Molecular Pathology

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER
[Advanced]

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this link to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Add article to my folders
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Herrington, C S
Right arrow Articles by Wolman, S R
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Herrington, C S
Right arrow Articles by Wolman, S R
J Clin Pathol: Mol Pathol 2001; 54:160-164
© 2001 Journal of Clinical Pathology

Loss of sequences on the short arm of chromosome 17 is a late event in squamous carcinoma of the cervix

C S Herrington1, M Worsham2, S A Southern1, P Mackowiak2 and S R Wolman3

1 Department of Pathology, University of Liverpool, Royal Liverpool University Hospital, Liverpool L69 3GA, UK
2 Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD20814, USA
3 Department of Pathology, Henry Ford Hospital, 2799 W Grand Boulevard, Detroit, MI 48202, USA

Correspondence: Professor Herringtonc.s.herrington{at}liv.ac.uk

Aims—To determine by fluorescence in situ hybridisation (FISH) whether deletion of D17S34, a subtelomeric probe for 17p, occurs in invasive squamous carcinoma of the cervix, and to determine the extent of such loss by analysis of the p53 and HER2/NEU genes.

Methods—Fourteen invasive squamous cell carcinomas of the cervix were investigated by FISH for D17S34, p53, and HER2/NEU. Dual hybridisation of each probe with the chromosome 17 {alpha} satellite (D17Z1) probe was performed on paraffin wax embedded sections, and the fluorescence ratios of the paired signals were determined. Broad spectrum human papillomavirus (HPV) typing by ISH and GP5+/6+ polymerase chain reaction was also performed.

Results—Twelve tumours were HPV positive, nine with HPV-16, and one each with types 18, 31, and 39. Loss of D17S34 was identified in four tumours, one of which was HPV negative. In one tumour, D17S34 loss was accompanied by loss of p53 only, suggesting that deletion was limited to the p arm. A second tumour showed simultaneous losses of all probes, indicative of whole chromosome 17 loss during tumour growth. The two remaining specimens showed loss of D17S34 only, diffuse in one, and localised within the tumour in the other. Aberrations of p53 or HER2/NEU were not seen independently of D17S34 loss, and loss did not correlate with HPV presence or type.

Conclusions—These data show that D17S34 loss is prevalent, marking 28% of the invasive squamous carcinomas in this study. The observed intratumoral heterogeneity indicates that, at least in some cases, this loss occurs after invasion and is therefore a late event in the path of cervical carcinogenesis.

Key Words: cervix • fluorescence in situ hybridisation • chromosome 17 • papillomavirus







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER
Molecular Pathology Journal of Clinical Pathology
Terms and conditions relating to subscriptions purchased online  ¦  Website terms and conditions  ¦  Privacy policy
Copyright © 2001 by the BMJ Publishing Group Ltd & Association of Clinical Pathologists.