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Objective:The feasibility of curative surgery for elderly patients with renal cell carcinoma (RCC) remains controversial and under discussion. The main aim of this study was to evaluate the long-term benefits of curative surgery as a treatment for RCC in elderly patients.Methods:We retrospectively considered 672 patients with RCC who underwent partial nephrectomy or radical nephrectomy between January 2004 and July 2014. X-tile program was used to determine the optimal age cutoff values with CSS as endpoint.Results:Patients were divided into the following groups according to their age using the method of X-tile program: a young group (< 40 years), a young-old group (40-75) and an old-old group (≥ 75). Following multivariate analysis age ≥ 75 years was determined to be an independent risk factor for overall survival (HR=4.36; 95% CI: 1.31-14.48; P=0.016); interestingly, this was not the case for cancer-specific survival (HR = 2.65; 95%CI: 0.77-9.16; P=0.124). Furthermore, an age of 40 to 75 years was not a risk factor according to univariate and multivariate analysis.Conclusion:After determining the age cutoff values, there was no significant difference in prognosis between young and old patients with RCC.

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Toxoplasma gondii excreted-secreted antigens (ESA) could lead to the fetal abortion especially in the early stage of pregnancy. Deficit in regulatory T cells is a critical event in the fetal abortion. Transcription factor forkhead box p3 (Foxp3) mediates differentiation and functional roles on regulatory T cells. Previously, we revealed that ESA inhibited Foxp3 through the suppression of transforming growth factor-β type II receptor, phosphorylation of Smad2, Smad3, and Smad4. Knockdown of Smad2 collaborated with ESA to further inhibit Foxp3. The decrease in Foxp3 caused by ESA reversed via forced expression of Smad2, Smad3, and Smad4, respectively. In this study, we investigate whether other signaling pathways are implicated in ESA-induced Foxp3 downregulation. EL4 cells were cultured and stimulated with ESA. Interleukin-2 receptor γ (IL-2Rγ) chain, Janus kinase 3 (JAK3), signal transducer and activator of transcription 5 (Stat5), Stat3, phosphorylation of Stat5 and Stat3 were assayed by Western blot analysis. Phosphorylation of Stat5 and Stat3 was further measured by cellular immunofluorescence. The expression plasmid of pcDNA3.1-Stat3 and pcDNA3.1-Stat5b was constructed, respectively. The concentration of interleukin-2 (IL-2) in the culture supernatants was detected by enzyme-linked immunosorbent assay. ESA inhibited the level of JAK3, phosphorylation of Stat5 and Stat3, and Foxp3 in EL4 cells. The suppressive effects of ESA on Foxp3 were attenuated by forced expression of Stat5 and Stat3. In addition, ESA suppressed IL-2Rγ in EL4 cells, while IL-2Rγ agonist could markedly reverse the diminished Foxp3 caused by ESA. Furthermore, ESA directly influenced the expression of IL-2Rγ, rather than the availability of IL-2 indirectly. ESA suppressed the level of Foxp3 via inhibiting IL-2Rγ/JAK3/Stats signaling pathway in EL4 cells.