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Le mésothéliome pleural malin, un cancer agressif affectant la plèvre, est provoqué principalement par une exposition aux fibres d'amiante. L'incidence de ce cancer dont le maximum est prévu en 2020 s'accroît progressivement. À ce jour, aucune stratégie thérapeutique ne permet d'améliorer significativement l'espérance de vie des patients. L'objectif de ce travail est d'étudier les mécanismes de tolérances aux dommages de l'ADN (DDT) dans 2 sous-types cellulaires (sarcomatoïde et épithéloïde). Ce travail a permis de mettre en évidence des différences dans l'activation de deux médiateurs de DDT (BAP1 et RAD18). L'inhibition de BAP1 et RAD18 pourrait avoir un potentiel thérapeutique dans le contexte d'une chimiosensibilisation du mésothéliome pleural malin. Malignant pleural mesothelioma, an aggressive cancer affecting the pleura, is mainly caused by asbestos exposure. Its incidence is increasing up to a predicted peak in 2020. To date, there is no therapy that allows a significant improvement of patient's life expectancy. The objective of this study was to evaluate the mechanisms of DNA damage tolerance (DDT) in 2 different cellular sub-types of mesothelioma. This work has highlighted mechanistic differences in activation of two DDT mediators (BAP1 and RAD18). Inhibition of BAP1 and RAD18 mediators may have therapeutic value in a context of chemosensibilization of malignant pleural mesothelioma.

Mésothéliome --- mécanisme de tolérance --- BAP1 --- RAD18 --- mesothelioma --- dna damages tolerance --- Sciences du vivant > Biochimie, biophysique & biologie moléculaire

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Malignant mesothelioma (MM) is a rare and aggressive cancer, related to chronic inflammation and oxidative stress caused mainly by exposure to asbestos. Although this mineral has been banned for decades in many countries, epidemiologists predict the MM epidemic will last past 2040, raising many concerns in public health given its late diagnosis, dismal prognosis, and lack of current efficient therapies.To deal with this situation, important breakthroughs have recently been made in the understanding of MM’s complex biology and the carcinogenic process of the different patterns of the disease. Examples of these include the development of new biomarkers and the deciphering of gene–environment interactions, molecular mechanisms of invasiveness, deregulated pathways, altered expression of miRNAs, DNA damage repair, or metabolic profile. From now on, MM’s aggressive and chemoresistant character appears linked to a polyclonal malignancy, and heterogeneity in molecular alterations.Given these improvements, new therapeutic targets are being explored to solve the double challenge faced by clinicians. The first is to reduce tumor development and its wasting consequences as soon as possible, without resistance and with limited toxicity. The second is to stimulate the recognition of tumor cells by the induction of a specific immune response. This Special Issue will highlight all these aspects.

Medicine --- well-differentiated papillary mesothelioma --- WDPM --- malignant mesothelioma --- DNA sequencing --- mutation --- mesothelioma --- tumor suppressor --- targeted therapy --- immunotherapy --- biomarkers --- proteomics --- macrophage-capping protein --- fatty acid-binding protein --- laminin subunit beta-2 --- selenium-binding protein 1 --- carcinogenesis --- malignant pleural mesothelioma --- asbestos exposure --- DNA methylation --- lymphocyte-to-monocyte ratio --- epigenome-wide analysis --- survival analysis --- metabolomics --- radiotherapy --- cancers --- inflammation --- infiltrating immune cells --- prognostic biomarker --- predictive biomarker --- immune therapy --- VATS --- extrapleural pneumonectomy --- pleurectomy decortication --- therapy response --- survival --- FDG --- PET-CT --- mesothelium --- oxidative stress --- redox-sensitive factors --- asbestos --- carbon nanotubes --- protein-protein interactions --- systems biology --- network analysis --- drug repurposing --- pleural mesothelioma --- gene expression --- immunogenicity --- sarcomatoid --- epithelioid --- first line --- meta-analysis --- systematic review --- MPM --- lurbinectedin --- DNA damage response --- histotype --- Hippo pathway --- NF2 --- BAP1 --- CDKN2A --- PTCH1 --- SETD2 --- MTAP --- liquid biopsies --- circulating tumor DNA --- plasma --- cancer-specific mutations --- genomics --- cancer biomarkers --- tumor microenvironment --- tumor-associated macrophages --- dendritic cells --- immunohistochemistry --- interaction analysis --- pleural effusion --- well-differentiated papillary mesothelioma --- WDPM --- malignant mesothelioma --- DNA sequencing --- mutation --- mesothelioma --- tumor suppressor --- targeted therapy --- immunotherapy --- biomarkers --- proteomics --- macrophage-capping protein --- fatty acid-binding protein --- laminin subunit beta-2 --- selenium-binding protein 1 --- carcinogenesis --- malignant pleural mesothelioma --- asbestos exposure --- DNA methylation --- lymphocyte-to-monocyte ratio --- epigenome-wide analysis --- survival analysis --- metabolomics --- radiotherapy --- cancers --- inflammation --- infiltrating immune cells --- prognostic biomarker --- predictive biomarker --- immune therapy --- VATS --- extrapleural pneumonectomy --- pleurectomy decortication --- therapy response --- survival --- FDG --- PET-CT --- mesothelium --- oxidative stress --- redox-sensitive factors --- asbestos --- carbon nanotubes --- protein-protein interactions --- systems biology --- network analysis --- drug repurposing --- pleural mesothelioma --- gene expression --- immunogenicity --- sarcomatoid --- epithelioid --- first line --- meta-analysis --- systematic review --- MPM --- lurbinectedin --- DNA damage response --- histotype --- Hippo pathway --- NF2 --- BAP1 --- CDKN2A --- PTCH1 --- SETD2 --- MTAP --- liquid biopsies --- circulating tumor DNA --- plasma --- cancer-specific mutations --- genomics --- cancer biomarkers --- tumor microenvironment --- tumor-associated macrophages --- dendritic cells --- immunohistochemistry --- interaction analysis --- pleural effusion

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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.

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