Abstract
Abstract Background: Regional lymph node metastasis is a common event in solid tumors and is considered a marker for dissemination, increased stage, and worse prognosis. In renal cell cancer (RCC) lymphatic tumor spread exists, but, despite impressive therapeutic advances in metastatic RCC, including targeting of VEGF induced angiogenesis, data on the role of vegfr-3 that's appears to be the signaling pathway for tumor-induced lymphangiogenesis in RCC are rare. In this study, we analyzed the expression and the presence of the soluble VEGFR-3 form in 30 RCC patients and results were correlated with clinicopathological parameters. Patients and Methods: Tumor and sera from 30 RCC patients (20 clear cell (ccRCC) and 10 papillary (pRCC) were included in this study. The expressions of VEGFR-3 on tumor were evaluated by immunohistochemestry. Using ELISA assays, sVEGFR–3 were measured in sera of RCC patients in comparison to 20 healthy controls. Results: A high expression of VEGFR-3 was observed in more than 55% of the patients as compared to the negative control. Regarding circulating VEGF R-3 the level were variable in all samples, but, the median sVEGF- R3 level was significantly higher (p=0.005) in RCC patients as compared to healthy donors. An inverse correlation between VEGFR-3 expression & its soluble form was noted (r=-0.33 p=0.040).. However, when patients were divided into subgroups, the expression as well as the circulating form of VEGFR-3 were significantly higher in pRCC than ccRCC (p= 0.035 and 0.022 respectively). No significant correlation with lymph node status was observed. Furthermore, there was no correlation with any clinicopathological variable in the two subgroups. Conclusions: we showed that in renal cell cancer, VEGFR-3 is expressed and present as soluble form, a different expression pattern in ccRCC and pRCC exist. Therefore, any clinical treatment strategy designed to target lymphangiogenesis in RCC should differentiate between ccRCC and pRCC Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 371.
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