Abstract
The frequencies of overexpression and mutation in the p53 tumor suppressor gene were examined in proliferative verrucous leukoplakia and oral squamous cell carcinoma with immunohistochemistry and single-strand conformation polymorphism analysis of DNA fragments amplified by polymerase chain reaction. Ten samples each of normal oral mucosa, proliferative verrucous leukoplakia, and squamous cell carcinoma were immunostained with antibodies against p53 protein; 8 of 10 cases of proliferative verrucous leukoplakia cases and 7 of 10 cases of oral squamous cell carcinoma were positive for p53 protein. Minimal staining was observed in normal oral tissues. The quantified labeling indexes demonstrated a range that corresponded to lesion progression. Single-strand conformation polymorphism analysis revealed p53 gene mutations within exons 5 to 8 in 40% (4 of 10) of the squamous cell carcinoma samples. Two of the 4 mutated squamous cell carcinoma samples lacked p53 expression. No p53 mutations were detected in proliferative verrucous leukoplakia tissues. Human papillomavirus 16 was identified in 2 of 7 p53 positive oral squamous cell carcinoma samples. Human papillomavirus 16 and 18 were identified in two of eight p53 positive proliferative verrucous leukoplakia samples. One p53 negative squamous cell carcinoma sample was positive for human papillomavirus 16 and had a mutation in exon 6 of the p53 gene. Human papillomavirus infection along with p53 expression plays a yet to be defined role in the pathogenesis of a limited number of cases of proliferative verrucous leukoplakia and squamous cell carcinoma. p53 Immunohistochemistry, p53 gene mutations, and human papillomavirus infection prevalence do not provide a means to differentiate between leukoplakia and carcinoma and do not provide a predictive test for progression of leukoplakia to carcinoma.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 471-477 |
| Number of pages | 7 |
| Journal | Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics |
| Volume | 83 |
| Issue number | 4 |
| DOIs | |
| State | Published - 1997 |
Bibliographical note
Funding Information:This work was supported in part by grants CA 16058-20 from The Ohio State University (GDS), IRGI 6-34 from American Cancer Society (CMW) and IR43CA62715-01 (TAL). Some tissues used for HPV analysis were provided by the Cooperative Human Tissue Network (CHTN) funded by NCI. aResearch Associate, Department of Pathology and Laboratory of Cancer Chemoprevention and Etiology, The Ohio State University. bAssistant Professor, School of Public Health and Laboratory of Cancer Chemoprevention and Etiology, The Ohio State University. CDirector, Research and Development, Bioserve Biotechnologies. aResearch Medical Officer, Office of Special Nutritionals, Clinical Research and Review of Staff, U.S. Food and Drag Administration. eResearch Assistant, Department of Pathology and Laboratory of Cancer Chemoprevention and Etiology, The Ohio State University. fResearch Scientist, School of Public Health and Laboratory of Cancer Chemoprevention and Etiology, The Ohio State University. gAssistant Professor, Department of Maxillofacial Surgery/Pathology, College of Dentistry, The Ohio State University. hprofessor and Chairperson, Department of Otolaryngology, The Ohio State University. iprofessor, School of Public Health, and Director, Laboratory of Cancer Chemoprevention and Etiology, The Ohio State University. Received for publication Oct. 28, 1996; returned for revision Feb. 26, 1996 and May 21, 1996; accepted for publication Oct. 14, 1996. Copyright © 1997 by Mosby Year Book, Inc. 1079-2104/97/$5.00 + 0 7/14/78679
