What influences preneoplastic colorectal lesion recurrence?

Abstract

The hypothesis of the local recurrence of preneoplastic lesions was first put forward in the 1950s. Disease recurrence may result from an inherent imbalance in cell proliferation that promotes carcinogenesis in apparently normal mucosa. Our review sheds light on how early preneoplastic lesions could be used to diagnose relapsed preneoplastic and, developing neoplastic lesions. We focus in detail on the clinical-pathological and molecular features of adenoma subtypes and their role in relapsed adenoma and their development into colorectal carcinoma. Moreover, we include the data available on microbiota and its metabolites and their role in recurrence. We strongly believe that a significant improvement could be achieved in colorectal screening by introducing personalized endoscopic surveillance for polyp-bearing patients on the basis of the presence of molecular markers that are predictive of recurrence.

Keywords: microbiota; preneoplastic lesions; recurrence; suppressor and serrated pathway.

Figure 1. Distribution of lesions according to molecular alterations involved in the etiology and/or recurrence of preneoplastic lesions

Schematic diagram of CRC progression and recurrence. Two pathways have been recognized, the suppressor and the serrated pathway. Both sequences involve the progression of normal colonocytes into early and advanced adenomas, with subsequent transformation into early and advanced cancer. Relapsed suppressor and serrated preneoplastic lesions retain the same histological subtype. The boxes show the typical molecular biomarkers for each lesion. The dotted arrows represent the potential connections between adenomas and polyps during their development.