PURPOSE: Oxidative DNA damage is one of the mechanisms associated to initial colorectal carcinogenesis, but how it interacts with β-catenin, an adherence protein related to cancer evolution, is not clear. This study investigates the relationship between oxidative DNA damage and β-catenin expression in normal mucosa and colon tumor tissue (adenoma and adenocarcinoma) in colorectal adenocarcinoma evolution. METHOD: One hundred and 13 samples were studied. Hematoxylin-eosin determined histological grade. β-Catenin expression was analyzed by immunohistochemistry. The oxidative DNA damage was evaluated using comet assay technique. The coefficient for rejection of the nullity hypothesis was taken to 5 %. Kruskal-Wallis, Spearman test, and partial correlation were used to analyze the data. RESULTS: There was oxidative DNA damage increase in colorectal cancer evolution (p < 0.01). Histological grade was correlated with oxidative DNA damage (p < 0.01). There were differences in β-catenin expression among normal, adenoma, and adenocarcinoma tissue with progressive increase of β-catenin expression (p < 0.00). Histological grade was correlated to β-catenin expression (p < 0.00). There was a relationship (p < 0.00) between β-catenin and histological grade while controlling for the effect of oxidative DNA damage. CONCLUSION: The findings of this study make it possible to establish a relationship between oxidative DNA damage and β-catenin expression in normal mucosa and colorectal tumor tissue. Additionally, they show a causal relationship between variations of β-catenin in different tissues analyzed while controlling for the effect of oxidative DNA damage.
PURPOSE: Oxidative DNA damage is one of the mechanisms associated to initial colorectal carcinogenesis, but how it interacts with β-catenin, an adherence protein related to cancer evolution, is not clear. This study investigates the relationship between oxidative DNA damage and β-catenin expression in normal mucosa and colon tumor tissue (adenoma and adenocarcinoma) in colorectal adenocarcinoma evolution. METHOD: One hundred and 13 samples were studied. Hematoxylin-eosin determined histological grade. β-Catenin expression was analyzed by immunohistochemistry. The oxidative DNA damage was evaluated using comet assay technique. The coefficient for rejection of the nullity hypothesis was taken to 5 %. Kruskal-Wallis, Spearman test, and partial correlation were used to analyze the data. RESULTS: There was oxidative DNA damage increase in colorectal cancer evolution (p < 0.01). Histological grade was correlated with oxidative DNA damage (p < 0.01). There were differences in β-catenin expression among normal, adenoma, and adenocarcinoma tissue with progressive increase of β-catenin expression (p < 0.00). Histological grade was correlated to β-catenin expression (p < 0.00). There was a relationship (p < 0.00) between β-catenin and histological grade while controlling for the effect of oxidative DNA damage. CONCLUSION: The findings of this study make it possible to establish a relationship between oxidative DNA damage and β-catenin expression in normal mucosa and colorectal tumor tissue. Additionally, they show a causal relationship between variations of β-catenin in different tissues analyzed while controlling for the effect of oxidative DNA damage.
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