N improved number of circulating PLTs correlates with poor prognosis. PLTs assistance cancer cells by modulating angiogenesis and/or directly binding cancer cells, which facilitates the metastatic procedure [1,2]. These cells and their soluble aspects can also defend cancer cells from immune attack by mechanisms which are poorly understood. Research focused on autoimmune circumstances, have shown that exhausted PLTs type aggregates with T cells, downregulating T cell activation, proliferation and interferon- production [3,4]. Nevertheless, no equivalent study has been performed in the context of cancer. Approaches Our study investigated the presence of circulating PLT-immune cell aggregates in myeloproliferative neoplasm (MPN) sufferers. To that objective, cryopreserved peripheral blood mononuclear cells had been analyzed by multicolor flow cytometry for PLT bound -T, -NK, -B and -CD3+/CD56+ cells, as well as CD4 and CD8 T cell subpopulations. Additionally, to assess the effect PLT-binding has on T and NK cell anti-tumor reactivity, in vitro cytotoxic response was constantly monitored over 40 hours, utilizing the xCELLigence technologies.Outcomes Our preliminary results show that, when compared to healthful donors, MPN individuals have an elevated number of PLT bound CD8+ T, NK and CD3+/CD56+ cells. Lastly, our final results indicate that platelets can modulate the T and NK cells tumor reactivity in distinct manners; the presence of PLTs impairs the killing capacity of T cell whereas it appears to improve it on NK cells. Having said that, additional research are needed to confirm our preliminary results. Conclusions N/mAChR4 manufacturer AReferences 1. Borsig L. The function of platelet activation in tumor metastasis. Specialist Rev Anticancer Ther. 2008;eight(8):1247-1255. doi:10.1586/14737140.8.eight.1247. 2. Bambace NM, Holmes CE. The platelet contribution to cancer progression. J Thromb Haemost. 2011;9(2):237- 249. doi:ten.1111/j.15387836.2010.04131.x. 3. Zamora C, Canto E, Nieto JC, et al. Functional consequences of platelet binding to T lymphocytes in inflammation. J Leukoc Biol. 2013;94(3):521529. doi:ten.1189/jlb.0213074. 4. Zamora C, CantE, Nieto JC, et al. Binding of platelets to lymphocytes: A possible anti-inflammatory therapy in rheumatoid arthritis. J Immunol. 2017;198(eight):3099-3108. doi:ten.4049/jimmunol.1601708.P479 NG-641: an oncolytic T-SIGn virus targeting cancer-associated fibroblasts inside the stromal microenvironment of human carcinomas Matthieu Besneux1, Brian Champion, PhD1, Nalini Marino1, Marilena Patsalidou1, Gianfranco di Genova1, Sam Illingworth1, Stefania Fedele1, Lorna Slater1, Darren Glutathione Peroxidase medchemexpress Plumb1, Katy West1, Joshua Freedman, BS2, Len Seymour2, Kerry Fisher, MD PhD1, Alice Brown, PhD1 1 PsiOxus Therapeutics Ltd, Abingdon, UK; 2Oxford University, Oxford, UK Correspondence: Brian Champion ([email protected]) Journal for ImmunoTherapy of Cancer 2018, 6(Suppl 1):P479 Background NG-641 is really a modified variant of enadenotucirev (EnAd), an Ad11p/ Ad3 chimeric group B adenovirus, which retains all of the functional properties of enadenotucirev, though also mediating the expression of transgenes designed to target the breakdown from the stromal barrier and reverse immune suppression inside the tumor microenvironment (TME). As an method to immunogene therapy targeting stromal wealthy tumors, we’ve made a transgene-modified variant of EnAd expressing a bi-specific T-cell activator molecule (FAP-TAC) recognizing human fibroblast activating protein (FAP) on cancer related fibroblasts (CAFs) and CD3 on T-cells.