Volume 160, Issue 6 pp. 1215-1221

Deregulation of the tumour suppressor genes p14ARF, p15INK4b, p16INK4a and p53 in basal cell carcinoma

P. Kanellou

P. Kanellou

Laboratory of Virology, Medical School, University of Crete, Heraklion 71100, Crete, Greece

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A. Zaravinos

A. Zaravinos

Laboratory of Virology, Medical School, University of Crete, Heraklion 71100, Crete, Greece

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M. Zioga

M. Zioga

A. Sygros Hospital, Department of Dermatology, Medical School, University of Athens, Athens, Greece

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D.A. Spandidos

D.A. Spandidos

Laboratory of Virology, Medical School, University of Crete, Heraklion 71100, Crete, Greece

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First published: 12 May 2009
Citations: 20
D.A. Spandidos.
E-mail:
[email protected]

Conflicts of interest
None declared.

P.K. and A.Z. contributed equally to this work and should be considered as first authors.

Summary

Background 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. p14ARF, 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.

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