Detection of Human Papillomavirus DNA in Cytologic Specimens Derived from Esophageal Precancer Lesions and Cancer

Abstract

A series of 80 esophageal cytologic specimens derived from the same number of patients with previously diagnosed squamous cell dysplasia of the esophagus were examined for the presence of human papillomavirus (HPV) infection by filter in situ hybridization (FISH), using a mixed DNA probe containing HPV types 11, 16, and 18. All the patients came from an area at high risk for esophageal cancer in China. A total of 53 cases (66.3%) were demonstrated as HPV-DNA-positive. HPV DNA was detected in 22.2% (2 of 9) of the patients without cytologic atypia, in 50% (3 of 6) with mild dysplasia, in 80.6% (25 of 31) with moderate dysplasia, in 67.9% (19 of 28) with severe dysplasia, and in 66.7% (4 of 6) with an invasive squamous cell carcinoma. The present results confirm the recent findings on HPV involvement in esophageal squamous cell lesions. They support the hypothesis that HPV is a possible etiologic agent in esophageal carcinogenesis, most probably acting synergistically with physical, chemical, and/or nutritional factors that have previously been related with this malignancy in the high-risk areas of China.

Dépistage du cancer épidermoïde de l’œsophage par endoscopie chez les sujets à risque élevé de cancer

“…L'infection par HPV est peu fréquemment associée au CEO dans les pays à faible incidence tels que les États-Unis ou certains pays d'Europe où son rôle est probablement négligeable. L'incidence de l'infection par HPV est, en revanche, particulièrement élevée dans les populations à haut risque de Chine présentant des anomalies cytologiques telles que la dysplasie [39]. Ce virus est retrouvé avec une incidence, allant de 13 à 63 % (22 % en moyenne) dans les cas de CEO survenant dans les zones géographiques à haut risque (Japon, Chine, Hong Kong, Inde, Pakistan, Corée, Afrique du Sud, Alaska, Australie) [40].…”

Oral HPV Infection: Current Strategies for Prevention and Therapy

“…HPVs are traditionally distinguished, on the base of specific epithelial tropism, in cutaneous and mucosal types: the firsts infect hands and feet skin, the second prefer mucosal surface of upper aero-digestive tract, anogenital district, urethra and conjunctive [35][36][37][38]. On the basis of epidemiologic data regarding the behaviour of the viral lesions, HPV have been also divided in two groups: those at "high risk" oncogenic [High Risk (HR) -HPV genotypes like 16-18-31-33-35, 39,45,51,52,53, 56,58,59, 66, 67,70,73,68, 82), associated with potentially and overtly malignant lesions (anogenital cancers, giant condyloma of Bruschke and Lowenstein) and those at "low risk" oncogenic [Low Risk (LR)-HPV genotypes like 2, 4, 27 (the skin types) and mucosal types 6,11,13,32,42), more commonly associated with benign diseases (ordinary wart, condyloma, focal epithelial hyperplasia, squamous cells papilloma, Bowen's papillomatosis) [39][40][41][42][43].…”

Genomic analysis of the first laboratory-mouse papillomavirus

“…To date, 120 types of human PV (HPV) and 69 non-human mammalian, avian and reptilian PVs have been isolated and characterized (de Villiers et al, 2004;Bernard et al, 2010). PVs infect cutaneous and mucosal epithelial cells and cause a variety of benign and malignant lesions (Chang et al, 1990;Jenson et al, 2001;Howley & Lowy, 2007). PVs seem to have existed for millions of years during which time they appear to have co-evolved with their natural hosts Herbst et al, 2009).…”