Abstract
Colorectal cancer is an ideal model in which to study malignant progression from the molecular-genetic perspective because different stages of the same malignancy coexist within each patient. Approximately 75% of colorectal cancer cases are sporadic and the remaining are familial disease, yet genetic mutations that have been identified account for only 5% to 6% of inherited cases. The two major pathways by which mutational changes leading to colorectal cancer occur are chromosomal instability and microsatellite instability. This article discusses genes and signaling pathways involved in development of inherited disease, as well as the association of some of these pathways with sporadic cases. Furthermore, therapies targeting active pathways in colorectal carcinogenesis, including the vascular endothelial growth factor and epidermal growth factor receptor tyrosine kinase, have shown promising results in clinical trials are now included in standard recommended treatment.
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