Colorectal carcinoma

Colorectal cancer (CRC) is one of the most common cancers between men and women that have high mortality rates.      CRC occupies the third position in common tumors. Many genetic and epigenetic changes in oncogenes and tumor suppressor genes result in CRC.  Numbers of modifiable and non-modifiable factors are contributing in the development of CRC. Mutations in DNA mismatch-repair genes or in the genes controlling oncogenes are the most common genetic problems associated with CRC. Lifestyle habits such as smoking, alcohol consumption, unbalanced diet, and obesity also can increase the CRC risk. Most cases discovered at late stage, where surgical excision, chemotherapy, and radiotherapy are useless. 

Signaling Pathways:

Several signaling including MAPK, Notch, PI3K, TGF-β and Wnt signaling pathways are implicated in the regulation of several biological processes involved in the pathogenesis of colorectal carcinoma, including cell proliferation, differentiation, angiogenesis, apoptosis and survival of colorectal cancer.

Induction of colorectal carcinoma:

Azoxymethane (AOM) intraperitoneal injection (20 mg/kg body weight) is used to induce CRC. In rodents, AOM induces colonic mucosal damage and neoplasia, particularly the occurrence of aberrant crypt foci (ACF). ACF are precursors of colon cancer and are being used as a surrogate end point for tumors in animals and humans. ACF are two to three times larger than normal crypts, are microscopically elevated, have a slit-like opening and a thick epithelial lining that stains darker than normal crypts with a large pericryptal zone.