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Polyps are well-known cancer precursors identified by colonoscopy. However, variability in their size, location, and surface largely affect identification, localisation, and characterisation. Moreover, colonoscopic surveillance and removal of polyps (referred to as polypectomy ) are highly operator-dependent procedures. There exist a high missed detection rate and incomplete removal of colonic polyps due to their variable nature, the difficulties to delineate the abnormality, the high recurrence rates, and the anatomical topography of the colon. There have been several developments in realising automated methods for both detection and segmentation of these polyps using machine learning. However, the major drawback in most of these methods is their ability to generalise to out-of-sample unseen datasets that come from different centres, modalities and acquisition systems. To test this hypothesis rigorously we curated a multi-centre and multi-population dataset acquired from multiple colonoscopy systems and challenged teams comprising machine learning experts to develop robust automated detection and segmentation methods as part of our crowd-sourcing Endoscopic computer vision challenge (EndoCV) 2021. In this paper, we analyse the detection results of the four top (among seven) teams and the segmentation results of the five top teams (among 16). Our analyses demonstrate that the top-ranking teams concentrated on accuracy (i.e., accuracy > 80% on overall Dice score on different validation sets) over real-time performance required for clinical applicability. We further dissect the methods and provide an experiment-based hypothesis that reveals the need for improved generalisability to tackle diversity present in multi-centre datasets., 26 pages

Esophageal cancer (EC) is a highly aggressive tumor, and the current monitoring procedures are partially inadequate to evaluate treatment efficacy. The aim of this study was to investigate whether allelic imbalance analysis in liquid biopsy could be used as an additional tool to monitor tumor burden in EC patients. For this purpose, circulating cell-free DNA (cfDNA) from 52 patients with a locally advanced EC, which underwent neoadjuvant treatment and resection, was analyzed. Data from four representative longitudinally followed patients are also reported. Furthermore, 17 DNAs from formalin-fixed paraffin-embedded (FFPE) tumor samples were analyzed and compared to time-matched cfDNAs. To look for allelic imbalance, which is the main genetic alteration in both EC histotypes, we used a panel of five microsatellites (MSs) and three single-nucleotide polymorphisms (SNPs) near genes described as frequently altered. The Fisher exact and Mann-Whitney U tests were used to analyze categorical and continuous data, respectively. The correlation coefficient between cfDNA and FFPE-DNA was calculated with the Pearson's correlation test. We found that the selected tumor-related alterations are present in cfDNA of both adenocarcinoma (EADC) and squamous cell carcinoma (ESCC) with similar frequencies. The only exception were the MSs, one downstream and one upstream, of SMAD4 of which the loss was only observed in EADC (26 vs. 0%, P = 0.018). More interestingly, longitudinal studies disclosed that in patients with disease progression, tumor-related alterations were present in cfDNA before overt clinical or instrumental signs of relapse. In conclusion, our data indicate that the evaluation of tumor-related gene allelic imbalance in cfDNA might be a useful tool to complement the current monitoring procedures for EC patients and to guide their management.

Alcohol consumption has a substantial importance in the causation of cancer of the oral cavity, pharynx, liver, colon, rectum; and in women, breast. It is also recognized as an independent risk factor for esophageal squamous cell carcinoma (ESCC). Nevertheless, the association with esophagus adenocarcinoma (EAC) is still not completely defined; as well as the association between alcohol intake and Barrett's Esophagus (BE). The aim of this mini-review is to summarize recent findings from population studies focused on the association between alcohol consumption and risk of BE. The research was carried out in PubMed, filtering for studies conducted in the period 2009-2015. Our mini-review has shown no association between the consumption of alcohol and BE. Some type of alcoholic beverages has shown an inverse association. Direct public health applications of these findings are limited, considering the causal link between moderate-to-heavy alcohol consumption with increased risks of several cancers. Given the rising incidence of BE and EAC, it is important to understand the interplay of dietary and lifestyle factors that influence the development of these conditions.

OBJECTIVES: The histological definition of Barrett's esophagus (BE) is debated, particularly regarding the phenotype of its metaplastic columnar epithelium. Histologically proven intestinal metaplasia (IM) was the sine qua non condition for a diagnosis of BE but, more recently, non-intestinalized (i.e., cardiac gastric-type; GM) columnar metaplasia has been re-included in the spectrum of Barrett's histology. MicroRNAs modulate cell commitment, and are also reportedly dysregulated in Barrett's carcinogenesis. This study investigates miRNA expression in the histological spectrum of esophageal columnar metaplastic changes, specifically addressing the biological profile of GM vs. IM. METHODS: A study was performed to discover microRNA microarray in 30 matching mucosa samples obtained from 10 consecutive BE patients; for each patient, biopsy tissue samples were obtained from squamous, GM and intestinalized epithelium. Microarray findings were further validated by qRT-PCR analysis in another bioptic series of 75 mucosa samples. RESULTS: MicroRNA profiling consistently disclosed metaplasia-specific microRNA signatures. Six microRNAs were significantly dysregulated across the histological phenotypes considered; five of them (two overexpressed (hsa-miR-192; -miR-215) and three under-expressed (hsa-miR-18a* -miR-203, and -miR-205)) were progressively dysregulated in the phenotypic sequence from squamous to gastric-type, to intestinal-type mucosa samples. CONCLUSIONS: A consistent microRNA expression signature underlies both gastric- and intestinal-type esophageal metaplasia. The pattern of microRNA dysregulation suggests that GM may further progress to IM. The clinico-pathological implications of these molecular profiles prompt further study on the “personalized” cancer risk associated with each of these metaplastic transformations.