritic spine --- S-adenosylmethionine --- beta amyloid --- ion channel --- inflammation --- sleep fragmentation --- cystathionine-?-lyase CTH gene --- DNA methylation --- heat shock response --- microglia --- drug target discovery --- amyloid-? oligomer --- therapy --- CR1 length polymorphism --- methylome --- APOE gene --- ubiquitin --- magnetic resonance imaging (MRI) --- neuronal degeneration --- type 2 diabetes --- Pin1 --- mild cognitive impairment --- dairy products --- endoplasmic reticulum --- oxidative stress --- Hispanics --- CDK5R1
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Designing immunotherapeutics, drugs, and anti-inflammatory reagents has been at the forefront of autoimmune research, in particular multiple sclerosis, for over 20 years. Delivery methods that are used to modulate effective and long-lasting immune responses have been the major focus. This Special Issue focused on delivery methods to be used for vaccines, immunotherapeutic approaches, drug design, and anti-inflammatories and their outcomes in preclinical studies and clinical trials.
Medicine --- multiple sclerosis --- inflammation --- oxidative --- biomarker --- sample size --- autoimmune encephalitis --- plasma exchange --- autoimmunity --- immunotherapeutics --- clinical outcomes --- major depression --- bupropion --- S-adenosylmethionine --- vitamin D3 --- yoga --- craniopharyngioma --- fractionated stereotactic radiation treatments --- sphenoid sinusitis --- cranial nerve-VI palsy --- autoimmune diseases --- immune thrombocytopenic purpura --- alemtuzumab --- antibodies against GluR3 peptide --- cognitive impairment --- diagnosis --- neuropsychological assessment --- short intracortical inhibition --- intracortical facilitation --- fampridine --- walking disability --- TSPAN32 --- tetraspanins --- cellular immunity --- memory T cells --- tDCS --- neuroimaging --- positron emission tomography --- cerebral blood flow --- probiotics --- Streptococcus thermophilus --- ST285 --- MBP83–99 peptide --- mannan --- immune modulation --- agonist peptide --- gut microbiome --- gut–brain axis --- metagenomics --- disease-modifying treatments --- MS --- vaccine --- immunomodulation --- carriers --- B cell receptor --- delivery methods --- immunotherapy --- monoclonal antibodies --- T cell receptor --- tolerance --- diagnostic markers --- immunoglobulins --- kappa --- free light chains --- antigen-specific immunotherapies --- tolerogenic vaccines --- tolerance induction --- central nervous system --- myelin peptides --- myelin basic protei --- proteolipid protein --- myelin oligodendrocyte glycoprotein --- nanotechnology --- drug delivery nanosystems --- lipids --- polymers --- vaccines --- nanoparticles --- antigen-specific immunotherapy --- experimental autoimmune encephalomyelitis --- neurodegeneration --- chloroquine --- EAE --- dendritic cells --- microglia --- astrocytes --- oligodendrocytes --- conformational analysis --- peptides --- altered peptide ligands --- NMR spectroscopy --- NOE-constraints --- molecular dynamic --- trimolecular complex --- Multiple Sclerosis --- early-onset --- adult-onset --- Human Leucocyte Antigens --- immunogenetics --- clinical phenotype --- clinical outcome --- therapeutics --- antibody detection --- ELISA --- multivalency --- N-glucosylated peptide epitopes --- peptide --- conjugation --- MOG35-55 --- Graphite/SiO2 electrode --- voltammetry --- HPLC --- MS drugs --- multiple sclerosis --- inflammation --- oxidative --- biomarker --- sample size --- autoimmune encephalitis --- plasma exchange --- autoimmunity --- immunotherapeutics --- clinical outcomes --- major depression --- bupropion --- S-adenosylmethionine --- vitamin D3 --- yoga --- craniopharyngioma --- fractionated stereotactic radiation treatments --- sphenoid sinusitis --- cranial nerve-VI palsy --- autoimmune diseases --- immune thrombocytopenic purpura --- alemtuzumab --- antibodies against GluR3 peptide --- cognitive impairment --- diagnosis --- neuropsychological assessment --- short intracortical inhibition --- intracortical facilitation --- fampridine --- walking disability --- TSPAN32 --- tetraspanins --- cellular immunity --- memory T cells --- tDCS --- neuroimaging --- positron emission tomography --- cerebral blood flow --- probiotics --- Streptococcus thermophilus --- ST285 --- MBP83–99 peptide --- mannan --- immune modulation --- agonist peptide --- gut microbiome --- gut–brain axis --- metagenomics --- disease-modifying treatments --- MS --- vaccine --- immunomodulation --- carriers --- B cell receptor --- delivery methods --- immunotherapy --- monoclonal antibodies --- T cell receptor --- tolerance --- diagnostic markers --- immunoglobulins --- kappa --- free light chains --- antigen-specific immunotherapies --- tolerogenic vaccines --- tolerance induction --- central nervous system --- myelin peptides --- myelin basic protei --- proteolipid protein --- myelin oligodendrocyte glycoprotein --- nanotechnology --- drug delivery nanosystems --- lipids --- polymers --- vaccines --- nanoparticles --- antigen-specific immunotherapy --- experimental autoimmune encephalomyelitis --- neurodegeneration --- chloroquine --- EAE --- dendritic cells --- microglia --- astrocytes --- oligodendrocytes --- conformational analysis --- peptides --- altered peptide ligands --- NMR spectroscopy --- NOE-constraints --- molecular dynamic --- trimolecular complex --- Multiple Sclerosis --- early-onset --- adult-onset --- Human Leucocyte Antigens --- immunogenetics --- clinical phenotype --- clinical outcome --- therapeutics --- antibody detection --- ELISA --- multivalency --- N-glucosylated peptide epitopes --- peptide --- conjugation --- MOG35-55 --- Graphite/SiO2 electrode --- voltammetry --- HPLC --- MS drugs
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The past decade has seen immunotherapy rise to the forefront of cancer treatment. This Special Issue of Cancers aims to elaborate on the latest developments, cutting-edge technologies, and prospects in cancer immunology and immunotherapy. Seventeen exceptional studies, including original contributions and review articles, written by international scientists and physicians, primarily concerning the fields of tumor biology, cancer immunology, therapeutics, and drug development, comprise the main body of this Special Issue.
Medicine --- NKG2D --- CAR T --- IL-7 --- prostate cancer --- cell therapy --- CD19-CAR-T --- B cell aplasia --- KIR --- PD-1 --- inhibitory CAR --- tumor-infiltrating lymphocytes --- tumor microenvironment --- immunotherapy --- NK cells --- cancer stem cells (CSCs) --- antibody-dependent cellular cytotoxicity (ADCC) --- differentiation --- cytotoxicity --- IFN-γ --- osteoclasts --- MICA/B mAb --- DNA methylation --- RNA methylation --- S-adenosylmethionine (SAM) --- cancer --- innate immunity --- adaptive immunity --- T cells --- m6A --- PD-L1 --- resistance --- immune checkpoints --- cancer vaccine --- combination immunotherapy --- TCR diversity --- organ transplantation --- carcinoma --- epidemiologic studies --- immunosuppression --- CTLA-4 --- Treg cells --- immune checkpoint inhibitors --- CD28 --- antigen-presenting cells --- IL15 --- colon cancer --- melanoma --- uveal --- BAP1 --- anti-PD-1 --- anti-CTLA-4 --- TIL --- classical and endemic Kaposi Sarcoma --- systemic treatment --- multi-state modelling --- treatment free interval --- chemotherapy --- interferon --- triple negative breast cancer --- immunomodulation --- bispecific antibody --- sortase A --- chemo-enzymatic approach --- anti-CD20 antibody --- Fab --- BiFab --- colorectal cancer --- dendritic cells --- Atypical Chemokine Receptor 4 (ACKR4) --- T-cell priming --- immune checkpoint blockade --- primary liver cancer --- kynurenine pathway --- immune evasion --- indoleamine 2,3 dioxygenase 1 --- tryptophan 2,3 dioxygenase 2 --- IDO inhibitor --- antigen presenting cells --- n/a
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Designing immunotherapeutics, drugs, and anti-inflammatory reagents has been at the forefront of autoimmune research, in particular multiple sclerosis, for over 20 years. Delivery methods that are used to modulate effective and long-lasting immune responses have been the major focus. This Special Issue focused on delivery methods to be used for vaccines, immunotherapeutic approaches, drug design, and anti-inflammatories and their outcomes in preclinical studies and clinical trials.
multiple sclerosis --- inflammation --- oxidative --- biomarker --- sample size --- autoimmune encephalitis --- plasma exchange --- autoimmunity --- immunotherapeutics --- clinical outcomes --- major depression --- bupropion --- S-adenosylmethionine --- vitamin D3 --- yoga --- craniopharyngioma --- fractionated stereotactic radiation treatments --- sphenoid sinusitis --- cranial nerve-VI palsy --- autoimmune diseases --- immune thrombocytopenic purpura --- alemtuzumab --- antibodies against GluR3 peptide --- cognitive impairment --- diagnosis --- neuropsychological assessment --- short intracortical inhibition --- intracortical facilitation --- fampridine --- walking disability --- TSPAN32 --- tetraspanins --- cellular immunity --- memory T cells --- tDCS --- neuroimaging --- positron emission tomography --- cerebral blood flow --- probiotics --- Streptococcus thermophilus --- ST285 --- MBP83–99 peptide --- mannan --- immune modulation --- agonist peptide --- gut microbiome --- gut–brain axis --- metagenomics --- disease-modifying treatments --- MS --- vaccine --- immunomodulation --- carriers --- B cell receptor --- delivery methods --- immunotherapy --- monoclonal antibodies --- T cell receptor --- tolerance --- diagnostic markers --- immunoglobulins --- kappa --- free light chains --- antigen-specific immunotherapies --- tolerogenic vaccines --- tolerance induction --- central nervous system --- myelin peptides --- myelin basic protei --- proteolipid protein --- myelin oligodendrocyte glycoprotein --- nanotechnology --- drug delivery nanosystems --- lipids --- polymers --- vaccines --- nanoparticles --- antigen-specific immunotherapy --- experimental autoimmune encephalomyelitis --- neurodegeneration --- chloroquine --- EAE --- dendritic cells --- microglia --- astrocytes --- oligodendrocytes --- conformational analysis --- peptides --- altered peptide ligands --- NMR spectroscopy --- NOE-constraints --- molecular dynamic --- trimolecular complex --- Multiple Sclerosis --- early-onset --- adult-onset --- Human Leucocyte Antigens --- immunogenetics --- clinical phenotype --- clinical outcome --- therapeutics --- antibody detection --- ELISA --- multivalency --- N-glucosylated peptide epitopes --- peptide --- conjugation --- MOG35-55 --- Graphite/SiO2 electrode --- voltammetry --- HPLC --- MS drugs
Choose an application
The past decade has seen immunotherapy rise to the forefront of cancer treatment. This Special Issue of Cancers aims to elaborate on the latest developments, cutting-edge technologies, and prospects in cancer immunology and immunotherapy. Seventeen exceptional studies, including original contributions and review articles, written by international scientists and physicians, primarily concerning the fields of tumor biology, cancer immunology, therapeutics, and drug development, comprise the main body of this Special Issue.
NKG2D --- CAR T --- IL-7 --- prostate cancer --- cell therapy --- CD19-CAR-T --- B cell aplasia --- KIR --- PD-1 --- inhibitory CAR --- tumor-infiltrating lymphocytes --- tumor microenvironment --- immunotherapy --- NK cells --- cancer stem cells (CSCs) --- antibody-dependent cellular cytotoxicity (ADCC) --- differentiation --- cytotoxicity --- IFN-γ --- osteoclasts --- MICA/B mAb --- DNA methylation --- RNA methylation --- S-adenosylmethionine (SAM) --- cancer --- innate immunity --- adaptive immunity --- T cells --- m6A --- PD-L1 --- resistance --- immune checkpoints --- cancer vaccine --- combination immunotherapy --- TCR diversity --- organ transplantation --- carcinoma --- epidemiologic studies --- immunosuppression --- CTLA-4 --- Treg cells --- immune checkpoint inhibitors --- CD28 --- antigen-presenting cells --- IL15 --- colon cancer --- melanoma --- uveal --- BAP1 --- anti-PD-1 --- anti-CTLA-4 --- TIL --- classical and endemic Kaposi Sarcoma --- systemic treatment --- multi-state modelling --- treatment free interval --- chemotherapy --- interferon --- triple negative breast cancer --- immunomodulation --- bispecific antibody --- sortase A --- chemo-enzymatic approach --- anti-CD20 antibody --- Fab --- BiFab --- colorectal cancer --- dendritic cells --- Atypical Chemokine Receptor 4 (ACKR4) --- T-cell priming --- immune checkpoint blockade --- primary liver cancer --- kynurenine pathway --- immune evasion --- indoleamine 2,3 dioxygenase 1 --- tryptophan 2,3 dioxygenase 2 --- IDO inhibitor --- antigen presenting cells --- n/a
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