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For the faultless function of the immune system, tight regulation of immune cell activation, immuno-suppression and the strength and efficiency of the immune response is essential. Immune checkpoint (ICP) molecules can amplify or dampen signals that lead to the modulation of specific immune activities. Under physiological conditions, immune checkpoints are essential to prevent autoimmune manifestations and to preserve self-tolerance. They help modulate immune responses by either promoting or inhibiting T-cell activation. However, in the context of cancer, malignant cells can dysregulate the expression of immune checkpoint proteins on immune cells in order to suppress anti-tumor immune responses and to gain immune resistance. Moreover, tumor cells themselves can also express some checkpoints proteins, thereby enabling these cells to externally orchestrate immune regulatory mechanisms. Several recent studies have confirmed that the expression of immune checkpoints could be an important prognostic parameter for cancer development and for patient outcome. Therefore, cancer immunotherapy based on the modulation of immune checkpoint molecules alone, or in combination with conventional tumor therapy (chemo- or/and radiotherapy), is now in focus as a means of developing new therapeutic strategies for different types of cancer. The two well-known molecules – CTLA4 and PD-1 - serve as important examples of such checkpoint proteins of important therapeutic potential. Thus far, inhibitors of CTLA4 and PD-1 have been approved to treat only a limited number of malignancies (e.g. malignant Melanoma, Non-Small Cell Lung Cancer). Many others are currently under investigation and the list of immune checkpoint molecules for potential therapeutic targeting is still growing. However, the clinical response to inhibitors of checkpoint molecules is not sufficient in all cases. Therefore, further studies are needed to improve our knowledge of such immunomodulatory proteins and their associated signaling pathways. Several key signaling pathways which are involved in the regulation of expression of checkpoint molecules in immune cells and in cancer cells have already been identified including MAPK, PI3K, NF-kB, JAKs and STATs. These (and future discovered) signaling pathways could give rise to the development of new strategies for modulating the expression of ICPs and thereby, improving anti-cancer immune responses. The main aim of the Research Topic is to collect novel findings from scientists involved in basic research on immune checkpoints as well as in translational studies investigating the use of checkpoint inhibtors in immunotherapy in experimental settings. We welcome the submission of Review, Mini-Review and Original Research articles that cover the following topics: 1. Molecular mechanisms underlying regulation of ICP expression in immune and/or cancer cells. 2. Characterization of signaling pathways downstream ICP molecules. 3. Cellular responses to ICP blockade. 4. Identification of new compounds interfering with ICP expression and/or signaling. 5. ICP-mediated interactions between cancer cells and immune cells. 6. Functional links between ICP and cytokines/chemokines. 7. Molecular mechanisms of ICP inhibition in the context of experimental cancer immunotherapy.

CTLA-4 (CD152) --- checkpoint blockade --- Immunosuppression --- cancer immunotherapy --- PD-1 (CD279) --- Tumor Microenvironment --- Metabolic checkpoints --- immune checkpoint molecules --- cytotoxic T lymphocytes --- PDL1

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For the faultless function of the immune system, tight regulation of immune cell activation, immuno-suppression and the strength and efficiency of the immune response is essential. Immune checkpoint (ICP) molecules can amplify or dampen signals that lead to the modulation of specific immune activities. Under physiological conditions, immune checkpoints are essential to prevent autoimmune manifestations and to preserve self-tolerance. They help modulate immune responses by either promoting or inhibiting T-cell activation. However, in the context of cancer, malignant cells can dysregulate the expression of immune checkpoint proteins on immune cells in order to suppress anti-tumor immune responses and to gain immune resistance. Moreover, tumor cells themselves can also express some checkpoints proteins, thereby enabling these cells to externally orchestrate immune regulatory mechanisms. Several recent studies have confirmed that the expression of immune checkpoints could be an important prognostic parameter for cancer development and for patient outcome. Therefore, cancer immunotherapy based on the modulation of immune checkpoint molecules alone, or in combination with conventional tumor therapy (chemo- or/and radiotherapy), is now in focus as a means of developing new therapeutic strategies for different types of cancer. The two well-known molecules – CTLA4 and PD-1 - serve as important examples of such checkpoint proteins of important therapeutic potential. Thus far, inhibitors of CTLA4 and PD-1 have been approved to treat only a limited number of malignancies (e.g. malignant Melanoma, Non-Small Cell Lung Cancer). Many others are currently under investigation and the list of immune checkpoint molecules for potential therapeutic targeting is still growing. However, the clinical response to inhibitors of checkpoint molecules is not sufficient in all cases. Therefore, further studies are needed to improve our knowledge of such immunomodulatory proteins and their associated signaling pathways. Several key signaling pathways which are involved in the regulation of expression of checkpoint molecules in immune cells and in cancer cells have already been identified including MAPK, PI3K, NF-kB, JAKs and STATs. These (and future discovered) signaling pathways could give rise to the development of new strategies for modulating the expression of ICPs and thereby, improving anti-cancer immune responses. The main aim of the Research Topic is to collect novel findings from scientists involved in basic research on immune checkpoints as well as in translational studies investigating the use of checkpoint inhibtors in immunotherapy in experimental settings. We welcome the submission of Review, Mini-Review and Original Research articles that cover the following topics: 1. Molecular mechanisms underlying regulation of ICP expression in immune and/or cancer cells. 2. Characterization of signaling pathways downstream ICP molecules. 3. Cellular responses to ICP blockade. 4. Identification of new compounds interfering with ICP expression and/or signaling. 5. ICP-mediated interactions between cancer cells and immune cells. 6. Functional links between ICP and cytokines/chemokines. 7. Molecular mechanisms of ICP inhibition in the context of experimental cancer immunotherapy.

CTLA-4 (CD152) --- checkpoint blockade --- Immunosuppression --- cancer immunotherapy --- PD-1 (CD279) --- Tumor Microenvironment --- Metabolic checkpoints --- immune checkpoint molecules --- cytotoxic T lymphocytes --- PDL1 --- CTLA-4 (CD152) --- checkpoint blockade --- Immunosuppression --- cancer immunotherapy --- PD-1 (CD279) --- Tumor Microenvironment --- Metabolic checkpoints --- immune checkpoint molecules --- cytotoxic T lymphocytes --- PDL1

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Dear Readers, Oncolytic Viruses (OV) are self-propagating agents that can selectively induce the lysis of cancer cells while sparing normal tissues. OV-mediated cancer cell death is often immunogenic and triggers robust anticancer immune responses and immunoconversion of tumor microenvironments. This makes oncolytic virotherapy a promising new form of immunotherapy and OVs ideal candidates for combination therapy with other anticancer agents, including other immunotherapeutics. There are more than 40 OVs from nine different families in clinical development and many more at the preclinical stage. Each OV has its own unique characteristics, its pros and cons. Although herpes simplex virus is currently the lead clinical agent, a real champion among the OVs has not yet emerged, justifying the continuous development and optimization of these agents. This book, “Oncolytic Virus Immunotherapy”, summarizes the state-of-the-art and gives a comprehensive overview of the OV arena with a particular focus on new trends, directions, challenges, and opportunities.

Medicine --- Clinical & internal medicine --- oncolytic viruses --- melanoma --- immunotherapy --- checkpoint inhibitors --- combinatory therapy --- reovirus --- oncolytic virus --- adenovirus --- oncolytic --- virotherapy --- targeting --- immunogenic cell death --- αvβ6 integrin --- oncolytic adenovirus --- cancer immunotherapy --- multi-stage --- immunostimulatory --- arming --- HSV-1 --- clinical trials --- newcastle disease virus --- NDV --- cancer --- immune checkpoint inhibitor --- PD-1 --- PD-L1 --- CTLA-4 --- type I interferon --- herpes simplex virus --- retargeted virus --- tropism retargeting --- tumor --- checkpoint inhibitor --- vaccination --- antigen-agnostic vaccination --- HER2 --- parvovirus --- tumor microenvironment --- combination therapy --- glioblastoma --- pancreatic cancer --- colorectal cancer --- measles virus --- vector engineering --- immune checkpoint blockade --- antitumor immune response --- delivery --- genetic modification --- biomarkers --- personalized oncolyticvirotherapy --- class I HLA --- immunosurveillance --- immunoediting --- oncogenic signaling --- RAS --- DNA methyltransferase inhibitor (DNMTi) --- viral mimicry --- epigenetic silencing --- adoptive T cell therapy --- CAR T cell --- pancreatic ductal adenocarcinoma --- vesicular stomatitis virus --- small molecule --- cancer immune therapy --- cancer therapy --- oncolytic viruses --- melanoma --- immunotherapy --- checkpoint inhibitors --- combinatory therapy --- reovirus --- oncolytic virus --- adenovirus --- oncolytic --- virotherapy --- targeting --- immunogenic cell death --- αvβ6 integrin --- oncolytic adenovirus --- cancer immunotherapy --- multi-stage --- immunostimulatory --- arming --- HSV-1 --- clinical trials --- newcastle disease virus --- NDV --- cancer --- immune checkpoint inhibitor --- PD-1 --- PD-L1 --- CTLA-4 --- type I interferon --- herpes simplex virus --- retargeted virus --- tropism retargeting --- tumor --- checkpoint inhibitor --- vaccination --- antigen-agnostic vaccination --- HER2 --- parvovirus --- tumor microenvironment --- combination therapy --- glioblastoma --- pancreatic cancer --- colorectal cancer --- measles virus --- vector engineering --- immune checkpoint blockade --- antitumor immune response --- delivery --- genetic modification --- biomarkers --- personalized oncolyticvirotherapy --- class I HLA --- immunosurveillance --- immunoediting --- oncogenic signaling --- RAS --- DNA methyltransferase inhibitor (DNMTi) --- viral mimicry --- epigenetic silencing --- adoptive T cell therapy --- CAR T cell --- pancreatic ductal adenocarcinoma --- vesicular stomatitis virus --- small molecule --- cancer immune therapy --- cancer therapy

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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 --- 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

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Nanomedicine is among the most promising emerging fields that can provide innovative and radical solutions to unmet needs in pharmaceutical formulation development. Encapsulation of active pharmaceutical ingredients within nano-size carriers offers several benefits, namely, protection of the therapeutic agents from degradation, their increased solubility and bioavailability, improved pharmacokinetics, reduced toxicity, enhanced therapeutic efficacy, decreased drug immunogenicity, targeted delivery, and simultaneous imaging and treatment options with a single system.Poly(lactide-co-glycolide) (PLGA) is one of the most commonly used polymers in nanomedicine formulations due to its excellent biocompatibility, tunable degradation characteristics, and high versatility. Furthermore, PLGA is approved by the European Medicines Agency (EMA) and the Food and Drug Administration (FDA) for use in pharmaceutical products. Nanomedicines based on PLGA nanoparticles can offer tremendous opportunities in the diagnosis, monitoring, and treatment of various diseases.This Special Issue aims to focus on the bench-to-bedside development of PLGA nanoparticles including (but not limited to) design, development, physicochemical characterization, scale-up production, efficacy and safety assessment, and biodistribution studies of these nanomedicine formulations.

Technology: general issues --- History of engineering & technology --- Materials science --- poly(lactic-co-glycolic acid) (PLGA) --- blood–brain barrier (BBB) --- current Good Manufacturing Practice (cGMP) --- Food and Drug Administration (FDA) --- nanotechnology --- PLGA nanoparticles --- neurodegenerative diseases --- drug delivery --- central nervous system --- neuroprotective drugs --- fluorescent labeling --- DiI --- coumarin 6 --- rhodamine 123 --- Cy5.5 --- quantum yield --- brightness --- stability of fluorescent label --- confocal microscopy --- intracellular internalization --- in vivo neuroimaging --- double-emulsion method --- dry powder inhalation --- antigen release --- porous PLGA particles --- microfluidics --- methotrexate --- chitosan --- PLA/PLGA --- sustained release --- micro-implant --- animal model --- minimally invasive --- drug delivery system --- nanoparticles --- poly (lactic-co-glycolic acid) (PLGA) --- microfluidic --- pharmacokinetics (PK) and biodistribution --- atorvastatin calcium --- poly(lactide-co-glycolide) --- polymeric nanoparticles --- carrageenan induced inflammation --- anti-inflammatory --- radiolabeled nanoparticles --- nuclear medicine --- photothermal therapy --- phthalocyanine --- SKOVip-kat --- Katushka --- TurboFP635 --- JO-4 --- PLGA --- orthotopic tumors --- 3D culture --- spheroids --- poly(lactic-co-glycolic acid) --- nanomedicine --- scale-up manufacturing --- clinical translation --- inline sonication --- tangential flow filtration --- lyophilization --- downstream processing --- H. pylori --- design of experiments --- poly(lactic-co-glycolic) acid --- size --- cancer --- chemoimmunotherapy --- immunogenic cell death --- immune checkpoint blockade --- PNA5 glycopeptide --- mas receptor --- angiotensin --- PLGA diblock copolymer --- ester and acid-end capped --- double emulsion solvent evaporation --- biocompatible --- biodegradable --- cardiovascular --- nanoparticle --- solid-state characterization --- in vitro --- drug release kinetics modeling --- PEGylation --- amine --- emulsion --- polyvinyl alcohol (PVA) --- Pluronic triblock copolymer --- trehalose --- sucrose --- Indomethacin --- solvents --- stabilizers --- morphology --- particle-size --- encapsulation --- drug release --- cytotoxicity