Abstract
This study was carried out for evaluating the interplay of p53, p21 and Ki-67 proteins along the colorectal adenoma-carcinoma oncogenic transformation sequel. Therefore, Fifty colorectal cancer and 14 adenoma patients were involved. The histopathological expression of p53, p21 and Ki-67 proteins was evaluated by immunohistochemistry assay. The results revealed that remarkable overexpression of p53 protein was seen in the tumorous sections of cancer patients more than that in adenoma patients (p
Highlights
Colonic epithelium to give way to precancerous adenoma development and eventually frank Colorectal Cancer (CRC) is the fourth commonest adenocarcinoma[3]
Risks for developing colorectal confirmed that sporadic CRC originate from colorectal adenoma, through adenoma-carcinoma sequence[4,5] and colorectal adenomas are fairly common in the general cancer include having inflammatory bowel disease, a personal or family history of colorectal cancer or colorectal polyps and certain hereditary syndromes
All CRC cases were of adenocarcinoma, 32 cases were left-sided, 12 right-sided and 6 at transverse colon .It was found that 6% of CRC patients were presented at B1 stage, 10% at B2 stage, 10% at C1 stage, 14% at C2 stage and 60% at D stage
Summary
Colonic epithelium to give way to precancerous adenoma development and eventually frank Colorectal Cancer (CRC) is the fourth commonest adenocarcinoma[3]. CRC arise through a series of colorectal tumor initiation and progression requires at genetic mutations that activates proto-oncogenes and least seven different somatic changes before a cell can disable tumor suppressor genes resulting in the normal develop into a carcinoma[10]. Loss of p53 tumor suppressor activity, results in cells tolerating DNA damage that can occur by genotoxic products, which eventually may lead to cancer formation due to inability to eliminate damaged cells by apoptosis[19] Another tumor suppressor protein is p21, which was identified as the product of the gene activated by wild-type p53 and it was named WAF1 (wild-type p53 activated factor) [20,21,22]. The obtained results could offer a better understanding of the entangled role of the oncogenic, proliferative and tumor suppressor factors in predisposing or causing CRC in human beings
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