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Background and Aim: Squamous papilloma of the esophagus is a rare benign tumor; less than 200 cases have been reported in the literature. The prevalence of endoscopically diagnosed squamous papilloma of the esophagus has been reported in only a very few series, and varies from 0.01 to 0.43%. Clinical relevance and possible association with other pathological conditions, namely if it is a premalignant lesion, remain a matter of debate. The etiology is controversial, although a role of human papilloma virus has been recently proposed. The aim of this study was to try to determine the prevalence, clinical relevance, possible association with other pathological conditions of the upper digestive tract, and possible etiological role of human papilloma virus on our series of squamous esophageal papillomas. Methods: Data from a total of 7618 upper gastrointestinal endoscopies consecutively performed in 4 years were obtained. A 4-year follow up was carried out. Results: Squamous esophageal papilloma was found in nine patients (0.01%). The mean size of polyps was 4 mm and the mean distance from the dental ridge was 25 cm. Only one patient had more than one polyp. Two patients had liver cirrhosis and three had peptic ulcer disease. All squamous esophageal papillomas were removed and tested for human papilloma virus with commercial available kits for in situ hybridization, but none was found positive. Conclusion: Squamous papilloma of the esophagus is an uncommon disease that does not appear to predispose to esophageal cancer. No association was found with human papilloma virus.

The p53 tumour suppressor gene has an important role in the the maintenance of genome stability and its mutational inactivation may be at the origin of aneuploidy in cancer cells. The aim of this study was to determine whether p53 mutations were associated to DNA aneuploidy, as assessed by flow cytometry, in colorectal adenocarcinomas. Analysis of p53 mutations spectrum of the sorted nuclei was done by Denaturing Gradient Gel Electrophoresis (DGGE) and DNA sequencing. Overall, we studied 20 adenocarcinomas, the corresponding control mucosa, and 7 lymph node metastases.Five tumours (25%) were DNA diploid, while 15 tumours (75%) were composed of DNA aneuploid and diploid subpopulations. DNA diploid control mucosa and adenocarcinomas showed no p53 mutations, while 60% of the tumours with DNA aneuploidy had p53 mutations. Therefore, p53 mutations occurred significantly more often in DNA aneuploid than in DNA diploid tumours (p< 0.04, Fisher’s exact test). Incidences of DNA aneuploidy and p53 mutations in lymph node metastases were 60 and 86%, respectively. In all tumours showing a p53 mutation, the wild-type allele was not or only bearly visible in DNA aneuploid cells suggesting that, in such cells, aneuploidy is accompanied by complete p53 functional inactivation.The present observations suggest that p53 mutations may have a role in the origin of aneuploidy at late stages of colorectal carcinogenesis.

This case-control study evaluated the real need for liver biopsy in subjects with persistently normal aminotransferase values over a long period by comparing the histological features of these subjects with those of patients with abnormal aminotransferase values. We considered as "Cases" all 32 consecutive anti-HCV/HCV-RNA positive subjects with at least eight normal serum ALT values during the last twelve months; for each "Case", we selected as a "Control" one anti-HCV/HCV-RNA positive patient with at least two abnormal serum ALT values during the last twelve months. The Cases and Controls were matched for age ( 5 years) and sex. In the Case group, 1 subject showed normal liver tissue, 18 minimal chronic hepatitis (CH) and 13 mild CH. In the Control group, 7 subjects showed minimal CH, 19 mild CH, 3 moderate CH, 1 severe CH and 2 cirrhosis. The subjects in the Control group showed a significantly higher HAI score (5.39+2.81) than those in the Case group (2.96+1.62, p0.001). The subjects in the Control group more frequently showed a fibrosis score greater than 1 (28.1%) compared to the Case group (9.4%; p0.05). Finally, steatosis was more frequent and more severe in the Control group than in the Case group (respectively, 78.1% vs 50%, p0.05; and 1.47+1.16 vs 0.6+0.71, p0.001). The HAI and fibrosis scores did not correlate with the ALT value, HCV genotype or HCV viral load in either the Case or Control group. Our findings showed that the subjects with a persistently normal serum ALT value had minimal or mild chronic hepatitis, thus demonstrating that a liver biopsy is not indicated for these subjects.