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Helicobacter pylori (H. pylori) is considered to be a major factor contributing to gastric mucosal damage by stimulating mucosal macrophage production of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), but the inflammatory responses within the gastric mucosa in vivo are not well known. Therefore, this study was designed to investigate the expression of TNF-α induced by H. pylori infection which is involved in the tumor initiation and promotion of gastric carcinogenesis. This study was carried out in 200 patients, consisting of normal gastric mucosa (n = 20), mucosa with chronic gastritis (n = 63), intestinal metaplasia (n = 20), dysplasia (n = 11), and gastric adenocarcinoma (n = 86), in which the H. pylori status has been analyzed. The expression of TNF-α was studied at mRNA as well as protein level using RT-PCR and western blotting, respectively. The localization of TNF-α was also studied semiquantitatively by immunohistochemistry. The RT-PCR and western blotting results of TNF-α mRNA and protein expressions were significantly increased in chronic gastritis, intestinal metaplasia, dysplasia and gastric adenocarcinoma patients, respectively. Immunohistochemical study also showed the increased expression of TNF-α in the similar way. Over expression of TNF-α showed a significant severity-dose–response as risk markers from preneoplastic lesions to gastric cancer.

Introduction: The proto-oncogene c-Kit encodes a tyrosine kinase receptor which is essential during embryonic and postnatal life but its expression in precancerous lesions has not been studied. Musashi-1 was initially identified as a neuronal stem cell marker and recently as an intestinal stem cell marker and is aberrantly expressed in several cancers including colorectal cancer, but its role in neoplastic tissues has not been elucidated. The present study aims to study the expression of c-Kit and Musashi-1 in precancerous lesions and colorectal carcinoma in correlation with etiological factors. Methods: Immunohistochemical analysis, western blot and RT-PCR were done to observe the expression of c-Kit and Musashi-1 in normal, ulcerative colitis, adenoma and adenocarcinoma of colorectal tissues. Results: c-Kit expression was observed to decrease from normal to adenocarcinoma. In contrast, Musashi-1 showed increased expression from adenoma to carcinoma stages. Furthermore, c-Kit showed statistically significant association with alcoholic and non-alcoholic patients (p Conclusions: Overall, these studies indicate that the decreased or loss of c-Kit and increase in the Musashi-1 expression in carcinoma can be attributed to the disease progression and malignant transformation of colorectal epithelium. A statistically significant negative correlation was found between c-Kit and Musashi-1 in colorectal carcinoma.