Colorectal Tumorigenesis

The development of a colorectal neoplasm is a multistep process of several genetic and phenotypic alterations of normal bowel epithelium leading to unregulated cell growth, proliferation, and tumor development. A genetic model has been proposed for colorectal tumorigenesis that describes a process of transformation from adenoma to carcinoma. This model of tumor development reflects an accumulation of mutations within colonic epithelium that give a selective growth advantage to the cancer cells.16 Genetic changes include activating mutations of oncogenes, mutations of tumor suppressor genes, and defects in DNA mismatch repair genes.

Additional genes and protein receptors are believed important in colorectal tumorigenesis. COX-2, which is induced in colorectal cancer cells, influences apoptosis and other cellular functions in colon cells, and overexpression of the epidermal growth factor receptor (EGFR), a transmembrane glycoprotein involved in signaling pathways that affect cell growth, differentiation, proliferation, and angiogenesis, occurs in

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the majority of colon cancers. These mechanisms are potentially important because of the availability of pharmacologic agents targeted to inhibit these processes.

Mucosa Larriina propria

Crypt of Lieberkuhn Musculsris mucosa

Submucosa

Circular 1 Muscuiaris Longitudinal J propria

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