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} </style> <meta name="follow.it-verification-code-YjBieUhIbjlSaTlwVGJ3TCttMnFRWTNDY2NxN1pUUlpTN2hkZm9zZ1BSTHdJTE1NVFZmU2I5MkF4Z1RPK3FqN0lNR2Vjd1l3NVE3eC9hVzJCR092MUhxNVY3ek52SlpyQ2kvdm9MUXViT0FYdSs1eW1YeWtYdEg3RFRqNm1lMEV8bzBEc0VDNjlTMzdxb3FrOUdNYzJrbmxEbEtaQlI5WTNGQTZIc3VQQVo5ND0=" content="d4BS8a1CMehBt5r4ASFd"/> <meta name="viewport" content="width=device-width, initial-scale=1"><meta property="og:image:secure_url" content="https://tron-mainz.de/de/wp-content/uploads/sites/9/2018/01/TRONPublications.jpg" data-id="sfsi-plus"/><meta property="og:image:type" content="" data-id="sfsi-plus"/><meta property="og:image:width" content="640" data-id="sfsi-plus"/><meta property="og:image:height" content="427" data-id="sfsi-plus"/><meta property="og:description" content=" [vc_row gap=15] [vc_column width=3/4][vc_column_text] Sethi R, Becker J, de Graaf J, Löwer M, Suchan M, Sahin U, Weber D. (2020) Integrative analysis of structural variations using short-reads and linked-reads yields highly specific and sensitive predictions. PLoS. Comput. Biol. 16(11):e1008397. DOI, PMID [su_spoiler title=Show abstract]Genetic diseases are driven by aberrations of the human genome. Identification of such aberrations including structural variations (SVs) is key to our understanding. Conventional short-reads whole genome sequencing (cWGS) can identify SVs to base-pair resolution, but utilizes only short-range information and suffers from high false discovery rate (FDR). Linked-reads sequencing (10XWGS) utilizes long-range information by linkage of short-reads originating from the same large DNA molecule. This can mitigate alignment-based artefacts especially in repetitive regions and should enable better prediction of SVs. However, an unbiased evaluation of this technology is not available. In this study, we performed a comprehensive analysis of different types and sizes of SVs predicted by both the technologies and validated with an independent PCR based approach. The SVs commonly identified by both the technologies were highly specific, while validation rate dropped for uncommon events. A particularly high FDR was observed for SVs only found by 10XWGS. To improve FDR and sensitivity, statistical models for both the technologies were trained. Using our approach, we characterized SVs from the MCF7 cell line and a primary breast cancer tumor with high precision. This approach improves SV prediction and can therefore help in understanding the underlying genetics in various diseases. [/su_spoiler] Becker S, Fink A, Podlech J, Giese I, Schmiedeke JK, Bukur T, Reddehase MJ, Lemmermann NA. (2020) Positive Role of the MHC Class-I Antigen Presentation Regulator m04/gp34 of Murine Cytomegalovirus in Antiviral Protection by CD8 T Cells. Front. Cell. Infect. Microbiol. 10:454. DOI, PMID [su_spoiler title=Show abstract]Murine cytomegalovirus (mCMV) codes for MHC class-I trafficking modulators m04/gp34, m06/gp48, and m152/gp40. By interacting with the MHC class-Iα chain, these proteins disconnect peptide-loaded MHC class-I (pMHC-I) complexes from the constitutive vesicular flow to the cell surface. Based on the assumption that all three inhibit antigen presentation, and thus the recognition of infected cells by CD8 T cells, they were referred to as “immunoevasins.” Improved antigen presentation mediated by m04 in the presence of m152 after infection with deletion mutant mCMV-Δm06W, compared to mCMV-Δm04m06 expressing only m152, led us to propose renaming these molecules “viral regulators of antigen presentation” (vRAP) to account for both negative and positive functions. In accordance with a positive function, m04-pMHC-I complexes were found to be displayed on the cell surface, where they are primarily known as ligands for Ly49 family natural killer (NK) cell receptors. Besides the established role of m04 in NK cell silencing or activation, an anti-immunoevasive function by activation of CD8 T cells is conceivable, because the binding site of m04 to MHC class-Iα appears not to mask the peptide binding site for T-cell receptor recognition. However, functional evidence was based on mCMV-Δm06W, a virus of recently doubted authenticity. Here we show that mCMV-Δm06W actually represents a mixture of an authentic m06 deletion mutant and a mutant with an accidental additional deletion of a genome region encompassing also gene m152. Reanalysis of previously published experiments for the authentic mutant in the mixture confirms the previously concluded positive vRAP function of m04. [/su_spoiler] Sahin U, Oehm P, Derhovanessian E, Jabulowsky RA, Vormehr M, Gold M, Maurus D, Schwarck-Kokarakis D, Kuhn AN, Omokoko T, Kranz LM, Diken M, Kreiter S, Haas H, Attig S, Rae R, Cuk K, Kemmer-Brück A, Breitkreuz A, Tolliver C, Caspar J, Quinkhardt J, Hebich L, Stein M, Hohberger A, Vogler I, Liebig I, Renken S, Sikorski J, Leierer M, Müller V, Mitzel-Rink H, Miederer M, Huber C, Grabbe S, Utikal J, Pinter A, Kaufmann R, Hassel JC, Loquai C, Türeci Ö. (2020) An RNA vaccine drives immunity in checkpoint-inhibitor-treated melanoma. Nature. 585(7823):107-112. DOI, PMID [su_spoiler title=Show abstract]Treating patients who have cancer with vaccines that stimulate a targeted immune response is conceptually appealing, but cancer vaccine trials have not been successful in late-stage patients with treatment-refractory tumours1,2. We are testing melanoma FixVac (BNT111)—an intravenously administered liposomal RNA (RNA-LPX) vaccine, which targets four non-mutated, tumour-associated antigens that are prevalent in melanoma—in an ongoing, first-in-human, dose-escalation phase I trial in patients with advanced melanoma (Lipo-MERIT trial, ClinicalTrials.gov identifier NCT02410733). We report here data from an exploratory interim analysis that show that melanoma FixVac, alone or in combination with blockade of the checkpoint inhibitor PD1, mediates durable objective responses in checkpoint-inhibitor (CPI)-experienced patients with unresectable melanoma. Clinical responses are accompanied by the induction of strong CD4+ and CD8+ T cell immunity against the vaccine antigens. The antigen-specific cytotoxic T-cell responses in some responders reach magnitudes typically reported for adoptive T-cell therapy, and are durable. Our findings indicate that RNA-LPX vaccination is a potent immunotherapy in patients with CPI-experienced melanoma, and suggest the general utility of non-mutant shared tumour antigens as targets for cancer vaccination. [/su_spoiler] Schrörs B, Boegel S, Albrecht C, Bukur T, Bukur V, Holtsträter C, Ritzel C, Manninen K, Tadmor AD, Vormehr M, Sahin U, Löwer M. (2020) Multi-Omics Characterization of the 4T1 Murine Mammary Gland Tumor Model. Front. Oncol. 10:1195. DOI, PMID [su_spoiler title=Show abstract]Background: Tumor models are critical for our understanding of cancer and the development of cancer therapeutics. The 4T1 murine mammary cancer cell line is one of the most widely used breast cancer models. Here, we present an integrated map of the genome, transcriptome, and immunome of 4T1. Results: We found Trp53 (Tp53) and Pik3g to be mutated. Other frequently mutated genes in breast cancer, including Brca1 and Brca2, are not mutated. For cancer related genes, Nav3, Cenpf, Muc5Ac, Mpp7, Gas1, MageD2, Dusp1, Ros, Polr2a, Rragd, Ros1, and Hoxa9 are mutated. Markers for cell proliferation like Top2a, Birc5, and Mki67 are highly expressed, so are markers for metastasis like Msln, Ect2, and Plk1, which are known to be overexpressed in triple-negative breast cancer (TNBC). TNBC markers are, compared to a mammary gland control sample, lower (Esr1), comparably low (Erbb2), or not expressed at all (Pgr). We also found testis cancer antigen Pbk as well as colon/gastrointestinal cancer antigens Gpa33 and Epcam to be highly expressed. Major histocompatibility complex (MHC) class I is expressed, while MHC class II is not. We identified 505 single nucleotide variations (SNVs) and 20 insertions and deletions (indels). Neoantigens derived from 22 SNVs and one deletion elicited CD8+ or CD4+ T cell responses in IFNγ-ELISpot assays. Twelve high-confidence fusion genes were observed. We did not observe significant downregulation of mismatch repair (MMR) genes or SNVs/indels impairing their function, providing evidence for 6-thioguanine resistance. Effects of the integration of the murine mammary tumor virus were observed at the genome and transcriptome level. Conclusions: 4T1 cells share substantial molecular features with human TNBC. As 4T1 is a common model for metastatic tumors, our data supports the rational design of mode-of-action studies for pre-clinical evaluation of targeted immunotherapies. [/su_spoiler] Salomon N, Vascotto F, Selmi A, Vormehr M, Quinkhardt J, Bukur T, Schrörs B, Löwer M, Diken M, Türeci Ö, Sahin U, Kreiter S. (2020) A liposomal RNA vaccine inducing neoantigen-specific CD4+ T cells augments the antitumor activity of local radiotherapy in mice. Oncoimmunology. 9:1771925. DOI, PMID [su_spoiler title=Show abstract] Antigen-encoding, lipoplex-formulated RNA (RNA-LPX) enables systemic delivery to lymphoid compartments and selective expression in resident antigen-presenting cells. We report here that the rejection of CT26 tumors, mediated by local radiotherapy (LRT), is further augmented in a CD8+ T cell-dependent manner by an RNA-LPX vaccine that encodes CD4+ T cell-recognized neoantigens (CD4 neoantigen vaccine). Whereas CD8+ T cells induced by LRT alone were primarily directed against the immunodominant gp70 antigen, mice treated with LRT plus the CD4 neoantigen vaccine rejected gp70-negative tumors and were protected from rechallenge with these tumors, indicating a potent poly-antigenic CD8+ T cell response and T cell memory. In the spleens of CD4 neoantigen-vaccinated mice, we found a high number of activated, poly-functional, Th1-like CD4+ T cells against ME1, the immunodominant CD4 neoantigen within the poly-neoantigen vaccine. LRT itself strongly increased CD8+ T cell numbers and clonal expansion. However, tumor infiltrates of mice treated with CD4 neoantigen vaccine/LRT, as compared to LRT alone, displayed a higher fraction of activated gp70-specific CD8+ T cells, lower PD-1/LAG-3 expression and contained ME1-specific IFNγ+ CD4+ T cells capable of providing cognate help. CD4 neoantigen vaccine/LRT treatment followed by anti-CTLA-4 antibody therapy further enhanced the efficacy with complete remission of gp70-negative CT26 tumors and survival of all mice. Our data highlight the power of combining synergistic modes of action and warrants further exploration of the presented treatment schema.[/su_spoiler] Barea Roldán D, Grimmler M, Hartmann C, Hubich-Rau S, Beiβert T, Paret C, Cagna G, Rohde C, Wöll S, Koslowski M, Türeci O, Sahin U. (2020) PLAC1 is essential for FGF7/FGFRIIIb-induced Akt-mediated cancer cell proliferation. Oncotarget. 11:1862-1875. DOI, PMID [su_spoiler title=Show abstract] PLAC1 (placenta enriched 1) is a mammalian trophoblast-specific protein. Aberrant expression of PLAC1 is observed in various human cancers, where it is involved in the motility, migration, and invasion of tumor cells, which are associated with the phosphoinositide 3-kinase (PI3K)/AKT pathway. We previously demonstrated that AKT activation mediates the downstream effects of PLAC1; however, the molecular mechanisms of PLAC1-induced AKT-mediated tumor-related processes are unclear. We studied human choriocarcinoma and breast cancer cell lines to explore the localization and receptor-ligand interactions, as well as the downstream effects of PLAC1. We show secretion and adherence of PLAC1 to the extracellular matrix, where it forms a trimeric complex with fibroblast growth factor 7 (FGF7) and its receptor, FGF receptor 2 IIIb (FGFR2IIIb). We further show that PLAC1 signaling via FGFR2IIIb activates AKT phosphorylation in cancer cell lines. As the FGF pathway is of major interest in anticancer therapeutic strategies, these data further promote PLAC1 as a promising anticancer drug target. [/su_spoiler] Schöpf B, Weissensteiner H, Schäfer G, Fazzini F, Charoentong P, Naschberger A, Rupp B, Fendt L, Bukur V, Giese I, Sorn P, Sant'Anna-Silva AC, Iglesias-Gonzalez J, Sahin U, Kronenberg F, Gnaiger E, Klocker H. (2020) OXPHOS remodeling in high-grade prostate cancer involves mtDNA mutations and increased succinate oxidation. Nat. Comm. 11(1):1487. DOI, PMID [su_spoiler title=Show abstract] Rewiring of energy metabolism and adaptation of mitochondria are considered to impact on prostate cancer development and progression. Here, we report on mitochondrial respiration, DNA mutations and gene expression in paired benign/malignant human prostate tissue samples. Results reveal reduced respiratory capacities with NADH-pathway substrates glutamate and malate in malignant tissue and a significant metabolic shift towards higher succinate oxidation, particularly in high-grade tumors. The load of potentially deleterious mitochondrial-DNA mutations is higher in tumors and associated with unfavorable risk factors. High levels of potentially deleterious mutations in mitochondrial Complex I-encoding genes are associated with a 70% reduction in NADH-pathway capacity and compensation by increased succinate-pathway capacity. Structural analyses of these mutations reveal amino acid alterations leading to potentially deleterious effects on Complex I, supporting a causal relationship. A metagene signature extracted from the transcriptome of tumor samples exhibiting a severe mitochondrial phenotype enables identification of tumors with shorter survival times. [/su_spoiler] Holtsträter C, Schrörs B, Bukur T, Löwer M. (2020) Bioinformatics for Cancer Immunotherapy. In: Methods Mol Biol. 2120:1-9. Springer. DOI, PMID [su_spoiler title=Show abstract] Our immune system plays a key role in health and disease as it is capable of responding to foreign antigens as well as acquired antigens from cancer cells. Latter are caused by somatic mutations, the so-called neoepitopes, and might be recognized by T cells if they are presented by HLA molecules on the surface of cancer cells. Personalized mutanome vaccines are a class of customized immunotherapies, which is dependent on the detection of individual cancer-specific tumor mutations and neoepitope (i.e., prediction, followed by a rational vaccine design, before on-demand production. The development of next generation sequencing (NGS) technologies and bioinformatic tools allows a large-scale analysis of each parameter involved in this process. Here, we provide an overview of the bioinformatic aspects involved in the design of personalized, neoantigen-based vaccines, including the detection of mutations and the subsequent prediction of potential epitopes, as well as methods for associated biomarker research, such as high-throughput sequencing of T-cell receptors (TCRs), followed by data analysis and the bioinformatics quantification of immune cell infiltration in cancer samples. [/su_spoiler] Reinhard K, Rengstl B, Oehm P, Michel K, Billmeier A, Hayduk N, Klein O, Kuna K, Ouchan Y, Wöll S, Christ E, Weber D, Suchan M, Bukur T, Birtel M, Jahndel V, Mroz K, Hobohm K, Kranz L, Diken M, Kühlcke K, Türeci Ö, Sahin U. (2020) An RNA vaccine drives expansion and efficacy of claudin-CAR-T cells against solid tumors. Science. 367:446-453. DOI, PMID [su_spoiler title=Show abstract] Chimeric antigen receptor (CAR)-T cells have shown efficacy in patients with B cell malignancies. Yet their application for solid tumors has challenges that include limited cancer-specific targets and non-persistence of adoptively transferred CAR-T cells. Here we introduce the developmentally regulated tight junction protein claudin 6 (CLDN6) as a CAR target in solid tumors, and a strategy to overcome inefficient CAR-T cell stimulation in vivo. We demonstrate that a nanoparticulate RNA vaccine, designed for body-wide delivery of the CAR antigen into lymphoid compartments, stimulates adoptively transferred CAR-T cells. Presentation of the natively folded target on resident dendritic cells promotes cognate and selective expansion of CAR-T cells. Improved engraftment of CAR-T cells and regression of large tumors in difficult-to-treat mouse models was achieved at sub-therapeutic CAR-T cell doses. [/su_spoiler] Vormehr M, Diken M, Türeci Ö, Sahin U, Kreiter S. (2020) Personalized Neo-Epitope Vaccines for Cancer Treatment. In: Theobald M. (eds) Current Immunotherapeutic Strategies in Cancer. Recent Results in Cancer Research. 214:153-167. Springer. DOI, PMID [su_spoiler title=Show abstract] After more than a century of efforts to establish cancer immunotherapy in clinical practice, the advent of checkpoint inhibition (CPI) therapy was a critical breakthrough toward this direction (Hodi et al. in Cell Rep 13(2):412–424, 2010; Wolchok et al. in N Engl J Med 369(2):122–133, 2013; Herbst et al. in Nature 515(7528):563–567, 2014; Tumeh et al. in Nature 515(7528):568–571, 2014). Further, CPIs shifted the focus from long studied shared tumor-associated antigens to mutated ones. As cancer is caused by mutations in somatic cells, the concept to utilize these correlates of ‘foreignness’ to enable recognition and lysis of the cancer cell by T cell immunity seems an obvious thing to do. 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ul.nav > .menu-item .sub-menu > .menu-item > a, #navigation > section > .side-nav .widget_shopping_cart, #navigation ul.cart .cart_list a { font-family: ; font-size: 1em ; font-style: normal ; font-weight: 400; color : !important; } #navigation > section > .primary-nav-container ul.nav > .menu-item .sub-menu > .menu-item > a:hover, #navigation > section > .side-nav .widget_shopping_cart { text-decoration: none; } #navigation > section > .primary-nav-container ul.nav .sub-menu { text-align: left !important ; } #navigation > section > .primary-nav-container ul.nav > .menu-item .sub-menu > .menu-item { border-top: px solid ; border-bottom: px solid ; border-left: px solid ; border-right: px solid ; } #navigation > section > .primary-nav-container ul.nav > .menu-item .sub-menu > .menu-item:hover { border-top: px solid ; border-bottom: px solid ; border-left: px solid ; border-right: px solid ; } #navigation > section > .primary-nav-container ul.nav > .menu-item .sub-menu, #navigation .side-nav > .cart > li > ul, #navigation .side-nav > .nav-search > li > ul { background-color: #ffffff !important; } #navigation > section > .primary-nav-container ul.nav > .menu-item .sub-menu > .menu-item:hover > a { color: #be3026 !important; } #navigation > section > .primary-nav-container ul.nav > .menu-item .sub-menu { padding-top: 0 !important; padding-bottom: 0 !important; } #navigation > section > .primary-nav-container ul.nav .sub-menu > .menu-item > a, #navigation > section > .side-nav .widget_shopping_cart { } #navigation > section > .primary-nav-container ul.nav .sub-menu, #navigation > section > .side-nav > .cart > li > ul { } body #navigation > section > .primary-nav-container ul.nav > .menu-item .sub-menu, #navigation > section > .side-nav > .cart > li > ul { border-radius: !important ; } #navigation > section > .primary-nav-container ul.nav > .menu-item .sub-menu > .menu-item:first-child { border-radius: 0 0 !important ; } #navigation > section > .primary-nav-container ul.nav > .menu-item .sub-menu > .menu-item:last-child { border-radius: 0 0 !important ; } #navigation > section > .primary-nav-container ul.nav { display: inline-block; vertical-align: middle; } #navigation > section > .side-nav { height:100%; vertical-align: middle; float:right; } #nav-container, #navigation { background-color: #ffffff !important; } #nav-container {border: none !important;}#nav-container { -moz-border-radius: 3px !important; -webkit-border-radius: 3px !important; border-radius: 3px !important; } #navigation ul.nav li ul { width:168px; font-size:14px; }#navigation ul.nav li { line-height:1.2em; }#navigation ul .sub-menu > li:first-child, #navigation ul .sub-menu > li:first-child > a { border-radius: 0 !important; -moz-border-radius: 0 !important; -webkit-border-radius: 0 !important; } #navigation { margin-top:0;margin-bottom:0; } #nav-container { margin-top: px; margin-bottom: px; } #navigation ul.nav > li > a { } #navigation ul.nav > li > a > i { margin-right: 5px; line-height: inherit; vertical-align: middle; color: ; } #navigation ul.nav > li > a:hover > i { color: ; } #navigation ul.nav > li.current-menu-item > a > i { color: ; } #navigation ul.nav > li ul li > a { line-height: ; } #navigation ul.nav > li ul li > a > i { float: left; margin-right: 5px; line-height: inherit; color: ; text-decoration: initial; } #nav-container #navigation ul#main-nav > li:first-child { border-left: none; } #navigation { transform: initial !important; }.primary-nav-container { display: inline-block; }#navigation ul.rss li.sub-rss a i,#navigation ul.rss li.sub-email a i{display:none;}body #navigation > section > .primary-nav-container ul.nav > .menu-item > .sub-menu > .menu-item:first { border-radius: 0 !important; } #navigation #main-nav > .menu-item > .sub-menu:before { content: ''; } #navigation #main-nav { font-size: 0; } #navigation #main-nav li { font-size: 14px; } #navigation #main-nav > .menu-item.parent:after { content: ''; position: absolute; top: 100%; display: none; } #navigation #main-nav > .menu-item.parent:hover:after { content: ''; position: absolute; top: 100%; display: block; } #navigation > section { height: auto; }#navigation .side-nav > .rss { position: relative; line-height: 100%; height: 100%; } #navigation .side-nav > .rss > li { line-height: 100%; height: 100%; } #navigation .side-nav > .rss > li > a { padding-top: 0; padding-bottom: 0; line-height: 100%; height: 100%; position: relative; overflow:hidden; } #navigation .side-nav > .rss > li > a:hover { text-decoration: none; } #navigation .side-nav > ul > li > a:before { position: absolute !important; top: 50% !important; margin-top: -0.5em !important; line-height:1; } #navigation .side-nav > .cart { line-height: 100%; height: 100% } #navigation .side-nav > .cart > li { height: 100% } #navigation .side-nav > .cart > li > .cart-contents { padding-top: 0; padding-bottom: 0; line-height: 100%; height: 100%; position: relative; } @media only screen and (min-width: 980px) { #navigation .side-nav > .cart > li { display: table; } #navigation .side-nav > .cart > li > a.cart-contents { display: table-cell; vertical-align: middle; } #navigation .side-nav > .cart > li > a.cart-contents:before { position: initial !important; } } #navigation ul.cart a.cart-contents + ul { box-sizing: content-box; } #navigation .side-nav > .nav-search { line-height: 100%; height: 100% } #navigation .side-nav > .nav-search > li { height: 100% } #navigation .side-nav > .nav-search > li > .search-contents { padding-top: 0; padding-bottom: 0; line-height: 100%; height: 100%; position: relative } #navigation .side-nav > ul > li > a:before { color: #be3026 !important; } #navigation .side-nav > ul > li > a:hover:before { color: !important; } #navigation #main-nav > .menu-item > a > span { vertical-align: middle; } .side-nav ul ul input , .side-nav ul ul :before { color: !important ; } } @media only screen and ( max-width: 767px ) { #navigation ul.nav > li > a > i { display: none; } #navigation ul.nav > li ul li > a > i { display: none } } </style> <style type="text/css">/* *** NEWS BOX - WP DYNAMIC CUSTOM THEME *** */ .lcnb_wpdt_theme .lcnb_loading { background: url('https://web.archive.org/web/20210320060850im_/https://tron-mainz.de/de/wp-content/gdprpatron/hts/tron-mainz.de/de/wp_content/plugins/swift_box_wp/js/sb//img/loader_d_gif.gif') no-repeat center center transparent; } .lcnb_wpdt_theme article.lcnb_news, .lcnb_wpdt_theme .lcnb_exp_block { background-color: #ffffff; } .lcnb_wpdt_theme.lcnb_wrap.lcnb_uniblock .lcnb_inner_wrapper { border-radius: 0px; } .lcnb_wpdt_theme.lcnb_wrap.lcnb_uniblock .lcnb_news, .lcnb_wpdt_theme.lcnb_wrap.lcnb_boxed article.lcnb_news, .lcnb_wpdt_theme.lcnb_wrap.lcnb_uniblock .lcnb_exp_block { border: 0px solid #D5D5D5; -moz-transition: box-shadow .2s linear, border-color .2s linear; -webkit-transition: box-shadow .2s linear, border-color .2s linear; -o-transition: box-shadow .2s linear, border-color .2s linear; -ms-transition: box-shadow .2s linear, border-color .2s linear; transition: box-shadow .2s linear, border-color .2s linear; } .lcnb_wpdt_theme.lcnb_wrap.lcnb_uniblock .lcnb_news:hover, .lcnb_wpdt_theme.lcnb_wrap.lcnb_boxed article.lcnb_news:hover { border-color: #C4C4C4; } /* IMPORANT - USE THE SAME VALUE OF THE .lcnb_news BORDER */ .lcnb_wpdt_theme.lcnb_vertical.lcnb_wrap.lcnb_uniblock .lcnb_news { margin-top: -0px; } .lcnb_wpdt_theme.lcnb_vertical.lcnb_wrap.lcnb_uniblock .lcnb_news:first-child { margin-top: 0px; } .lcnb_wpdt_theme.lcnb_horizontal.lcnb_wrap.lcnb_uniblock .lcnb_news { margin-left: -0px; } .lcnb_wpdt_theme.lcnb_horizontal.lcnb_wrap.lcnb_uniblock .lcnb_news:first-child { margin-left: 0px; } /* **** */ .lcnb_wpdt_theme.lcnb_wrap.lcnb_boxed article.lcnb_news, .lcnb_wpdt_theme.lcnb_boxed .lcnb_exp_block { border: 0px solid #D5D5D5; border-radius: 0px; box-shadow: none; } .lcnb_wpdt_theme .lcnb_title { color: #164679 !important; border-bottom: 1px solid #FFFFFF; font-weight: bold; } .lcnb_wpdt_theme .lcnb_txt, .lcnb_wpdt_theme .lcnb_exp_txt { color: #555555; } .lcnb_wpdt_theme .lcnb_txt a { color: #be3026 !important; } .lcnb_wpdt_theme .lcnb_img { background: url('https://web.archive.org/web/20210320060850im_/https://tron-mainz.de/de/wp-content/gdprpatron/hts/tron-mainz.de/de/wp_content/plugins/swift_box_wp/js/sb//img/loader_d_gif.gif') no-repeat center center transparent; } .lcnb_wpdt_theme .lcnb_social_box li { color: #164679; } /* navigation commands */ .lcnb_wpdt_theme.lcnb_has_cmd .lcnb_prev, .lcnb_wpdt_theme.lcnb_has_cmd .lcnb_next { border: 1px solid #D5D5D5; background-color: #ffffff; } .lcnb_wpdt_theme.lcnb_has_cmd .lcnb_prev:hover, .lcnb_wpdt_theme.lcnb_has_cmd .lcnb_next:hover { border-color: #C4C4C4; } .lcnb_wpdt_theme .lcnb_cmd span:before { color: #164679; } /* source logos */ .lcnb_wpdt_theme.lcnb_src_logo .lcnb_type_twitter > div { background-image: url("https://web.archive.org/web/20210320060850im_/https://tron-mainz.de/de/wp-content/gdprpatron/hts/tron-mainz.de/de/wp_content/plugins/swift_box_wp/js/sb//img/social_src_logos/dark/twitter_png.png"); } .lcnb_wpdt_theme.lcnb_src_logo .lcnb_type_rss > div { background-image: url("https://web.archive.org/web/20210320060850im_/https://tron-mainz.de/de/wp-content/gdprpatron/hts/tron-mainz.de/de/wp_content/plugins/swift_box_wp/js/sb//img/social_src_logos/dark/rss_png.png"); } .lcnb_wpdt_theme.lcnb_src_logo .lcnb_type_pinterest > div { background-image: url("https://web.archive.org/web/20210320060850im_/https://tron-mainz.de/de/wp-content/gdprpatron/hts/tron-mainz.de/de/wp_content/plugins/swift_box_wp/js/sb//img/social_src_logos/dark/pinterest_png.png"); } .lcnb_wpdt_theme.lcnb_src_logo .lcnb_type_facebook > div { background-image: url("https://web.archive.org/web/20210320060850im_/https://tron-mainz.de/de/wp-content/gdprpatron/hts/tron-mainz.de/de/wp_content/plugins/swift_box_wp/js/sb//img/social_src_logos/dark/facebook_png.png"); } .lcnb_wpdt_theme.lcnb_src_logo .lcnb_type_google > div { background-image: url("https://web.archive.org/web/20210320060850im_/https://tron-mainz.de/de/wp-content/gdprpatron/hts/tron-mainz.de/de/wp_content/plugins/swift_box_wp/js/sb//img/social_src_logos/dark/google_png.png"); } .lcnb_wpdt_theme.lcnb_src_logo .lcnb_type_youtube > div { background-image: url("https://web.archive.org/web/20210320060850im_/https://tron-mainz.de/de/wp-content/gdprpatron/hts/tron-mainz.de/de/wp_content/plugins/swift_box_wp/js/sb//img/social_src_logos/dark/youtube_png.png"); } .lcnb_wpdt_theme.lcnb_src_logo .lcnb_type_soundcloud > div { background-image: url("https://web.archive.org/web/20210320060850im_/https://tron-mainz.de/de/wp-content/gdprpatron/hts/tron-mainz.de/de/wp_content/plugins/swift_box_wp/js/sb//img/social_src_logos/dark/soundcloud_png.png"); } .lcnb_wpdt_theme.lcnb_src_logo .lcnb_type_tumblr > div { background-image: url("https://web.archive.org/web/20210320060850im_/https://tron-mainz.de/de/wp-content/gdprpatron/hts/tron-mainz.de/de/wp_content/plugins/swift_box_wp/js/sb//img/social_src_logos/dark/tumblr_png.png"); } /* bottom ant top bar */ .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_date, .lcnb_wpdt_theme .lcnb_top_bar .lcnb_date, .lcnb_wpdt_theme .lcnb_exp_date time, .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_rm_btn, .lcnb_wpdt_theme .lcnb_top_bar .lcnb_rm_btn { background-color: #F3F3F3; color: #164679; padding: 4px 8px; border-radius: 2px; } .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_link, .lcnb_wpdt_theme .lcnb_top_bar .lcnb_link, .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_social_trigger, .lcnb_wpdt_theme .lcnb_top_bar .lcnb_social_trigger, .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_btn_expand, .lcnb_wpdt_theme .lcnb_top_bar .lcnb_btn_expand { border-right: 1px solid #FFFFFF; box-shadow: none; } .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_link, .lcnb_wpdt_theme .lcnb_top_bar .lcnb_link, .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_social_trigger, .lcnb_wpdt_theme .lcnb_top_bar .lcnb_social_trigger, .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_btn_expand, .lcnb_wpdt_theme .lcnb_top_bar .lcnb_btn_expand { color: #164679; } .lcnb_wpdt_theme .lcnb_btm_bar.lcnb_narrow_txt, .lcnb_wpdt_theme .lcnb_top_bar.lcnb_narrow_txt { background: #ffffff; background: rgba(255,255,255, 0.9); } .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_link, .lcnb_wpdt_theme .lcnb_top_bar .lcnb_link, .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_social_trigger, .lcnb_wpdt_theme .lcnb_top_bar .lcnb_social_trigger, .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_btn_expand, .lcnb_wpdt_theme .lcnb_top_bar .lcnb_btn_expand { opacity: 0.8; filter: alpha(opacity=80); } .lcnb_wpdt_theme .lcnb_rm_btn:hover { background-color: #E8E8E8 !important; color: #303030 !important; } /* social flap */ .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_social_box, .lcnb_wpdt_theme .lcnb_top_bar .lcnb_social_box, .lcnb_wpdt_theme .lcnb_exp_data .lcnb_social_box { background-color: #ffffff; border: 1px solid #D5D5D5; } .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_social_box:after, .lcnb_wpdt_theme .lcnb_exp_data .lcnb_social_box:after { border-top-color: #D5D5D5; } .lcnb_wpdt_theme .lcnb_top_bar .lcnb_social_box:before { border-bottom-color: #D5D5D5; } .lcnb_wpdt_theme .lcnb_btm_bar .lcnb_social_box > li, .lcnb_wpdt_theme .lcnb_top_bar .lcnb_social_box > li, .lcnb_wpdt_theme .lcnb_exp_data .lcnb_social_box > li { border-bottom: 1px solid #D5D5D5; } /* lightbox overlays */ .lcnb_wpdt_theme .lcnb_lb_icon:before { color: #333333; } .lcnb_wpdt_theme .lcnb_lb_overlay { background-color: #FFFFFF; opacity: 0.7; filter: alpha(opacity=70); } /*** vertical ***/ .lcnb_wpdt_theme.lcnb_vertical.lcnb_side_cmd .lcnb_prev span { background-position: -132px 7px; } .lcnb_wpdt_theme.lcnb_vertical.lcnb_side_cmd .lcnb_next span { background-position: -168px 5px; } .lcnb_wpdt_theme.lcnb_vertical .lcnb_img { border-width: 0px 0px 0px 0px; border-style: solid; border-color: transparent; } .lcnb_wpdt_theme.lcnb_vertical .lcnb_img .lcnb_img_lb, .lcnb_wpdt_theme.lcnb_vertical .lcnb_img .lcnb_video_lb { margin: 0px 0 0 0px; /* IMPORANT - set the same value as .lcnb_img border */ } .lcnb_wpdt_theme.lcnb_vertical .lcnb_buttons { background-color: #ffffff; background-color: rgba(255,255,255, 0.85); border-right: 1px solid #FFFFFF; border-radius: 0px 0 0 0px; } .lcnb_wpdt_theme.lcnb_vertical .lcnb_buttons > div { border-color: #FFFFFF; border-left-color: #FFFFFF; opacity: 0.9; filter: alpha(opacity=90); } .lcnb_wpdt_theme.lcnb_vertical .lcnb_buttons > div:hover { opacity: 1; filter: alpha(opacity=100); } .lcnb_wpdt_theme.lcnb_vertical .lcnb_buttons { color: #164679; } .lcnb_wpdt_theme.lcnb_vertical .lcnb_buttons .lcnb_social_trigger.socials_shown { background-color: #ffffff; } .lcnb_wpdt_theme.lcnb_vertical .lcnb_buttons ul.lcnb_social_box { background-color: #ffffff; border: 1px solid #FFFFFF; } .lcnb_wpdt_theme.lcnb_vertical .lcnb_buttons .lcnb_social_box li { border-right: 1px solid #FFFFFF; } .lcnb_wpdt_theme.lcnb_vertical .lcnb_buttons .lcnb_social_box li:last-child { border-right: none !important; } .lcnb_wpdt_theme.lcnb_vertical .lcnb_buttons > div:hover, .lcnb_wpdt_theme.lcnb_vertical .lcnb_buttons > div.lcnb_active { background-color: #ffffff; } /*** horizontal ***/ .lcnb_wpdt_theme.lcnb_horizontal.lcnb_side_cmd .lcnb_prev span { background-position: -85px center; } .lcnb_wpdt_theme.lcnb_horizontal.lcnb_side_cmd .lcnb_next span { background-position: -115px center; } .lcnb_wpdt_theme.lcnb_horizontal .lcnb_img { border-width: 0px 0px 0; border-style: solid; border-color: transparent; } /**** EXPANDED NEWS ****/ .lcnb_wpdt_theme .lcnb_exp_block .lcnb_close:before { color: #164679; } .lcnb_wpdt_theme .lcnb_exp_data { border-top: 1px solid #FFFFFF; } .lcnb_wpdt_theme .lcnb_exp_data .lcnb_social_trigger, .lcnb_wpdt_theme .lcnb_exp_data .lcnb_link { border-left: 1px solid #FFFFFF; color: #164679; } .lcnb_wpdt_theme .lcnb_exp_img_wrap, .lcnb_wpdt_theme .lcnb_exp_body_img > div:first-child { border: 3px solid #FFFFFF; box-shadow: 0 0 1px #FFFFFF; } </style><style type="text/css">.entry img {padding: 0px;border: none;} .lcnb_wpdt_theme .lcnb_title {border-bottom: none;} .lcnb_wpdt_theme.lcnb_has_cmd .lcnb_prev, .lcnb_wpdt_theme.lcnb_has_cmd .lcnb_next {background-color: #f3f3f3!important;border: none!important;} .lcnb_horizontal.lcnb_side_cmd .lcnb_prev, .lcnb_horizontal.lcnb_side_cmd .lcnb_next {border-radius: 3px;} .lcnb_lb_icon {display:none;} .lcnb_lb_overlay {display:none;} .lcnb_horizontal.lcnb_has_cmd.lcnb_side_cmd {margin: 0!important;} .entry p {color: #164679;} .lcnb_wpdt_theme .lcnb_cmd span:before {color: #555555!important;} .lcnb_horizontal.lcnb_side_cmd .lcnb_next, .lcnb_horizontal.lcnb_side_cmd .lcnb_prev {height: 44px;} .lcnb_wpdt_theme.lcnb_has_cmd .lcnb_prev:hover, .lcnb_wpdt_theme.lcnb_has_cmd .lcnb_next:hover {background-color: #be3026!important;border: none!important;} .lcnb_horizontal.lcnb_side_cmd .lcnb_next, .lcnb_horizontal.lcnb_side_cmd .lcnb_prev {margin-top: 100px;} .lcnb_horizontal .lcnb_btm_bar {padding: 0px 6px 7px 10px;} .lcnb_horizontal .lcnb_contents {padding: 6px 14px 0px;}.lcnb_linked_title, .lcnb_title {font-size: 16px;} .lcnb_txt {font-size: 14px;} </style><noscript><style> .wpb_animate_when_almost_visible { opacity: 1; }</style></noscript></head> <body data-rsssl="1" class="page-template-default page page-id-8994 chrome alt-style-default one-col width-1200 one-col-1200 full-width full-header full-footer wpb-js-composer js-comp-ver-6.6.0 vc_responsive"> <?php echo DISPLAY_ULTIMATE_PLUS(); ?> <div id="wrapper"> <div id="inner-wrapper">  <div id="header-container"> <h3 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Wissenschaftsallianz</span></a></li> </ul> </li> </ul></div> <div class="side-nav"> <ul class="nav-search"> <li> <a class="search-contents" href="#"></a> <ul> <li> <div class="widget widget_search"><div class="search_main"> <form method="get" class="searchform" action="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/"> <input type="text" class="field s" name="s" value="Search..." onfocus="if (this.value == 'Search...') {this.value = '';}" onblur="if (this.value == '') {this.value = 'Search...';}"/> <button type="submit" class="fa fa-search submit" name="submit" value="Search"></button> </form> <div class="fix"></div> </div></div> </li> </ul> </li> </ul> </div> </section> <a href="#top" class="nav-close"> <i class="fa fa-times"></i> <span>Return to Content</span> </a> </nav> </div> </header> </div>  <div id="content" class="col-full"> <div id="main-sidebar-container">  <section id="main"> <article class="post-8994 page type-page status-publish has-post-thumbnail hentry category-publications"> <header> <h1 class="title entry-title">2020</h1> </header> <section class="entry"> <div class="vc_row wpb_row vc_row-fluid vc_column-gap-15 mpc-row"> <div class="wpb_column vc_column_container vc_col-sm-9 mpc-column" data-column-id="mpc_column-3760559172c9c4b"><div class="vc_column-inner"><div class="wpb_wrapper"> <div class="wpb_text_column wpb_content_element "> <div class="wpb_wrapper"> <p>Sethi R, Becker J, de Graaf J, Löwer M, Suchan M, Sahin U, Weber D. (2020) <strong>Integrative analysis of structural variations using short-reads and linked-reads yields highly specific and sensitive predictions</strong>.  <em>PLoS. Comput. Biol.</em> 16(11):e1008397.</p> <p><a href="https://web.archive.org/web/20210320060850/https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1008397">DOI</a>, <a href="https://web.archive.org/web/20210320060850/https://pubmed.ncbi.nlm.nih.gov/33226985/">PMID</a></p> <p> </p> <div class="su-spoiler su-spoiler-style-default su-spoiler-icon-plus su-spoiler-closed" data-scroll-offset="0" data-anchor-in-url="no"><div class="su-spoiler-title" tabindex="0" role="button"><span class="su-spoiler-icon"></span>Show abstract</div><div class="su-spoiler-content su-u-clearfix su-u-trim">Genetic diseases are driven by aberrations of the human genome. Identification of such aberrations including structural variations (SVs) is key to our understanding. Conventional short-reads whole genome sequencing (cWGS) can identify SVs to base-pair resolution, but utilizes only short-range information and suffers from high false discovery rate (FDR). Linked-reads sequencing (10XWGS) utilizes long-range information by linkage of short-reads originating from the same large DNA molecule. This can mitigate alignment-based artefacts especially in repetitive regions and should enable better prediction of SVs. However, an unbiased evaluation of this technology is not available. In this study, we performed a comprehensive analysis of different types and sizes of SVs predicted by both the technologies and validated with an independent PCR based approach. The SVs commonly identified by both the technologies were highly specific, while validation rate dropped for uncommon events. A particularly high FDR was observed for SVs only found by 10XWGS. To improve FDR and sensitivity, statistical models for both the technologies were trained. Using our approach, we characterized SVs from the MCF7 cell line and a primary breast cancer tumor with high precision. This approach improves SV prediction and can therefore help in understanding the underlying genetics in various diseases. </div></div> <p> </p> <p>Becker S, Fink A, Podlech J, Giese I, Schmiedeke JK, Bukur T, Reddehase MJ, Lemmermann NA. (2020) <strong>Positive Role of the MHC Class-I Antigen Presentation Regulator m04/gp34 of Murine Cytomegalovirus in Antiviral Protection by CD8 T Cells</strong>.  <em>Front. Cell. Infect. Microbiol</em>. 10:454.</p> <p><a href="https://web.archive.org/web/20210320060850/https://pubmed.ncbi.nlm.nih.gov/32984075/">DOI</a>, <a href="https://web.archive.org/web/20210320060850/https://pubmed.ncbi.nlm.nih.gov/32984075/">PMID</a></p> <div class="su-spoiler su-spoiler-style-default su-spoiler-icon-plus su-spoiler-closed" data-scroll-offset="0" data-anchor-in-url="no"><div class="su-spoiler-title" tabindex="0" role="button"><span class="su-spoiler-icon"></span>Show abstract</div><div class="su-spoiler-content su-u-clearfix su-u-trim">Murine cytomegalovirus (mCMV) codes for MHC class-I trafficking modulators m04/gp34, m06/gp48, and m152/gp40. By interacting with the MHC class-Iα chain, these proteins disconnect peptide-loaded MHC class-I (pMHC-I) complexes from the constitutive vesicular flow to the cell surface. Based on the assumption that all three inhibit antigen presentation, and thus the recognition of infected cells by CD8 T cells, they were referred to as “immunoevasins.” Improved antigen presentation mediated by m04 in the presence of m152 after infection with deletion mutant mCMV-Δm06<sup>W</sup>, compared to mCMV-Δm04m06 expressing only m152, led us to propose renaming these molecules “viral regulators of antigen presentation” (vRAP) to account for both negative and positive functions. In accordance with a positive function, m04-pMHC-I complexes were found to be displayed on the cell surface, where they are primarily known as ligands for Ly49 family natural killer (NK) cell receptors. Besides the established role of m04 in NK cell silencing or activation, an anti-immunoevasive function by activation of CD8 T cells is conceivable, because the binding site of m04 to MHC class-Iα appears not to mask the peptide binding site for T-cell receptor recognition. However, functional evidence was based on mCMV-Δm06<sup>W</sup>, a virus of recently doubted authenticity. Here we show that mCMV-Δm06<sup>W</sup> actually represents a mixture of an authentic <i>m06</i> deletion mutant and a mutant with an accidental additional deletion of a genome region encompassing also gene <i>m152</i>. Reanalysis of previously published experiments for the authentic mutant in the mixture confirms the previously concluded positive vRAP function of m04. </div></div> <p> </p> <p>Sahin U, Oehm P,  Derhovanessian E, Jabulowsky RA, Vormehr M, Gold M, Maurus D, Schwarck-Kokarakis D, Kuhn AN, Omokoko T, Kranz LM, Diken M, Kreiter S, Haas H, Attig S, Rae R, Cuk K, Kemmer-Brück A, Breitkreuz A, Tolliver C, Caspar J, Quinkhardt J, Hebich L, Stein M, Hohberger A, Vogler I, Liebig I, Renken S, Sikorski J, Leierer M, Müller V, Mitzel-Rink H, Miederer M, Huber C, Grabbe S, Utikal J, Pinter A, Kaufmann R, Hassel JC, Loquai C, Türeci Ö. (2020) <strong>An RNA vaccine drives immunity in checkpoint-inhibitor-treated melanoma</strong><em><strong>.</strong> Nature</em>. 585(7823):107-112.</p> <p><a href="https://web.archive.org/web/20210320060850/https://www.nature.com/articles/s41586-020-2537-9">DOI</a>, <a href="https://web.archive.org/web/20210320060850/https://pubmed.ncbi.nlm.nih.gov/32728218/">PMID</a></p> <div class="su-spoiler su-spoiler-style-default su-spoiler-icon-plus su-spoiler-closed" data-scroll-offset="0" data-anchor-in-url="no"><div class="su-spoiler-title" tabindex="0" role="button"><span class="su-spoiler-icon"></span>Show abstract</div><div class="su-spoiler-content su-u-clearfix su-u-trim">Treating patients who have cancer with vaccines that stimulate a targeted immune response is conceptually appealing, but cancer vaccine trials have not been successful in late-stage patients with treatment-refractory tumours1,2. We are testing melanoma FixVac (BNT111)—an intravenously administered liposomal RNA (RNA-LPX) vaccine, which targets four non-mutated, tumour-associated antigens that are prevalent in melanoma—in an ongoing, first-in-human, dose-escalation phase I trial in patients with advanced melanoma (Lipo-MERIT trial, ClinicalTrials.gov identifier NCT02410733). We report here data from an exploratory interim analysis that show that melanoma FixVac, alone or in combination with blockade of the checkpoint inhibitor PD1, mediates durable objective responses in checkpoint-inhibitor (CPI)-experienced patients with unresectable melanoma. Clinical responses are accompanied by the induction of strong CD4+ and CD8+ T cell immunity against the vaccine antigens. The antigen-specific cytotoxic T-cell responses in some responders reach magnitudes typically reported for adoptive T-cell therapy, and are durable. Our findings indicate that RNA-LPX vaccination is a potent immunotherapy in patients with CPI-experienced melanoma, and suggest the general utility of non-mutant shared tumour antigens as targets for cancer vaccination. </div></div> <p> </p> <p>Schrörs B, Boegel S, Albrecht C, Bukur T, Bukur V, Holtsträter C, Ritzel C, Manninen K, Tadmor AD, Vormehr M, Sahin U, Löwer M. (2020) <strong>Multi-Omics Characterization of the 4T1 Murine Mammary Gland Tumor Model</strong><em>. Front. Oncol</em>. 10:1195.</p> <p><a href="https://web.archive.org/web/20210320060850/https://www.frontiersin.org/articles/10.3389/fonc.2020.01195/full">DOI</a>, <a href="https://web.archive.org/web/20210320060850/https://pubmed.ncbi.nlm.nih.gov/32793490/">PMID</a></p> <div class="su-spoiler su-spoiler-style-default su-spoiler-icon-plus su-spoiler-closed" data-scroll-offset="0" data-anchor-in-url="no"><div class="su-spoiler-title" tabindex="0" role="button"><span class="su-spoiler-icon"></span>Show abstract</div><div class="su-spoiler-content su-u-clearfix su-u-trim">Background: Tumor models are critical for our understanding of cancer and the development of cancer therapeutics. The 4T1 murine mammary cancer cell line is one of the most widely used breast cancer models. Here, we present an integrated map of the genome, transcriptome, and immunome of 4T1. <p>Results: We found Trp53 (Tp53) and Pik3g to be mutated. Other frequently mutated genes in breast cancer, including Brca1 and Brca2, are not mutated. For cancer related genes, Nav3, Cenpf, Muc5Ac, Mpp7, Gas1, MageD2, Dusp1, Ros, Polr2a, Rragd, Ros1, and Hoxa9 are mutated. Markers for cell proliferation like Top2a, Birc5, and Mki67 are highly expressed, so are markers for metastasis like Msln, Ect2, and Plk1, which are known to be overexpressed in triple-negative breast cancer (TNBC). TNBC markers are, compared to a mammary gland control sample, lower (Esr1), comparably low (Erbb2), or not expressed at all (Pgr). We also found testis cancer antigen Pbk as well as colon/gastrointestinal cancer antigens Gpa33 and Epcam to be highly expressed. Major histocompatibility complex (MHC) class I is expressed, while MHC class II is not. We identified 505 single nucleotide variations (SNVs) and 20 insertions and deletions (indels). Neoantigens derived from 22 SNVs and one deletion elicited CD8+ or CD4+ T cell responses in IFNγ-ELISpot assays. Twelve high-confidence fusion genes were observed. We did not observe significant downregulation of mismatch repair (MMR) genes or SNVs/indels impairing their function, providing evidence for 6-thioguanine resistance. Effects of the integration of the murine mammary tumor virus were observed at the genome and transcriptome level.</p> <p>Conclusions: 4T1 cells share substantial molecular features with human TNBC. As 4T1 is a common model for metastatic tumors, our data supports the rational design of mode-of-action studies for pre-clinical evaluation of targeted immunotherapies. </p></div></div> <p> </p> <p>Salomon N, Vascotto F, Selmi A, Vormehr M, Quinkhardt J, Bukur T, Schrörs B, Löwer M, Diken M, Türeci Ö, Sahin U, Kreiter S. (2020) <strong>A liposomal RNA vaccine inducing neoantigen-specific CD4+ T cells augments the antitumor activity of local radiotherapy in mice</strong>. <em>Oncoimmunology</em>.  9:1771925. </p> <p><a href="https://web.archive.org/web/20210320060850/https://www.tandfonline.com/doi/full/10.1080/2162402X.2020.1771925">DOI</a>, <a href="https://web.archive.org/web/20210320060850/https://pubmed.ncbi.nlm.nih.gov/32923128/">PMID</a></p> <div class="su-spoiler su-spoiler-style-default su-spoiler-icon-plus su-spoiler-closed" data-scroll-offset="0" data-anchor-in-url="no"><div class="su-spoiler-title" tabindex="0" role="button"><span class="su-spoiler-icon"></span>Show abstract</div><div class="su-spoiler-content su-u-clearfix su-u-trim"> Antigen-encoding, lipoplex-formulated RNA (RNA-LPX) enables systemic delivery to lymphoid compartments and selective expression in resident antigen-presenting cells.  We report here that the rejection of CT26 tumors, mediated by local radiotherapy (LRT), is further augmented in a CD8+ T cell-dependent manner by an RNA-LPX vaccine that encodes CD4+ T cell-recognized neoantigens (CD4 neoantigen vaccine).  Whereas CD8+ T cells induced by LRT alone were primarily directed against the immunodominant gp70 antigen, mice treated with LRT plus the CD4 neoantigen vaccine rejected gp70-negative tumors and were protected from rechallenge with these tumors, indicating a potent poly-antigenic CD8+ T cell response and T cell memory.  In the spleens of CD4 neoantigen-vaccinated mice, we found a high number of activated, poly-functional, Th1-like CD4+ T cells against ME1, the immunodominant CD4 neoantigen within the poly-neoantigen vaccine.  LRT itself strongly increased CD8+ T cell numbers and clonal expansion.  However, tumor infiltrates of mice treated with CD4 neoantigen vaccine/LRT, as compared to LRT alone, displayed a higher fraction of activated gp70-specific CD8+ T cells, lower PD-1/LAG-3 expression and contained ME1-specific IFNγ+ CD4+ T cells capable of providing cognate help.  CD4 neoantigen vaccine/LRT treatment followed by anti-CTLA-4 antibody therapy further enhanced the efficacy with complete remission of gp70-negative CT26 tumors and survival of all mice.  Our data highlight the power of combining synergistic modes of action and warrants further exploration of the presented treatment schema.</div></div> <p> </p> <p>Barea Roldán D, Grimmler M, Hartmann C, Hubich-Rau S, Beiβert T, Paret C, Cagna G, Rohde C, Wöll S, Koslowski M, Türeci O, Sahin U. (2020) <strong>PLAC1 is essential for FGF7/FGFRIIIb-induced Akt-mediated cancer cell proliferation</strong>. <em>Oncotarget</em>. 11:1862-1875.</p> <p><a href="https://web.archive.org/web/20210320060850/https://www.oncotarget.com/article/27582/text/">DOI</a>, <a href="https://web.archive.org/web/20210320060850/https://pubmed.ncbi.nlm.nih.gov/32499871/">PMID</a></p> <div class="su-spoiler su-spoiler-style-default su-spoiler-icon-plus su-spoiler-closed" data-scroll-offset="0" data-anchor-in-url="no"><div class="su-spoiler-title" tabindex="0" role="button"><span class="su-spoiler-icon"></span>Show abstract</div><div class="su-spoiler-content su-u-clearfix su-u-trim"> PLAC1 (placenta enriched 1) is a mammalian trophoblast-specific protein. Aberrant expression of PLAC1 is observed in various human cancers, where it is involved in the motility, migration, and invasion of tumor cells, which are associated with the phosphoinositide 3-kinase (PI3K)/AKT pathway. We previously demonstrated that AKT activation mediates the downstream effects of PLAC1; however, the molecular mechanisms of PLAC1-induced AKT-mediated tumor-related processes are unclear. We studied human choriocarcinoma and breast cancer cell lines to explore the localization and receptor-ligand interactions, as well as the downstream effects of PLAC1. We show secretion and adherence of PLAC1 to the extracellular matrix, where it forms a trimeric complex with fibroblast growth factor 7 (FGF7) and its receptor, FGF receptor 2 IIIb (FGFR2IIIb). We further show that PLAC1 signaling via FGFR2IIIb activates AKT phosphorylation in cancer cell lines. As the FGF pathway is of major interest in anticancer therapeutic strategies, these data further promote PLAC1 as a promising anticancer drug target. </div></div> <p> </p> <p>Schöpf B, Weissensteiner H, Schäfer G, Fazzini F, Charoentong P, Naschberger A, Rupp B, Fendt L, Bukur V, Giese I, Sorn P, Sant’Anna-Silva AC, Iglesias-Gonzalez J, Sahin U, Kronenberg F, Gnaiger E, Klocker H. (2020) <strong>OXPHOS remodeling in high-grade prostate cancer involves mtDNA mutations and increased succinate oxidation</strong>. <em>Nat. Comm</em>. 11(1):1487.</p> <p><a href="https://web.archive.org/web/20210320060850/https://www.nature.com/articles/s41467-020-15237-5">DOI</a>, <a href="https://web.archive.org/web/20210320060850/https://www.ncbi.nlm.nih.gov/pubmed/32198407">PMID</a></p> <div class="su-spoiler su-spoiler-style-default su-spoiler-icon-plus su-spoiler-closed" data-scroll-offset="0" data-anchor-in-url="no"><div class="su-spoiler-title" tabindex="0" role="button"><span class="su-spoiler-icon"></span>Show abstract</div><div class="su-spoiler-content su-u-clearfix su-u-trim"> Rewiring of energy metabolism and adaptation of mitochondria are considered to impact on prostate cancer development and progression. Here, we report on mitochondrial respiration, DNA mutations and gene expression in paired benign/malignant human prostate tissue samples. Results reveal reduced respiratory capacities with NADH-pathway substrates glutamate and malate in malignant tissue and a significant metabolic shift towards higher succinate oxidation, particularly in high-grade tumors. The load of potentially deleterious mitochondrial-DNA mutations is higher in tumors and associated with unfavorable risk factors. High levels of potentially deleterious mutations in mitochondrial Complex I-encoding genes are associated with a 70% reduction in NADH-pathway capacity and compensation by increased succinate-pathway capacity. Structural analyses of these mutations reveal amino acid alterations leading to potentially deleterious effects on Complex I, supporting a causal relationship. A metagene signature extracted from the transcriptome of tumor samples exhibiting a severe mitochondrial phenotype enables identification of tumors with shorter survival times. </div></div> <p> </p> <p>Holtsträter C, Schrörs B, Bukur T, Löwer M. (2020) <strong>Bioinformatics for Cancer Immunotherapy</strong>. In: <em>Methods Mol Biol</em>.  2120:1-9.  Springer.</p> <p><a href="https://web.archive.org/web/20210320060850/https://link.springer.com/protocol/10.1007%2F978-1-0716-0327-7_1">DOI</a>, <a href="https://web.archive.org/web/20210320060850/https://www.ncbi.nlm.nih.gov/pubmed/32124308">PMID</a></p> <div class="su-spoiler su-spoiler-style-default su-spoiler-icon-plus su-spoiler-closed" data-scroll-offset="0" data-anchor-in-url="no"><div class="su-spoiler-title" tabindex="0" role="button"><span class="su-spoiler-icon"></span>Show abstract</div><div class="su-spoiler-content su-u-clearfix su-u-trim"> Our immune system plays a key role in health and disease as it is capable of responding to foreign antigens as well as acquired antigens from cancer cells. Latter are caused by somatic mutations, the so-called neoepitopes, and might be recognized by T cells if they are presented by HLA molecules on the surface of cancer cells. Personalized mutanome vaccines are a class of customized immunotherapies, which is dependent on the detection of individual cancer-specific tumor mutations and neoepitope (i.e., prediction, followed by a rational vaccine design, before on-demand production. The development of next generation sequencing (NGS) technologies and bioinformatic tools allows a large-scale analysis of each parameter involved in this process. Here, we provide an overview of the bioinformatic aspects involved in the design of personalized, neoantigen-based vaccines, including the detection of mutations and the subsequent prediction of potential epitopes, as well as methods for associated biomarker research, such as high-throughput sequencing of T-cell receptors (TCRs), followed by data analysis and the bioinformatics quantification of immune cell infiltration in cancer samples. </div></div> <p> </p> <p>Reinhard K, Rengstl B, Oehm P, Michel K, Billmeier A, Hayduk N, Klein O, Kuna K, Ouchan Y, Wöll S, Christ E, Weber D, Suchan M, Bukur T, Birtel M, Jahndel V, Mroz K, Hobohm K, Kranz L, Diken M, Kühlcke K, Türeci Ö, Sahin U. (2020) <strong>An RNA vaccine drives expansion and efficacy of claudin-CAR-T cells against solid tumors</strong>. <em>Science</em>. 367:446-453.</p> <p><a href="https://web.archive.org/web/20210320060850/https://science.sciencemag.org/content/early/2019/12/30/science.aay5967.long">DOI</a>, <a href="https://web.archive.org/web/20210320060850/https://www.ncbi.nlm.nih.gov/pubmed/31896660">PMID</a></p> <div class="su-spoiler su-spoiler-style-default su-spoiler-icon-plus su-spoiler-closed" data-scroll-offset="0" data-anchor-in-url="no"><div class="su-spoiler-title" tabindex="0" role="button"><span class="su-spoiler-icon"></span>Show abstract</div><div class="su-spoiler-content su-u-clearfix su-u-trim"> Chimeric antigen receptor (CAR)-T cells have shown efficacy in patients with B cell malignancies. Yet their application for <span class="highlight">solid</span> <span class="highlight">tumors</span> has challenges that include limited cancer-specific targets and non-persistence of adoptively transferred CAR-T cells. Here we introduce the developmentally regulated tight junction protein claudin 6 (CLDN6) as a CAR target in <span class="highlight">solid</span> <span class="highlight">tumors</span>, and a strategy to overcome inefficient CAR-T cell stimulation in vivo. We demonstrate that a nanoparticulate RNA vaccine, designed for body-wide delivery of the CAR antigen into lymphoid compartments, stimulates adoptively transferred CAR-T cells. Presentation of the natively folded target on resident dendritic cells promotes cognate and selective expansion of CAR-T cells. Improved engraftment of CAR-T cells and regression of large <span class="highlight">tumors</span> in difficult-to-treat mouse models was achieved at sub-therapeutic CAR-T cell doses. </div></div> <p> </p> <p>Vormehr M, Diken M, Türeci Ö, Sahin U, Kreiter S. (2020) <strong>Personalized Neo-Epitope Vaccines for Cancer Treatment</strong>. In: Theobald M. (eds) <em>Current Immunotherapeutic Strategies in Cancer</em>. Recent Results in Cancer Research.  214:153-167.  Springer.</p> <p><a href="https://web.archive.org/web/20210320060850/https://link.springer.com/chapter/10.1007%2F978-3-030-23765-3_5">DOI</a>, <a href="https://web.archive.org/web/20210320060850/https://www.ncbi.nlm.nih.gov/pubmed/31473852">PMID</a></p> <div class="su-spoiler su-spoiler-style-default su-spoiler-icon-plus su-spoiler-closed" data-scroll-offset="0" data-anchor-in-url="no"><div class="su-spoiler-title" tabindex="0" role="button"><span class="su-spoiler-icon"></span>Show abstract</div><div class="su-spoiler-content su-u-clearfix su-u-trim"> After more than a century of efforts to establish cancer immunotherapy in clinical practice, the advent of checkpoint inhibition (CPI) therapy was a critical breakthrough toward this direction (Hodi et al. in Cell Rep 13(2):412–424, <span class="CitationRef"><a title="View reference" role="button" href="https://web.archive.org/web/20210320060850/https://link.springer.com/chapter/10.1007/978-3-030-23765-3_5#CR29">2010</a></span>; Wolchok et al. in N Engl J Med 369(2):122–133, <span class="CitationRef"><a title="View reference" role="button" href="https://web.archive.org/web/20210320060850/https://link.springer.com/chapter/10.1007/978-3-030-23765-3_5#CR92">2013</a></span>; Herbst et al. in Nature 515(7528):563–567, <span class="CitationRef"><a title="View reference" role="button" href="https://web.archive.org/web/20210320060850/https://link.springer.com/chapter/10.1007/978-3-030-23765-3_5#CR28">2014</a></span>; Tumeh et al. in Nature 515(7528):568–571, <span class="CitationRef"><a title="View reference" role="button" href="https://web.archive.org/web/20210320060850/https://link.springer.com/chapter/10.1007/978-3-030-23765-3_5#CR83">2014</a></span>). Further, CPIs shifted the focus from long studied shared tumor-associated antigens to mutated ones. As cancer is caused by mutations in somatic cells, the concept to utilize these correlates of ‘foreignness’ to enable recognition and lysis of the cancer cell by T cell immunity seems an obvious thing to do. </div></div> </div> </div> </div></div></div><div class="wpb_column vc_column_container vc_col-sm-3 mpc-column"><div class="vc_column-inner"><div class="wpb_wrapper"> <div class="vc_grid-container-wrapper vc_clearfix"> <div class="vc_grid-container vc_clearfix wpb_content_element vc_basic_grid" data-initial-loading-animation="fadeIn" data-vc-grid-settings="{"page_id":8994,"style":"all","action":"vc_get_vc_grid_data","shortcode_id":"1516780861471-483aff06-d626-10","tag":"vc_basic_grid"}" data-vc-request="https://tron-mainz.de/de/wp-admin/admin-ajax.php" data-vc-post-id="8994" data-vc-public-nonce="660a59436e"> <style data-type="vc_shortcodes-custom-css">.vc_custom_1484316837418{background-color: #164679 !important;background-position: center !important;background-repeat: no-repeat 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style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2021-2/" class="vc_gitem-link" title="2021">2021</a></h3></div></div></div></div></div></div></div><div class="vc_clearfix"></div></div><div class="vc_grid-item vc_clearfix vc_col-sm-12"><div class="vc_grid-item-mini vc_clearfix "><div class="vc_gitem-animated-block vc_gitem-animate vc_gitem-animate-none" data-vc-animation="none"><div class="vc_gitem-zone vc_gitem-zone-a vc_custom_1484316837418 vc-gitem-zone-height-mode-auto vc-gitem-zone-height-mode-auto-16-9 vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2019-2/" title="2019" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920202167 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2019-2/" class="vc_gitem-link" title="2019">2019</a></h3></div></div></div></div></div><div class="vc_gitem-zone vc_gitem-zone-b vc_custom_1484317192348 vc-gitem-zone-height-mode-auto vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2019-2/" title="2019" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920211292 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2019-2/" class="vc_gitem-link" title="2019">2019</a></h3></div></div></div></div></div></div></div><div class="vc_clearfix"></div></div><div class="vc_grid-item vc_clearfix vc_col-sm-12"><div class="vc_grid-item-mini vc_clearfix "><div class="vc_gitem-animated-block vc_gitem-animate vc_gitem-animate-none" data-vc-animation="none"><div class="vc_gitem-zone vc_gitem-zone-a vc_custom_1484316837418 vc-gitem-zone-height-mode-auto vc-gitem-zone-height-mode-auto-16-9 vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2018-2/" title="2018" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920202167 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2018-2/" class="vc_gitem-link" title="2018">2018</a></h3></div></div></div></div></div><div class="vc_gitem-zone vc_gitem-zone-b vc_custom_1484317192348 vc-gitem-zone-height-mode-auto vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2018-2/" title="2018" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920211292 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2018-2/" class="vc_gitem-link" title="2018">2018</a></h3></div></div></div></div></div></div></div><div class="vc_clearfix"></div></div><div class="vc_grid-item vc_clearfix vc_col-sm-12"><div class="vc_grid-item-mini vc_clearfix "><div class="vc_gitem-animated-block vc_gitem-animate vc_gitem-animate-none" data-vc-animation="none"><div class="vc_gitem-zone vc_gitem-zone-a vc_custom_1484316837418 vc-gitem-zone-height-mode-auto vc-gitem-zone-height-mode-auto-16-9 vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2017-2/" title="2017" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920202167 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2017-2/" class="vc_gitem-link" title="2017">2017</a></h3></div></div></div></div></div><div class="vc_gitem-zone vc_gitem-zone-b vc_custom_1484317192348 vc-gitem-zone-height-mode-auto vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2017-2/" title="2017" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920211292 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2017-2/" class="vc_gitem-link" title="2017">2017</a></h3></div></div></div></div></div></div></div><div class="vc_clearfix"></div></div><div class="vc_grid-item vc_clearfix vc_col-sm-12"><div class="vc_grid-item-mini vc_clearfix "><div class="vc_gitem-animated-block vc_gitem-animate vc_gitem-animate-none" data-vc-animation="none"><div class="vc_gitem-zone vc_gitem-zone-a vc_custom_1484316837418 vc-gitem-zone-height-mode-auto vc-gitem-zone-height-mode-auto-16-9 vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2016-2/" title="2016" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920202167 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2016-2/" class="vc_gitem-link" title="2016">2016</a></h3></div></div></div></div></div><div class="vc_gitem-zone vc_gitem-zone-b vc_custom_1484317192348 vc-gitem-zone-height-mode-auto vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2016-2/" title="2016" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920211292 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2016-2/" class="vc_gitem-link" title="2016">2016</a></h3></div></div></div></div></div></div></div><div class="vc_clearfix"></div></div><div class="vc_grid-item vc_clearfix vc_col-sm-12"><div class="vc_grid-item-mini vc_clearfix "><div class="vc_gitem-animated-block vc_gitem-animate vc_gitem-animate-none" data-vc-animation="none"><div class="vc_gitem-zone vc_gitem-zone-a vc_custom_1484316837418 vc-gitem-zone-height-mode-auto vc-gitem-zone-height-mode-auto-16-9 vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2015-2/" title="2015" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920202167 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2015-2/" class="vc_gitem-link" title="2015">2015</a></h3></div></div></div></div></div><div class="vc_gitem-zone vc_gitem-zone-b vc_custom_1484317192348 vc-gitem-zone-height-mode-auto vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2015-2/" title="2015" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920211292 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2015-2/" class="vc_gitem-link" title="2015">2015</a></h3></div></div></div></div></div></div></div><div class="vc_clearfix"></div></div><div class="vc_grid-item vc_clearfix vc_col-sm-12"><div class="vc_grid-item-mini vc_clearfix "><div class="vc_gitem-animated-block vc_gitem-animate vc_gitem-animate-none" data-vc-animation="none"><div class="vc_gitem-zone vc_gitem-zone-a vc_custom_1484316837418 vc-gitem-zone-height-mode-auto vc-gitem-zone-height-mode-auto-16-9 vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2014-2/" title="2014" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920202167 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2014-2/" class="vc_gitem-link" title="2014">2014</a></h3></div></div></div></div></div><div class="vc_gitem-zone vc_gitem-zone-b vc_custom_1484317192348 vc-gitem-zone-height-mode-auto vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2014-2/" title="2014" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920211292 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/2014-2/" class="vc_gitem-link" title="2014">2014</a></h3></div></div></div></div></div></div></div><div class="vc_clearfix"></div></div><div class="vc_grid-item vc_clearfix vc_col-sm-12"><div class="vc_grid-item-mini vc_clearfix "><div class="vc_gitem-animated-block vc_gitem-animate vc_gitem-animate-none" data-vc-animation="none"><div class="vc_gitem-zone vc_gitem-zone-a vc_custom_1484316837418 vc-gitem-zone-height-mode-auto vc-gitem-zone-height-mode-auto-16-9 vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/publications/2013-2/" title="2013" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920202167 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/publications/2013-2/" class="vc_gitem-link" title="2013">2013</a></h3></div></div></div></div></div><div class="vc_gitem-zone vc_gitem-zone-b vc_custom_1484317192348 vc-gitem-zone-height-mode-auto vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/publications/2013-2/" title="2013" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920211292 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/publications/2013-2/" class="vc_gitem-link" title="2013">2013</a></h3></div></div></div></div></div></div></div><div class="vc_clearfix"></div></div><div class="vc_grid-item vc_clearfix vc_col-sm-12"><div class="vc_grid-item-mini vc_clearfix "><div class="vc_gitem-animated-block vc_gitem-animate vc_gitem-animate-none" data-vc-animation="none"><div class="vc_gitem-zone vc_gitem-zone-a vc_custom_1484316837418 vc-gitem-zone-height-mode-auto vc-gitem-zone-height-mode-auto-16-9 vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/publications/2012-2/" title="2012" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920202167 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/publications/2012-2/" class="vc_gitem-link" title="2012">2012</a></h3></div></div></div></div></div><div class="vc_gitem-zone vc_gitem-zone-b vc_custom_1484317192348 vc-gitem-zone-height-mode-auto vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/publications/2012-2/" title="2012" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920211292 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/publications/2012-2/" class="vc_gitem-link" title="2012">2012</a></h3></div></div></div></div></div></div></div><div class="vc_clearfix"></div></div><div class="vc_grid-item vc_clearfix vc_col-sm-12"><div class="vc_grid-item-mini vc_clearfix "><div class="vc_gitem-animated-block vc_gitem-animate vc_gitem-animate-none" data-vc-animation="none"><div class="vc_gitem-zone vc_gitem-zone-a vc_custom_1484316837418 vc-gitem-zone-height-mode-auto vc-gitem-zone-height-mode-auto-16-9 vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/publications/2011-2/" title="2011" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div class="vc_gitem_row vc_row vc_gitem-row-position-middle"><div class="vc_col-sm-12 vc_gitem-col vc_gitem-col-align-"><div class="vc_custom_heading sidegrid vc_custom_1486920202167 vc_gitem-post-data vc_gitem-post-data-source-post_title"><h3 style="color: #ffffff;text-align: center;font-family:Lato;font-weight:700;font-style:normal"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/publications/2011-2/" class="vc_gitem-link" title="2011">2011</a></h3></div></div></div></div></div><div class="vc_gitem-zone vc_gitem-zone-b vc_custom_1484317192348 vc-gitem-zone-height-mode-auto vc_gitem-is-link"><a href="https://web.archive.org/web/20210320060850/https://tron-mainz.de/de/publications/2011-2/" title="2011" class="vc_gitem-link vc-zone-link"></a><div class="vc_gitem-zone-mini"><div 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