the function of Cyclin D1 (CycD1) has been widely studied in the cell nucleus as a regulatory subunit of the cyclindependent kinases Cdk4/6 involved in the control of proliferation and development in mammals. CycD1 has been also localized in the cytoplasm, where its function nevertheless is poorly characterized. In this work we have observed that in normal skin as well as in primary cultures of human keratinocytes, cytoplasmic localization of CycD1 correlated with the degree of differentiation of the keratinocyte. In these conditions, CycD1 co-localized in cytoplasmic foci with exocyst components (Sec6) and regulators (ralA), and with β1 integrin, suggesting a role for CycD1 in the regulation of keratinocyte adhesion during differentiation. Consistent with this hypothesis, CycD1 overexpression increased β1 integrin recycling and drastically reduced the ability of keratinocytes to adhere to the extracellular matrix. We propose that localization of CycD1 in the cytoplasm during skin differentiation could be related to the changes in detachment ability of keratinocytes committed to differentiation.Cyclin D1 localizes in the cytoplasm of keratinocytes during skin differentiation and regulates cell-matrix adhesion

Tophi develop during the most advanced clinical stage of gout, and are usually located on or around the joints. However, unusual skin features caused by intradermal and/or subcutaneous deposition of tophaceous material at locations other than articular regions have been reported. We present the case of a patient with a condition that has been recently termed 'miliarial gout'. which is only the second such case, to our knowledge. A 51-year-old woman, who had a chronic joint disease that had been diagnosed and treated as psoriatic arthritis, presented with multiple asymptomatic, yellowish-white, firm papules (1-3 mm in size) on erythematous areas on the outside of her left leg. On histological examination of a skin biopsy, uric acid crystals were seen in the dermis and subcutis. The patient also had a raised level of serum urate, consistent with a diagnosis of gout. Treatment with allopurinol led to rapid improvement. Intake of corticosteroids and diuretics was a possible triggering factor for the development of cutaneous tophi in this patient.

The authors have indicated no significant interest with commercial supporters. N evus sebaceous (or Jadassohn's sebaceous nevus or organoid nevus) is a well-known congenital skin hamartoma involving ectodermand mesoderm-derived structures that usually appears in the head and face area. During childhood, the lesion remains static but, during puberty, grows and becomes more evident and verrucous. These changes reveal growth of pilosebaceous and apocrine elements, probably because of the influence of androgens. 1,2Depending on location and size, nevus sebaceous causes only aesthetic problems, although in adulthood, benign and malignant neoplasms develop in approximately 15% of cases. 2 Of malignant tumors, the most common is basal cell carcinoma (BCC), which has an estimated incidence in nevus sebaceous of less than 2%. Other malignant tumors are rare. 3 To our knowledge, only 12 squamous cell carcinomas (SCCs) and eight adnexal have been described. [4][5][6][7][8][9][10][11][12][13][14] We are reporting an unusual case of SCC that appeared on a Jadassohn's sebaceous nevus in a 41-year-old man. Its clinical and evolutive features are compared with those of previously published cases. Case ReportIn December 2002, a 41-year-old man sought medical advice for a 3-month history of a growing nodule on a congenital lesion of his face. Clinical examination revealed, on the inferior portion of his left cheek, a pink-yellowish verrucous plaque, 2 Â 0.8 cm in size, with a centrally ulcerated and crusted erythematous nodule, 1 Â 0.8 cm in size, arising on the external end of the plaque (Figure 1). Enlarged regional lymph nodes were not detected. The patient had no history of cutaneous cancer, immunosuppression, or local trauma.The lesion was completely excised with wide margins. Histopathologic examination showed the presence of a large number of mature sebaceous glands and papillomatous hyperplasia of the epidermis (Figure 2). A SCC developed within the nevus sebaceous. The squamous carcinoma cells invaded the upper dermis without desmoplasia. There was a moderate infiltrate of lymphocytes between the carcinomatous cells (Figures 3 and 4). The lesion also showed mature apocrine glands located in the lower dermis.The patient remains well, without clinical evidence of recurrence, after more than 8 years of follow-up. DiscussionJadassohn's sebaceous nevus is an hamartomatous skin malformation present in 0.3% of newborns. 15