1. ¹Institute and Department of Pathology, Rikshospitalet, University of Oslo, Oslo, Norway
2. ²Centre for Cutaneous Research, Bart's and The London Queen Mary's School of Medicine and Dentistry, University of London, and Cancer Research UK Skin Tumour Laboratory, London, UK
3. ³Department of Medical Genetics, Ullevål University Hospital, Oslo, Norway
4. ⁴Department of Cancer Genetics, The Norwegian Radium Hospital, Oslo, Norway
5. ⁵Institute of Human Genetics, University of Aarhus, Aarhus, Denmark
6. ⁶Department of Clinical Genetics, Vejle Hospital, Vejle, Denmark

Correspondence: Dr Ole Petter F. Clausen, Institute and Department of Pathology, Rikshospitalet, Sognsvannsvn.20, Oslo 0027, Norway. E-mail: ole.petter.clausen@rikshospitalet.no

⁷These authors contributed equally to this work.

Received 9 March 2006; Accepted 4 April 2006; Published online 25 May 2006.

Abstract

Keratoacanthoma (KA) is a benign keratinocytic neoplasm that usually presents as a solitary nodule on sun-exposed areas, develops within 6–8 weeks and spontaneously regresses after 3–6 months. KAs share features such as infiltration and cytological atypia with squamous cell carcinomas (SCCs). Furthermore, there are reports of KAs that have metastasized, invoking the question of whether or not KA is a variant of SCC. To date no reported criteria are sensitive enough to discriminate reliably between KA and SCC, and consequently there is a clinical need for discriminating markers. We screened fresh frozen material from 132 KAs and 37 SCCs for gross chromosomal aberrations by using comparative genomic hybridization (CGH). Forty-nine KAs (37.1%) and 31 SCCs (83.7%) showed genomic aberrations, indicating a higher degree of chromosomal instability in SCCs. Gains of chromosomal material from 1p, 14q, 16q, 20q, and losses from 4p were seen significantly more frequently in SCCs compared with KAs (P-values 0.0033, 0.0198, 0.0301, 0.0017, and 0.0070), whereas loss from 9p was seen significantly more frequently in KAs (P-value 0.0434). The patterns of recurrent aberrations were also different in the two types of neoplasms, pointing to different genetic mechanisms involved in their developments.