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Angiogenesis buy me a boat lyrics the formation of new vasculature from an existing vascular network, plays a critical role in various pathological processes, such as tumor progression, and both acute and chronic inflammation [17, 35, 36]. It has been also suggested that this process is integral part of IBD pathology [37]. VEGF is the key mediator of angiogenesis but the role of tumor suppressor genes in angiogenesis still remains elucidated. In our study, we found higher systemic values of TNF-α and IL-6 in UC patients with positive staining of p16, p53 and VEGF, respectively (Fig 2D). Few studies revealed that alteration of tumor suppressor genes may contribute to neovascularization, guided by altered cytokine milieu [38, 39]. Wild type p53 down regulates VEGF expression and subsequently inhibits angiogenesis, in several tumors [40, 41]. In line with this, mutant-type p53 expression correlates with VEGF in few different tumors [42, 43]. Also, wild type p16 reduce angiogenesis, via down regulation of VEGF [44] and, in rheumatoid arthritis model, p16 impairs IL-6 secretion by mononuclear cells [45]. We proposed that expressed antioncogene p16 and p53 are mutated and they are not functional [46]. Rodrugues et al. analyzed p53 cDNA by using the polymerase chain raction in 10 colorectal cancer cell lines and showed that all cell lines that expressed high levels of p53 were synthesizing mRNAs that encoded mutant p53 proteins, indicating that high expression of p53 protein correlates with the presence of p53 gene mutations in these colorectal cancer cell lines [47]. The similar results were obtained in breast cancer cell lines [48] and primary lung tumors [49]. These findings implicate that when p53 is detected immunohistologically, it is probably mutant. Lang et al. also reported that 65% of patients with overexpression of p16 in squamous cell carcinoma of the head and neck showed p16-specific gene alterations [50]. These antioncogenes may induce VEGF over expression and stimulate angiogenesis. Positive staining of p16 and VEGF was detected in significantly higher percentages of UC patients with histological grade III (Table 1), indicating that disease progression is followed by higher expression of antioncogenes and subsequently VEGF. Besides its well-known role in angiogenesis, it has been suggested that VEGF also have a role in inflammation and immunity. For example, the study of Kim YS et al [51] revealed that VEGF is key mediator in the development of T cell priming in the airways. Their results suggest that VEGF mediates the recruitment of inflammatory cells and enhances expression of co-stimulatory molecules on recruited and resident mononuclear cells, leading to up-regulation of pro-inflammatory, Th1 and Th17 cytokines. Additionally, Basu A et al [52] confirmed facilitating role of VEGF on pro-inflammatory response, by affecting memory T cell function..

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