Unique expression of human papilloma virus type 5 and type 16 in esophageal squamous cell carcinoma-a case report.

The role of human papilloma virus (HPV) in esophageal cancers from the low-incidence area (Western population) is unclear. We report a case of esophageal squamous papillomatosis associated with underlying esophageal squamous cell carcinoma (OSCC). The esophagectomy specimen confirmed presence of HPV-5 and HPV-16 suggesting a viral etiology. The significance of this dual infection is not known, but it suggests that esophageal papillomatosis is premalignant and should receive regular endoscopic follow-up. This is the first report of both HPV-5 and HPV-16 DNA detected in an esophageal cancer occurring in the Western population.

Effect of systemic corticosteroid therapy on risk for intra-abdominal or pelvic abscess in non-operated Crohn's disease.

BACKGROUND & AIMS: Systemic corticosteroid therapy increases risk of postoperative sepsis in Crohn's disease. This study investigates its effect on risk for sepsis in non-operated patients. METHODS: A retrospective case-control study was performed in 432 patients with Crohn's disease (the 94% of our database for whom adequate documentation could be retrieved). Two analyses were performed. The first tested the hypothesis that patients with perforating Crohn's disease (n = 86) were more likely to develop intra-abdominal or pelvic abscess (n = 29) if they had received systemic corticosteroids during the previous 3 months. The second analysis, confined to interventions since 1998, tested the hypothesis that corticosteroid therapy was more common during the 3 months before presentation with intra-abdominal or pelvic abscess (n = 12) than during the 3 months after presentation with a relapse of nonperforating disease (n = 24 consecutive patients). In both analyses adjustment was made for any other significant variable. RESULTS: Systemic corticosteroid therapy was associated with an adjusted odds ratio (OR) for intra-abdominal or pelvic abscess of 9.03 (95% confidence interval [CI], 2.40-33.98) in patients with perforating Crohn's disease. Patients receiving prednisolone > or = 20 mg per day had an OR of 2.81 (95% CI, 0.99-7.99) for abscess compared with those receiving a lower dose. In patients with relapsed active disease, corticosteroid therapy was associated with an unadjusted OR of 9.31 (95% CI, 1.03-83.91) for intra-abdominal or pelvic abscess. Neither smoking nor azathioprine usage was associated with increased risk for abscess. CONCLUSIONS: Systemic corticosteroid therapy for Crohn's disease is associated with increased risk for intra-abdominal or pelvic abscess.

Three different subsite classification systems for carcinomas in the proximity of the GEJ, but is it all one disease?

BACKGROUND AND AIM: Currently there are three different subsite classification systems for carcinomas in the region of the gastroesophaeal junction (GEJ), namely ICD-O, Munich and Liverpool. The aim of the present study was to compare clinicoepidemiological, pathological and molecular features of adenocarcinomas in the proximity of the GEJ, classified according to their position with respect to the GEJ initially, and then classified according to ICD-O, Munich and Liverpool classifications. METHODS: Forty-seven adenocarcinomas in the proximity of the GEJ were subdivided into groups 1 (exclusively within esophagus), 2 (mainly within esophagus but extending distally across GEJ), 3 (equally present in esophagus and stomach) or 4 (mainly in stomach but extending proximally across GEJ), and analysis of their clinicoepidemiological, pathological and molecular features was performed. Molecular characterization included loss of heterozygosity (LOH) and microsatellite instability analyses. RESULTS: Group 3 carcinomas were younger than other carcinomas in the proximity of the GEJ, but otherwise these carcinomas were similar in their clinicoepidemiological, pathological and molecular features. There were no significant differences between esophageal (groups 1 and 2) and gastric (groups 3 and 4) carcinomas as classified by ICD-O. Munich types I (groups 1 and 2), II (group 3) and III (group 4) carcinomas of the GEJ were also similar. LOH at the site of the Rb tumor suppressor gene and at 17p11.1-p12 was more common in GEJ (groups 2, 3 and 4) than lower third (group 1) esophageal carcinomas classified according to the Liverpool system. CONCLUSION: Overall, adenocarcinomas of the lower esophagus and adenocarcinomas involving the GEJ have similar clinicoepidemiological, pathological and molecular features no matter which subsite classification is used, adding further evidence that they represent the same disease.

Loss of heterozygosity on chromosome 17p predicts neoplastic progression in Barrett's esophagus.

BACKGROUND AND AIM: Endoscopic surveillance for adenocarcinoma in patients with Barrett's esophagus is costly, with one cancer detected every 48-441 patient years of follow up. Genetic abnormalities, including loss of heterozygosity at sites of tumor suppressor genes, have been detected in malignant and premalignant Barrett's esophagus. The aim of this prospective study was to determine if loss of heterozygosity analysis could identify patients with Barrett's esophagus at greatest risk of adenocarcinoma, for whom endoscopic surveillance is most appropriate. METHODS: Loss of heterozygosity analysis was performed on endoscopic biopsies from 48 patients as part of a Barrett's surveillance program using 14 microsatellite markers shown previously to detect loss of heterozygosity in more than 30% of esophageal adenocarcinomas. Patients were followed up endoscopically for a median of 5 years. RESULTS: Loss of heterozygosity was detected in nine patients. Three patients with loss of heterozygosity on chromosome 5q or 9p did not progress beyond metaplasia. Loss of heterozygosity at 17p11.1-p13 was detected in six patients, all of whom demonstrated dysplasia and/or carcinoma during follow up (four low-grade dysplasia, one high-grade dysplasia and one adenocarcinoma). CONCLUSION: Loss of heterozygosity at 17p11.1-p13 on chromosome 17p identifies patients with Barrett's esophagus at risk of neoplastic progression and can supplement histology in determining the frequency of endoscopy during surveillance.