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dc.contributor.authorOgmundsdottir, H M
dc.contributor.authorHilmarsdottir, H
dc.contributor.authorBjornsson, J
dc.contributor.authorHolbrook, W P
dc.date.accessioned2010-10-29T11:51:47Z
dc.date.available2010-10-29T11:51:47Z
dc.date.issued2009-10-01
dc.date.submitted2010-10-29
dc.identifier.citationJ. Oral Pathol. Med. 2009, 38(9):716-21en
dc.identifier.issn1600-0714
dc.identifier.pmid19473449
dc.identifier.doi10.1111/j.1600-0714.2009.00767.x
dc.identifier.urihttp://hdl.handle.net/2336/114011
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links fielden
dc.description.abstractOBJECTIVES: 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.
dc.language.isoenen
dc.relation.urlhttp://dx.doi.org/10.1111/j.1600-0714.2009.00767.xen
dc.subject.meshAdulten
dc.subject.meshAgeden
dc.subject.meshAged, 80 and overen
dc.subject.meshCarcinoma, Squamous Cellen
dc.subject.meshCell Transformation, Neoplasticen
dc.subject.meshDNA Mutational Analysisen
dc.subject.meshExonsen
dc.subject.meshFemaleen
dc.subject.meshGene Expression Regulation, Neoplasticen
dc.subject.meshGenes, p53en
dc.subject.meshHumansen
dc.subject.meshLeukoplakia, Oralen
dc.subject.meshLichen Planus, Oralen
dc.subject.meshLongitudinal Studiesen
dc.subject.meshMaleen
dc.subject.meshMiddle Ageden
dc.subject.meshMouth Neoplasmsen
dc.subject.meshMutationen
dc.subject.meshPolymerase Chain Reactionen
dc.subject.meshPrecancerous Conditionsen
dc.subject.meshRetrospective Studiesen
dc.subject.meshTumor Suppressor Protein p53en
dc.titleLongitudinal study of TP53 mutations in eight patients with potentially malignant oral mucosal disordersen
dc.typeArticleen
dc.contributor.departmentMolecular and Cell Biology Laboratory, Icelandic Cancer Society, Iceland. helgaogm@hi.isen
dc.identifier.journalJournal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathologyen
html.description.abstractOBJECTIVES: 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.


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