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dc.contributor.authorKanellou, Peggy
dc.contributor.authorZaravinos, Apostolos
dc.contributor.authorZioga, M.
dc.contributor.authorSpandidos, Demetrios A.
dc.date.accessioned2018-11-08T08:09:18Z
dc.date.available2018-11-08T08:09:18Z
dc.date.issued2009-06-01
dc.identifierSCOPUS_ID:66149100107
dc.identifier.issn00070963
dc.identifier.otherPubMed ID: 19298278
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=66149100107&origin=inward
dc.identifier.urihttps://repo.euc.ac.cy/handle/123456789/757
dc.description.abstractBackground Basal cell carcinoma (BCC) is a locally aggressive slowly growing tumour that rarely metastasizes and is mostly seen in older members of the population. Objectives To determine the involvement of the tumour suppressor genes p14ARF, p15INK4b, p16INK4a and p53 in BCC. Methods We investigated the integrity of the CDKN2A locus in 15 BCC samples by analysing the presence of allelic imbalance/loss of heterozygosity (LOH). Moreover, we studied the mRNA expression levels of the tumour suppressor genes p14ARF, p15INK4b, p16INK4a and p53 in the BCC samples and compared them with mRNA levels in the corresponding normal tissue. The presence of mutations was examined by sequencing for exons 1a and 2 of p16INK4a. Results We found LOH in one BCC sample for the marker D9S1748. A polymorphism (G442A) of exon 2 was detected in three cases. p14 ARF, p15INK4b and p53 presented high expression levels, whereas p16INK4a exhibited low mRNA levels compared with the corresponding normal tissue. Significant correlations were detected among the genes studied. Conclusions Our results demonstrate a different expression profile between p16INK4a and p14ARF, p15INK4b and p53 in BCC. Moreover, we found a low percentage of LOH and of a polymorphic sequence variant (Ala148Thr) for the CDKN2A locus.
dc.relation.ispartofBritish Journal of Dermatology
dc.titleDeregulation of the tumour suppressor genes p14ARF, p15 INK4b, p16INK4a and p53 in basal cell carcinoma
elsevier.identifier.doi10.1111/j.1365-2133.2009.09079.x
elsevier.identifier.eid2-s2.0-66149100107
elsevier.identifier.scopusidSCOPUS_ID:66149100107
elsevier.volume160
elsevier.issue.identifier6
elsevier.coverdate2009-06-01
elsevier.coverdisplaydateJune 2009
elsevier.openaccess0
elsevier.openaccessflagfalse
elsevier.aggregationtypeJournal


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