Comparison of HPV infection, p53 mutation and allelic losses in post-transplant and non-posttransplant oral squamous cell carcinomas
Article first published online: 19 MAR 2002
Journal of Oral Pathology & Medicine
Volume 31, Issue 3, pages 134–141, March 2002
How to Cite
Zhang, L., Epstein, J. B., Poh, C. F., Berean, K., Lam, W. L., Zhang, X. and Rosin, M. P. (2002), Comparison of HPV infection, p53 mutation and allelic losses in post-transplant and non-posttransplant oral squamous cell carcinomas. Journal of Oral Pathology & Medicine, 31: 134–141. doi: 10.1034/j.1600-0714.2002.310302.x
- Issue published online: 19 MAR 2002
- Article first published online: 19 MAR 2002
- Accepted for publication June 7, 2001
- human papilloma virus (HPV);
- loss of heterozygosity (LOH);
- oral squamous cell carcinoma;
- p53 mutation;
Background: Oral squamous cell carcinoma (SCC) is increasingly found in transplant recipients, although little is known of the natural history of the disease or the mechanism underlying this increase.
Methods: In this article we describe the history of development of 5 oral post-transplant SCCs (PSCCs) and compare their genetic profiles to 34 non-posttransplant SCCs (NPSCCs).
Results: Of the five patients with PSCCs, 3 had bone marrow transplants and two, kidney. All three PSCCs from bone marrow recipients were preceded locally by graft-vs.-host disease (GVHD). Two of the GVHD were biopsied and demonstrated dysplasia. Similar frequencies of loss of heterozygosity (LOH) occurred in PSCCs and NPSCCs at 3p, 9p, 17p and 8p, with lower frequencies in PSCCs at 4q (39% vs. 0%), 11q (53% vs. 20%) and 13q (45% vs. 20%), although the latter were not significantly different. Only 1 PSCC had a p53 mutation, compared to historical values of 40–60% for NPSCC. Interestingly, human papillomavirus (HPV) DNA was detected in 3 (60%) PSCCs, in comparison to only 4 (12%) of the 34 NPSCCs (P = 0.0346).
Conclusions: Dysplasia in oral GVHD may be a strong indicator of cancer risk and should not be regarded as reactive changes to lichenoid mucosites. The low level of p53 mutation and increased HPV infection support the involvement of HPV in the development of PSCC, while the similarity in LOH patterns suggests that other aspects of carcinogenesis may be comparable in these two types of SCCs.