Genomic instability in obesity-associated colon cancer

Epidemiological studies have demonstrated the association between obesity and colon cancer. Many studies using animal models have also confirmed that obesity increases colon cancer incidence. Multiple cancer risk factors in obesity have been identified, which can activate multiple signalling pathways to promote cell proliferation and decrease apoptosis. The mechanisms for obesity-associated colon cancer, however, are not fully elucidated. In this review, the possible roles of genomic instability in obesity-associated colon cancer are summarized. It is known that genomic instability is critical for the carcinogenesis of colon cancer. Recent studies have provided convincing evidence that obesity can increase genomic instability. Therefore, it is highly possible that genomic instability has an important role in obesity-associated colon cancer. Particularly, the activation of phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) and mitogen activated protein kinases (MAPK) signalling pathways in obesity may mediate genomic instability in obesityassociated colon cancer.