Interobserver Agreement Among Pathologists in the Differentiation of Sessile Serrated From Hyperplastic Polyps

Abstract

Colorectal cancer (CRC) is the third most common cancer in the United States, with approximately 135,430 new cases and 50,260 deaths every year. 1 Jemal A. et al. J Natl Cancer Inst. 2017; 109: djx030 Crossref Scopus (777) Google Scholar ,2 Siegel R.L. et al. CA Cancer J Clin. 2017; 67: 177-193 Crossref PubMed Scopus (2659) Google Scholar It has been widely recognized now that approximately 20%–30% of CRCs arise from serrated polyps through a serrated/methylated pathway that includes BRAF mutation and DNA methylation that is distinct from the traditional adenoma-carcinoma sequence. 3 Noffsinger A.E. Serrated polyps and colorectal cancer: new pathway to malignancy. Annu Rev Pathol. 2009; 4: 343-364 Crossref PubMed Scopus (178) Google Scholar , 4 Ogino S. et al. CpG island methylator phenotype, microsatellite instability, BRAF mutation and clinical outcome in colon cancer. Gut. 2009; 58: 90-96 Crossref PubMed Scopus (613) Google Scholar , 5 Kambara T. et al. BRAF mutation is associated with DNA methylation in serrated polyps and cancers of the colorectum. Gut. 2004; 53: 1137-1144 Crossref PubMed Scopus (594) Google Scholar Sessile serrated polyps are flat/sessile and have similar color to the surrounding mucosa, making it difficult to differentiate between the normal colonic mucosa and the polyp itself. Serrated lesions are classified pathologically per the World Health Organization (WHO) criteria 6 Bosman F.T. et al. WHO classification of tumours of the digestive system. World Health Organization, 2010 Google Scholar into (1) hyperplastic polyp (HP), (2) sessile serrated adenoma (SSA)/sessile serrated polyp (SSP) with or without cytologic dysplasia, and (3) traditional serrated adenoma (TSA). Differentiating sessile serrated adenomas from hyperplastic polyps is difficult but clinically important because it guides surveillance intervals.