1687 - VEGF and VEGF Receptors in Thymic Epithelial Tumors (Tet): Pathological Features and Clinical Implications

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ABSTRACT Background Thymic Epithelial Tumors (TET) are very rare cancers. They derives from Thymic gland and are associated with different clinical syndromes, such as miastenic and Good syndrome and other immunological and paraneoplastic disorders. The principal treatment of these patients is chemotherapy with schedule containing cisplatin characterized by high response rates (60%). Unfortunately some patients do not respond at all and most patients do not achieve long-lasting remission. For these patients have not other therapeutic chances at the moment. There are few data of the efficacy of anti-angiogenetic drugs in TET but new knowledges are emerging on the potential use of this class of drugs in patients with TET on the basis of laboratory and preclinical translational findings. Materials and methods we investigated the expression of Vascular Endothelial Growth Factor (VEGF) and its receptors (VEGFR1, 2 and 3) in 200 TET arranged in Tissue Micro Array (TMA). We observed both histotype distribution and modulation of angiogenetic factors (both VEGFRs and VEGFs) in TET. Results we observed that, when compared with the low-grade counterpart, high grade TET (B2, B3 and Carcinomas) contained significantly higher numbers of VEGFA, VEGFC, VEGFD, VEGFR1 and VEGFR2 expressing tumor cells. In addition, in high grade TET, strong positive correlations between staining for VEGFA and those for all other markers were found. In the same tumors, VEGFC staining was not associated with VEGFR1, VEGFR3 and PDGFRB staining and no correlation was obtained between VEGFD and VEGFR1 or VEGFR3 staining. The co-expression in epithelial cells of growth factors and their receptors suggests the presence of autocrine mechanisms in TET. Conclusions according to our data VEGFs and VEGFRs in TET are potential targets of anti-angiogenesis drugs. Further studies are needed to investigate the potential role of anti-angiogenetic agents. Disclosure All authors have declared no conflicts of interest.