Abstract
Historically, the founding paradigm has been that cancers of the gastrointestinal tract are preceded by a pre-invasive stage of intraepi-thelial neoplasia. From the morphological standpoint the term “dysplasia” has been conventionally applied to the collection of changes in cellular morphology and tissue architecture that define intraepithelial neo-plasia. Although morphologically different according to the specific GI tract anatomic location (Barrett-associated, gastritis- and non-gastritis-associated, adenomatous and serrated dysplasia; Odze et al., 2010 ) the sever -ity of intraepithelial neoplasia is estimated from the degree of deviation from the normal tissue of origin, and the neoplastic process has been thought to progress univocally toward carcinoma through dysplasia of increasing severity. There now exists evidence to con-strue the natural history of tumor progression in GI tract in accordance with a stochastic model, in which each stage is probabilistically linked with different evolutive pathways (pro-gression, stabilization, regression) rather than deterministically associated with the onset of carcinoma (Risio, 2010). Moreover, even if biological reasons support dysplasia as the most predictive marker of the cancerization risk, the links between non-morphological features of precursors and their malignant transformation is greater than the one link-ing dysplasia and malignancy, at least in the colonic carcinogenesis. New biomarkers are therefore needed, to define the magnitude of risk and the times of progression for each step of tumorigenesis, in order to ration-ally schedule surveillance and follow-up of patients with diagnosed GI tract neoplasia and to plan suitable population-based cancer prevention interventions.
Highlights
Equivocal Cancer Precursors: Old Mimickers or New Entities? “Origin of Colorectal Cancers in Hyperplastic Polyps and Serrated Adenomas: Another Truism Bites the Dust” was the title-page of the Editorial by Hamilton (2001)
Ten years later we are fully aware of those serrated polyps, mainly with sessile configuration that, though obscured by a low histopathologic diagnostic reproducibility (Vieth et al, 2011), subtly mimic the innocent, non-cancerous, hyperplastic polyps
Worries persist considering that a subset of these lesions appears to give rise to carcinoma when less than a few millimeters in size and, most importantly, that the vast majority of interval colon cancers are more likely than non-interval colon cancers to arise from serrated lesions (Sawhney et al, 2006)
Summary
Equivocal Cancer Precursors: Old Mimickers or New Entities? “Origin of Colorectal Cancers in Hyperplastic Polyps and Serrated Adenomas: Another Truism Bites the Dust” was the title-page of the Editorial by Hamilton (2001). Two critical issues, which need to be addressed, are the following: (i) To profile the morphological and/ or genetic phenotype of the serrated lesions engaged in the “serrated polyp neoplasia pathway”; (ii) To standardize the effective use of the new endoscopic techniques (e.g.,: magnifying chromoendoscopy) in order to improve the detection rates of those not identifiable GI cancer precursors, such as sessile serrated and non-polypoid adenomatous lesions.
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