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Malav P. Parikh [1] and Sujit Muthukuru [1] and Yash Jobanputra [1] and Kushal Naha [2] and Niyati M. Gupta [1] and Vaibhav Wadhwa [1] and Rocio Lopez [3] and Prashanthi N. Thota [1] and Madhusudhan R. Sanaka [1]

Academic Editor: Robert Odze

1, Department of Gastroenterology and Hepatology, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA, clevelandclinic.org

2, Department of Internal Medicine, Presence Saint Francis Hospital, 355 Ridge Ave, Evanston, IL 60202, USA, presencehealth.org

3, Department of Biostatistics and Quantitative Health Sciences, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA, clevelandclinic.org

Received Aug 21, 2017; Revised Nov 4, 2017; Accepted Nov 23, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

In recent times, the serrated adenoma-neoplasia pathway has emerged as an alternative mechanism to the conventional adenoma-carcinoma pathway for the development of colorectal cancer (CRC) [1–6]. This alternate pathway can account for almost 15–20% of the incident CRCs and majority of the interval cancers after a screening colonoscopy [7, 8]. These tumors have a high frequency of BRAF mutations, microsatellite instability, and hypermethylation of genes [9–11]. Serrated lesions are often difficult to detect during a screening colonoscopy as they are flat or sessile, have an indiscriminate edge, may be covered by a mucous cap, and are located mostly in the proximal colon [12, 13].

Originally, all the serrated lesions were believed to be hyperplastic polyps (HP) with no malignant potential; however, now, it has been identified that few subtypes of serrated lesions do harbor malignant potential [3–6, 14]. According to the world health organization (WHO), serrated lesions are classified into (1) hyperplastic polyps; (2) sessile serrated adenomas (SSA) with or without dysplasia; and (3) traditional serrated adenomas (TSA) [15]. HPs are essentially benign. TSAs have malignant potential; however, they are uncommon. Hence, SSAs, which are located mostly in the proximal colon, appear to be the principal precursor lesions leading to CRC via the alternate pathway. It has been shown that serrated polyp detection rate is dependent on the endoscopist, experience of the pathologist, and colonoscopy withdrawal times [13, 16, 17]. However, there is only limited...

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