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Background:Gliosis is a characteristic pathology in many central nervous system (CNS) diseases. Cytokines are considered to be effectors of gliosis. It has been shown that pro-inflammatory cytokines such as interleukin (IL)-1 and IL-6 boost glia scar formation. On the other hand, anti-inflammatory cytokines, such as IL-10 and IL-1 receptor antagonist (ra), can act neuroprotectively. Furthermore, various immune mediators and neurotransmitters can modulate the onset of gliosis.Material/Methods: We analysed, on the one hand, the predictive powers for recurrent disease of the immunohistochemical expressions of p53 and the endothelial markers CD34 and CD105 in 53 NSCLC tumor samples, and, on the other hand, their correlations to serum VEGF and bFGF levels. Moreover, we sequenced the whole coding region of the p53 gene in 32 tumor samples for the presence of p53 mutations (exons 2–11) using a cDNA technique.Results: The two endothelial markers correlated with each other. CD105 expression correlated with p53 expression, which was overexpressed in 49%. No other significant correlations between markers could be demonstrated. A significant correlation between p53 overexpression and recurrent disease was demonstrated (p=0.029). The mutational status of p53 correlated to p53 protein overexpression, but did not correlate with either of the immunohistochemical markers. The mutational status could not confirm an immunohistochemical correlation between p53 and recurrences (p=0.068).Conclusions: The present study demonstrates that p53 expression correlates with CD105 expression, and that p53 overexpression may indicate a lower recurrence risk in patients undergoing surgery for NSCLC stage I-IIIA, although future larger prospective studies are needed to fully elucidate this finding.