Clinical Research Papers:
Clinicopathologic distribution of KRAS and BRAF mutations in a Chinese population with colorectal cancer precursor lesions
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Chenghao Yi1,*, Yanqing Huang1,*, Xing Yu1, Xiaofen Li1, Shu Zheng1, Kefeng Ding1,2 and Jinghong Xu3
1 Cancer Institute, Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
2 Department of Surgical Oncology, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
3 Department of Pathology, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
* Co-first authors have contributed equally to this study
Jinghong Xu, email:
Kefeng Ding, email:
Keywords: KRAS, BRAF, serrated lesion, conventional adenoma, colorectal cancer precursor lesions
Received: July 29, 2015 Accepted: January 13, 2016 Published: February 19, 2016
Investigating the clinical features and corresponding histomorphologic and molecular profiles of precursor lesions of colorectal cancer in a natural population provides new insights into the nature of colorectal cancer, uncovers new screening markers and establishes new prevention strategies for colorectal cancer. In this study, 4302 patients with at least one colorectal polyp from a large colorectal cancer screening program were evaluated and genetic mutations in either KRAS or BRAF were detected in 495 patients. The population-based mutation rates of KRAS and BRAF genes in colorectal polyps within this Chinese patient population were 21.8% and 12.1% respectively. Interestingly, considerable variability in the KRAS and BRAF mutations rates were found among different types of polyps. In a multivariate analysis, presence of villous histology and high-grade dysplasia was associated with KRAS mutations (OR, 3.0; 95% CI, 1.7-5.4 and OR, 3.5; 95% CI 1.9-6.5, respectively), while serrated adenomas and hyperplastic polyps were associated with BRAF V600E mutations (OR, 20.6; 95% CI, 8.2–51.8 and OR, 11.9; 95% CI 4.9–29.0, respectively). KRAS mutations may, in part, drive the histologic progression of adenomas toward a villous histology and higher grades of dysplasia. Mutant BRAF may, in part, drive the histologic progression of adenomas toward serrated histology. Dysplasia may arise from hyperplastic polyps, resulting in the formation of serrated adenomas and potentially the development of colorectal carcinoma.
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