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J Oral Pathol Med. 2009 Oct;38(9):716-21. doi: 10.1111/j.1600-0714.2009.00767.x. Epub 2009 Mar 14.

Longitudinal study of TP53 mutations in eight patients with potentially malignant oral mucosal disorders.

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  • 1Molecular and Cell Biology Laboratory, Icelandic Cancer Society, Iceland. helgaogm@hi.is

Abstract

OBJECTIVES:

In a previous cross-sectional study, the authors found a higher rate of TP53 mutation in oral lichen planus (OLP) than in hyperkeratosis. By analysing for TP53 mutations in serial samples from patients on long-term follow-up of their oral lesions, it was hoped to determine if these mutations were related to disease progression.

METHODS:

Eight patients presenting with lesions diagnosed clinically as oral leukoplakia or lichen planus were followed from 2 to 12 years. Two to five samples of archival biopsy tissue were analysed from each patient by constant denaturant gradient gel electrophoresis for hotspots A, B, C, D and exon 6.

RESULTS:

Four patients were diagnosed clinically as OLP: two of these were confirmed histopathologically, one was diagnosed as non-specific hyperkeratosis and one as cancer. Four patients had leukoplakia only, with a histopathological diagnosis of hyperkeratosis. Seven patients had TP53 mutations, three of them on repeated occasions. All five patients who developed squamous-cell carcinoma had mutations. Two of them had mutated pre-malignant lesions, and one of these previously had a non-mutated cancer. Three patients had two different primary cancers, only one of them mutated. One patient developed a mutated cancer 5 years after the last mutation-free biopsy. Of the cancer-free patients, a lesion regarded clinically as cancer-suspicious in one case was mutated, in another patient two OLP lesions were mutated, the third had five biopsies taken during 8 years, all non-mutated.

CONCLUSIONS:

TP53 mutations may occur early or late in the development of oral squamous-cell carcinoma.

[PubMed - indexed for MEDLINE]
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