Pattern of mRNA expression of β-defensins in basal cell carcinoma

Twenty-two non-ulcerated BCCs (12 nodular type, 10 superficial type) have been analysed for the presence of hBD (1–3) mRNA by quantitative real-time RT-PCR. As controls, non-lesional skin specimens of BCC patients as well as samples of healthy subjects were assessed by RT-PCR.hBD-1 levels in healthy controls and non-lesional skin of BCC patients were significantly (P < 0.05) higher than the levels observed in tumour tissue. Moreover, BCCs showed significantly (P < 0.05) increased mRNA expression of hBD-2 as compared to controls. There was no significant (P > 0.05) difference between lesional mRNA levels for hBD-3 and those levels observed in controls. The mRNA expression of hBDs (1–3) found in nodular and superficial BCCs did not significantly (P > 0.05) differ.The gene expression patterns of hBD-1 and hBD-2 are for the first time shown to be significantly altered in non-ulcerated BCCs as compared to intra-individual and inter-individual controls, respectively. The present findings may indicate that beside the antimicrobial activity of AMPs, hBDs may also play a role in the pathogenesis of BCC. However, functional and immunohistological studies investigating hBDs in patients with BCC are needed to confirm our data.Basal cell carcinoma (BCC) is the most common cancer in humans. It is classified, together with squamous cell carcinoma, as non-melanoma skin cancer. The incidence of BCC is increasing worldwide by up to 10% a year. Although mortality is low as BCC rarely metastasises, this malignancy causes considerable morbidity and places a huge burden on healthcare services worldwide. Three main types of BCCs are generally distinguished with regard to the histopathological growth pattern: nodular, superficial, and morphoeic. BCCs are believed to derive from the epidermis, specifically the basal cell layer and the outer root sheath of the hair follicle. The development of BCC is clearly associated with mutated p53 tumour-suppressor gene and constitutive activation of so