Colorectal carcinoma is a highly lethal malignant epithelial tumor involving humans. The incidence of colorectal carcinoma is steadily increasing in developing countries, this could be assigned to low physical activity together with high consumption of animal fat-rich food. malignancy of the colon is a multistep process which is initiated by adenoma that proceeds to carcinoma, the latter includes a wide variety of tumor phenotypes. During the adenoma-carcinoma process; a series of genetic and epigenetic alterations occur. Detection of these genetic alterations is of great benefit in the future management of colorectal carcinomas. Cortactin (CTTN) is a Src kinase substrate, encoded by a gene located on chromosome 11. CTTN anchors the dynamic actin assembly . CTTN is implicated in the formation of the leading-edges cellular protrusions.the aim of this study is to evaluate expression of CTTN in 50 cases of colorectal adenocarcinomas and their adjacent normal colonic mucosae.
Colorectal carcinoma is one of the most aggressive malignant epithelial neoplasms affecting the gastrointestinal tract. The incidence of colorectal carcinoma is obviously increasing in developing countries, where the physical inactivity and the consumption of animal fat-rich food became more evident. Colorectal tumorigenesis is a multistep process which is initiated by adenoma and is terminated by carcinoma, the latter shows variable degrees of tumor differentiation and invasiveness. During the adenoma-carcinoma process; a series of genetic mutations occur. Detection of these genetic mutations will help in the development of novel therapeutic agents, which in turn will improve patients' outcomes. Cortactin (CTTN) is a Src kinase substrate, encoded by a gene located on chromosome 11. CTTN binds to and activates Arp 2/3 and stabilizes the dynamic actin assembly after its formation. So, it become clear that CTTN is involved in the formation of the leading-edges cellular protrusions.