KRAS and TP53 mutations in inflammatory bowel disease-associated colorectal cancer: a meta-analysis

// Lijun Du 1 , John J. Kim 1,2 , Jinhua Shen 1,3 , Binrui Chen 1 and Ning Dai 1 1 Department of Gastroenterology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China 2 Division of Gastroenterology, Loma Linda University Medical Center, Loma Linda, USA 3 Department of Gastroenterology, Affiliated Hospital of Shaoxing University, Shaoxing, China Correspondence to: Ning Dai, email: // Keywords : KRAS, TP53, mutation, inflammatory bowel disease, colorectal cancer Received : September 18, 2016 Accepted : December 27, 2016 Published : January 07, 2017 Abstract Although KRAS and TP53 mutations are common in both inflammatory bowel disease-associated colorectal cancer (IBD-CRC) and sporadic colorectal cancer (S-CRC), molecular events leading to carcinogenesis may be different. Previous studies comparing the frequency of KRAS and TP53 mutations in IBD-CRC and S-CRC were inconsistent. We performed a meta-analysis to compare the presence of KRAS and TP53 mutations among patients with IBD-CRC, S-CRC, and IBD without dysplasia. A total of 19 publications (482 patients with IBD-CRC, 4,222 with S-CRC, 281 with IBD without dysplasia) met the study inclusion criteria. KRAS mutation was less frequent (RR=0.71, 95%CI 0.56-0.90; P =0.004) while TP53 mutation was more common (RR=1.24, 95%CI 1.10-1.39; P <0.001) in patients with IBD-CRC compared to S-CRC. Both KRAS (RR=3.09, 95%CI 1.47-6.51; P =0.003) and TP53 (RR=2.15, 95%CI 1.07-4.31 P =0.03) mutations were more prevalent in patients with IBD-CRC compared to IBD without dysplasia. In conclusion, IBD-CRC and S-CRC appear to have biologically different molecular pathways. TP53 appears to be more important than KRAS in IBD-CRC compared to S-CRC. Our findings suggest possible roles of TP53 and KRAS as biomarkers for cancer and dysplasia screening among patients with IBD and may also provide targeted therapy in patients with IBD-CRC.