Oral lichen planus has a high rate of TP53 mutations. A study of oral mucosa in icelanD.

Authors: Ogmundsdottir, HM  Hilmarsdottir, H  Astvaldsdottir, A  Johannsson, JH  Holbrook, WP 
Citation: Ogmundsdottir HM, etal., Eur J Oral Sci. 2002 Jun;110(3):192-8.
Pubmed: (View Article at PubMed) PMID:12120703

Oral squamous cell carcinoma (OSCC) is a world-wide health problem. In addition to external exposure (smoking and alcohol), certain oral lesions may increase the risk of oral cancer (e.g. leukoplakia, erythroplakia, and oral lichen planus). TP53 has been implicated in OSCC, but there are limited studies of mutations in premalignant oral lesions. In this study, 55 samples from OSCC, 47 from hyperkeratotic (HK) oral mucosa, clinically diagnosed as white patches, 48 samples from oral lichen planus (OLP), and 12 biopsies from normal oral mucosa were studied immunohistochemically for expression of TP53 protein. From all the carcinoma samples and selected non-malignant samples showing moderate or strong TP53 protein expression, malignant cells or TP53-positive nuclei were microdissected and screened for mutations in exons 5-8 by constant denaturation gel electrophoresis. Moderate to strong TP53 protein staining was seen in 56% of OSCC, 32% of OLP but only in 13% of HK. All OLP samples showed a characteristic pattern of positive nuclei confined to the basal layer, whereas TP53 staining was seen in suprabasal nuclei in HK. Mutation rate was 11 out of 52 for OSCC, three out of 20 tested for HK and, remarkably, nine out 27 tested for OLP. There was no correlation between TP53 protein staining and TP53 mutations. No associations were found with anatomical sites or disease progression. The unexpectedly high mutation rate of OLP might explain the premalignant potential of this lesion.


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RGD ID: 8547838
Created: 2014-02-26
Species: All species
Last Modified: 2014-02-26
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.