Show simple item record

dc.contributor.authorOgmundsdottir, H M
dc.contributor.authorBjornsson, J
dc.contributor.authorHolbrook, W P
dc.date.accessioned2010-10-29T11:56:21Z
dc.date.available2010-10-29T11:56:21Z
dc.date.issued2009-08-01
dc.date.submitted2010-10-29
dc.identifier.citationJ. Oral Pathol. Med. 2009, 38(7):565-71en
dc.identifier.issn1600-0714
dc.identifier.pmid19473450
dc.identifier.doi10.1111/j.1600-0714.2009.00766.x
dc.identifier.urihttp://hdl.handle.net/2336/113991
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links fielden
dc.description.abstractBACKGROUND: Prediction of progression from pre-malignant oral mucosal lesions to malignancy, or recurrence of an existing oral squamous cell carcinoma (OSCC), is an important clinical problem in oral medicine. METHODS: This study presents a follow-up of a study published in 2002. Samples from 54 patients with OSCC, 45 with oral lichen planus (OLP) and 45 with hyperkeratosis (clinically leukoplakia), diagnosed between 1987 and 1996, were analysed for TP53 protein expression and TP53 mutation. Follow-up was 11-17 years for OSCC (mean 13.3), 12-22 years for OLP (mean 15.9) and 12-17 years for hyperkeratosis (mean 14.5). RESULTS: Of the 54 OSCC patients, 28 experienced recurrent disease, 21 died of OSCC, 22 died of other causes. Of the 14 OSCC patients with mutated TP53 (n = 11), the cancer recurred in eight (57%) and in 20/39 (51%) without mutation. Expression of TP53 protein was significantly associated with reduced overall survival. Among OLP patients, nine were TP53-mutated out of 31 tested. One TP53-mutated OLP patient developed OSCC in a different site. Of the hyperkeratosis patients, three were mutated of 22 tested. One hyperkeratosis patient (non-mutated) developed OSCC in the same site. CONCLUSION: TP53 mutations can exist in benign oral mucosal lesions for many years without progression to malignancy. No association was found between TP53 protein expression or TP53 mutation and recurrence of OSCC or disease-related survival. Overall survival was reduced in patients with positive TP53 protein expression.
dc.language.isoenen
dc.relation.urlhttp://dx.doi.org/10.1111/j.1600-0714.2009.00766.xen
dc.subject.meshAdulten
dc.subject.meshAgeden
dc.subject.meshAged, 80 and overen
dc.subject.meshCarcinoma, Squamous Cellen
dc.subject.meshDisease Progressionen
dc.subject.meshDisease-Free Survivalen
dc.subject.meshFemaleen
dc.subject.meshFollow-Up Studiesen
dc.subject.meshGene Expression Regulation, Neoplasticen
dc.subject.meshHumansen
dc.subject.meshLeukoplakia, Oralen
dc.subject.meshLichen Planus, Oralen
dc.subject.meshMaleen
dc.subject.meshMiddle Ageden
dc.subject.meshMouth Mucosaen
dc.subject.meshMouth Neoplasmsen
dc.subject.meshMutationen
dc.subject.meshPrecancerous Conditionsen
dc.subject.meshSurvival Analysisen
dc.subject.meshTumor Suppressor Protein p53en
dc.titleRole of TP53 in the progression of pre-malignant and malignant oral mucosal lesions. A follow-up study of 144 patientsen
dc.typeArticleen
dc.contributor.departmentFaculty of Medicine, University of Iceland, Vatnsmyrarvegur 16, 101 Reykjavik, 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.abstractBACKGROUND: Prediction of progression from pre-malignant oral mucosal lesions to malignancy, or recurrence of an existing oral squamous cell carcinoma (OSCC), is an important clinical problem in oral medicine. METHODS: This study presents a follow-up of a study published in 2002. Samples from 54 patients with OSCC, 45 with oral lichen planus (OLP) and 45 with hyperkeratosis (clinically leukoplakia), diagnosed between 1987 and 1996, were analysed for TP53 protein expression and TP53 mutation. Follow-up was 11-17 years for OSCC (mean 13.3), 12-22 years for OLP (mean 15.9) and 12-17 years for hyperkeratosis (mean 14.5). RESULTS: Of the 54 OSCC patients, 28 experienced recurrent disease, 21 died of OSCC, 22 died of other causes. Of the 14 OSCC patients with mutated TP53 (n = 11), the cancer recurred in eight (57%) and in 20/39 (51%) without mutation. Expression of TP53 protein was significantly associated with reduced overall survival. Among OLP patients, nine were TP53-mutated out of 31 tested. One TP53-mutated OLP patient developed OSCC in a different site. Of the hyperkeratosis patients, three were mutated of 22 tested. One hyperkeratosis patient (non-mutated) developed OSCC in the same site. CONCLUSION: TP53 mutations can exist in benign oral mucosal lesions for many years without progression to malignancy. No association was found between TP53 protein expression or TP53 mutation and recurrence of OSCC or disease-related survival. Overall survival was reduced in patients with positive TP53 protein expression.


This item appears in the following Collection(s)

Show simple item record