DNA Damage Is a Potential Marker for TP53 Mutation in Colorectal Carcinogenesis.

Purpose: The ability to measure oxidative DNA damage in a tissue allows establishment of the relationship between DNA damage and mutations in normal and neoplastic cells. It is well known that TP53 is a key inhibitor of tumor development and preserves the genome integrity in each cell. The aim of the present study was to investigate the relationship between DNA damage and TP53 mutation in colorectal adenoma and adenocarcinoma, and the value of DNA damage as potential marker of TP53 mutation in non-tumor tissues adjacent to colon malignant lesions.

Microenvironment influence on human colon adenocarcinoma phenotypes and matrix metalloproteinase-2, p53 and β-catenin tumor expressions from identical monoclonal cell tumor in the orthotopic model in athymic nude rats.

The present study aims to identify differences between left and right colon adenocarcinoma arising from identical clonal cell and to find out if microenvironment has any influence on matrix metalloproteinase-2 (MMP2), p53 and β-catenin tumor expressions. MATERIAL AND METHODS. Rats (RNU) were submitted to cecostomy to obtain the orthotopic model of right colon tumor (n = 10), while for the left colon model (n = 10), a colon diversion and distal mucous fistula in the descending colon was used.

Oxidative DNA damage and β-catenin expression in colorectal cancer evolution.

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.