Genetic pathways, prevention, and treatment of sporadic colorectal cancer

Rasika Mundade1, Thomas F. Imperiale2, Lakshmi Prabhu1, Patrick J. Loehrer3, Tao Lu1,4

1 Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN USA

2 Division of Gastroenterology and Hepatology, Regenstrief Health Center, Roudebush VA Medical Center, Indianapolis, IN USA

3 Division of Hematology and Oncology, Indiana Cancer Pavilion, Indianapolis, IN USA

4 Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN USA


Tao Lu, email:

Keywords: colon cancer, genetic pathway, sporadic

Received: April 19, 2014 Accepted: June 28, 2014 Published: June 30, 2014


Epithelial cancer of the colon and rectum, also known as colorectal cancer (CRC), results from a progressive accumulation of genetic and epigenetic alterations that lead to uncontrolled growth of colonocytes, the cells lining the colon and rectum. CRC is the second leading cause of cancer-related deaths and the third most common cancer in men and in women in the U.S. Of all the patients diagnosed with CRC every year, it is estimated that the vast majority of CRCs are non-hereditary “sporadic cancers” with no apparent evidence of an inherited component. Sporadic CRC results from the cumulative effects of multiple genetic and epigenetic alterations caused by somatic mutations, which may themselves be the indirect result of several environmental factors. This review examines our current understanding of the major genetic alterations leading to colon cancer, options for prevention and early detection of CRC, and the currently available treatment approaches that may target these different genetic alterations.

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