SCREENING FOR HUMAN PAPILLOMAVIRUS INFECTIONS IN ESOPHAGEAL SQUAMOUS-CELL CARCINOMAS BY IN-SITU HYBRIDIZATION

Citation
Fj. Chang et al., SCREENING FOR HUMAN PAPILLOMAVIRUS INFECTIONS IN ESOPHAGEAL SQUAMOUS-CELL CARCINOMAS BY IN-SITU HYBRIDIZATION, Cancer, 72(9), 1993, pp. 2525-2530
Citations number
40
Categorie Soggetti
Oncology
Journal title
CancerACNP
ISSN journal
0008543X
Volume
72
Issue
9
Year of publication
1993
Pages
2525 - 2530
Database
ISI
SICI code
0008-543X(1993)72:9<2525:SFHPII>2.0.ZU;2-2
Abstract
Background. Infections with specific types of human papillomavirus (HP V) have been closely linked with human squamous cell carcinomas, those of the anogenital tract in particular. Increasing number of reports a lso suggest that HPV infection could be a risk factor for esophageal c ancer. However, most of the previous studies on HPV involvement in eso phageal carcinomas have included only small numbers of biopsy specimen s, thus necessitating additional studies based on extensive series of esophageal samples. Methods. A series of 776 biopsy specimens derived from 363 patients who had undergone esophagectomy for squamous cell ca rcinoma in the high-incidence area of China were analyzed for the pres ence of HPV DNA by screening and specific typing in situ hybridization with biotinylated HPV DNA probes. Results. Under low-stringency condi tions, 85 (23.4%) tumors were demonstrated to contain HPV DNA. Positiv e signals were found on the nuclei of cancer cells in 71 (19.6%), in t he surrounding epithelial cells with hyperplastic or dysplastic change s in 13 (3.6%), in the cancer cells and the surrounding epithelial cel ls in 10 (2.8%), and in the resected margins in 1 (0.3%). Thirty-four (40%) of the 85 HPV-positive tumors were shown to contain at least one type of HPV 6, 11, 16, 18, or 30 DNA sequences. HPV 16 was the type f ound most frequently, occurring in 18.8% of the 85 HPV-positive specim ens. In addition to the primary tumors, HPV DNA sequences were found i n 12.3% (7 of 57) of the lymph node metastases. Conclusion. The result s confirm the previously reported HPV involvement in esophageal squamo us cell lesions and implicate HPV as a potential etiologic agent in th e multifactorial pathogenesis of esophageal carcinoma.