It has long been believed that colorectal cancer evolves from a precursor lesion, the adenomatous polyp. This concept was based on the elegant pathology studies from the St Mark's Hospital, London, published by Lockhart-Mummery and Dukes in 1928,¹ and culminating in the concept of the polyp-cancer sequence published in 1975 by Muto and colleagues.² The introduction of colonoscopy in the early 1970s, followed by the demonstration of the feasibility of colonoscopic polypectomy, provided the technology for the application of this concept to clinical practice.³ The entire colon could be examined, polyps identified and removed and, it was believed, colorectal cancer prevented. Evidence for this belief was provided by observations from the prospective National Polyp Study (NPS) in the USA that demonstrated a reduction in the incidence of colorectal cancer by 76-90% following colonoscopic polypectomy.⁴

The paper in this issue of Gut by Citarda et al addressed a common questionthat is, . . . [Full text of this article]