tacrolimus on GLI1 expression, and provide strength to the hypothesis that GLI1 regulates the expression of BCL-2 and of basal lamina molecules including laminin. Acknowledgements This paper is devoted to the memory of Paolo Carli, M.D., who passed away on April 6, 2007, while the results of this research, that had been launched and strongly promoted by him, were still generated. Additional funds were provided by the University of Florence and by Tuscany region (project TRESOR—scientific director Prof. M. Serio). Appendix A. Supplementary data Supplementary data associated with this article can be found, in the online version, at doi:10.1016/j.jdermsci.2008.10.006. Conflict of interest The study was supported in part by Fujisawa GmbH (Munich, Germany), now Astellas Europe (Staines, UK). References [1] Villavicencio EH, Walterhouse DO, Iannaccone PM. The sonic hedgehog- patched-gli pathway in human development and disease. Am J Hum Genet 2000;67:1047–54. [2] Ghali L, Wong ST, Green J, Tidman N, Quinn AG. Gli1 protein is expressed in basal cell carcinomas, outer root sheath keratinocytes and a subpopulation of mesenchymal cells in normal human skin. J Invest Dermatol 1999;113:595–9. [3] Green J, Leigh IM, Poulsom R, Quinn AG. Basal cell carcinoma development is associated with induction of the expression of the transcription factor Gli-1. Br J Dermatol 1998;139:911–5. [4] Hatta N, Hirano T, Kimura T, Hashimoto K, Mehregan DR, Ansai S, et al. Molecular diagnosis of basal cell carcinoma and other basaloid cell neoplasms of the skin by the quantification of Gli1 transcript levels. J Cutan Pathol 2005;32:131–6. [5] Goto T, Kino T, Hatanaka H, Nishiyama M, Okuhara M, Kohsaka M, et al. Discovery of FK-506, a novel immunosuppressant isolated from Streptomyces tsukubaensis. Transplant Proc 1987;19:4–8. [6] Kim A, DiCarlo J, Cohen C, McCall C, Johnson D, McAlpine B, et al. Are keloids really ‘‘gli-loids’’?: High-level expression of gli-1 oncogene in keloids. J Am Acad Dermatol 2001;45:707–11. [7] Macaron NC, Cohen C, Chen SC, Arbiser JL. GLI-1 oncogene is highly expressed in granulomatous skin disorders, including sarcoidosis, granuloma annulare, and necrobiosis lipoidica diabeticorum. Arch Dermatol 2005;141:259–62. [8] Zhan M, Zhao H, Han ZC. Signalling mechanisms of anoikis. Histol Histopathol 2004;19:973–83. [9] Evans AV. The expanding role of topical tacrolimus in dermatology. Clin Exp Dermatol 2005;30:111–5. [10] Niwa Y, Terashima T, Sumi H. Topical application of the immunosuppressant tacrolimus accelerates carcinogenesis in mouse skin. Br J Dermatol 2003;149:960–7. P. Di Gennaro a R. Sestini b S. Bacci a A. Pacini a P. Pinzani L. Domenici a A. Toscano a D. Massi c P. Carli d M. Genuardi b P. Romagnoli a, * a Department of Anatomy, Histology, and Forensic Medicine, University of Florence, Viale Pieraccini 6, Florence 50139, Italy b Department of Clinical Physiopathology, University of Florence, Viale Pieraccini 6, Florence 50139, Italy c Department of Human Pathology and Oncology, University of Florence, Viale Morgagni 85, Florence 50134, Italy d Department of Dermatological Sciences, University of Florence, Via della Pergola 58-64, Florence 50121, Italy *Corresponding author. Tel.: +39 055 4271389; fax: +39 055 4271385 E-mail address: paolo.romagnoli@unifi.it 13 May 2008 6 October 2008 25 October 2008 doi:10.1016/j.jdermsci.2008.10.006 Letter to the Editor Clinical, histological and genetic investigation of Buschke– Fischer–Brauer’s disease in Tunisian families Dear Editor, Buschke–Fischer–Brauer’s disease or the type I of punctate PPK (MIM 148600) is a rare hereditary skin disease that is usually inherited as an autosomal dominant trait and its incidence was reported as 1.17/100,000 inhabitants in Croatia [1]. Punctate PPK is characterized by multiple punctate keratoses over the entire palmoplantar surfaces. The age of onset ranged between 12 and 30 years [2]. The molecular basis of punctate PPK is still unknown. Recently, two punctate PPK loci were found to map to 15q22–15q24 and to 8q24.13–8q24.21 [3,4]. However, in a recent study, Gao et al. failed to confirm genetic linkage to their previous locus on 8q and showed significant evidence for linkage to 15q22–15q24 (9.98 cM). This candidate region was reduced to 5.06 cM on 15q22.2–15q22.31 [5]. In the present study, we report the clinical, histological and genetic findings in five Tunisian families (PPK1 to PPK5) with a total of 15 patients (6 women and 9 men). The diagnosis was established based on clinical examination and confirmed by histopathological findings. The explored patients exhibited classi- cal PPK phenotype and a positive family history was observed which confirmed the autosomal mode of transmission of the disease in informative families. Patients presented with hyperker- atosis and verrucoid punctate lesions on the palmoplantar area. Lesions were yellowish, of 2–3 mm in diameter and usually coalesce on the soles subject to continuous high pressure. There was no nail involvement. The age of onset of the disease ranged from 10 to 35 years. However, for the patient (IV-1) in family PPK1, ARTICLE INFO Keywords: Palmoplantar keratoderma; Punctate PPK; Haplotype; Linkage analysis Letters to the Editor / Journal of Dermatological Science 54 (2009) 43–63 54