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Introduction An atrophic dermatofibroma is a benign fibrohistiocytic neoplasm. It typically presents as an asymptomatic patch with a depressed central area. Methods The PubMed database was used to search the following words: atrophic, dermatofibroma, elastic and fibers. The relevant papers and their references generated by the search were reviewed. Images of the clinical and pathological features of two patients with an atrophic dermatofibroma are presented. In addition, a comprehensive review of the characteristics of this unique dermatofibroma is provided. Results An atrophic dermatofibroma has been reported in 102 patients: 53 women, 11 men and 38 individuals whose gender was not provided. It typically appeared as an asymptomatic solitary patch with a central umbilication—most commonly on the shoulder or lower extremity or back—of women aged 48 years or older. Dermoscopy typically showed white scar-like patches; a patchy pigment network was also noted in some lesions. The pathology of an atrophic dermatofibroma has the same features that can be observed in a common fibrous dermatofibroma; there is acanthosis, basal layer hyperpigmentation, and induction of basal cell carcinoma-like features, hair follicle formation or sebaceous hyperplasia in the epidermis and a proliferation of spindle-shaped fibroblasts in the dermis. However, atrophic dermatofibromas also demonstrate depression of the central surface and thinning of the dermis; in many cases, the dermal atrophy is at least 50%. Elastic fibers are either decreased or absent. Similar to non-atrophic dermatofibromas, the immunoperoxidase profile of atrophic dermatofibromas is factor XIIIa-positive and cluster of differentiation 34 (CD34)-negative. The pathogenesis of atrophic dermatofibromas remains to be established. Conclusion An atrophic dermatofibroma is an uncommon benign variant of a dermatofibroma. The diagnosis can be suspected based on clinical features and dermatoscopic findings. A biopsy of the lesion will confirm the diagnosis. Periodic evaluation of the lesion site is a reasonable approach to the management of the residual tumor.

Tattoos may be associated with medical complications including, albeit rarely, skin cancer. The features of a 46-year-old man who developed a basal cell carcinoma within a tattoo on his left scapula are described and the characteristics of the other 13 patients (7 men and 6 women) with tattoo-associated basal cell carcinoma are reviewed. The tumor usually occurs on the sun-exposed skin of individuals aged 60 years and older whose tattoo has often been present for 20 years or more. The pathogenesis of a basal cell carcinoma developing within a tattoo may merely be a coincidence. However, there is supporting evidence that the tattoo and the subsequent basal cell carcinoma may be coincident events whereby either tattoo injectionassociated trauma or the tattoo pigments and dyes (in their native state or after ultraviolet radiation alteration) or both have a carcinogenic impact on the development of the basal cell carcinoma at that location.

During early development, progenitors of the heart valves and septa are formed by epithelial-mesenchymal transformation (EMT) of endothelial cells in the atrioventricular (AV) canal. Previously, we showed that pertussis toxin, a specific inhibitor of a subset of G proteins, inhibited EMT in chick AV canal cultures. This study examines in detail the effects of pertussis toxin on the process of EMT. One of the major mediators of EMT is Transforming Growth Factor beta 3 (TGF3) which acts through the TGF Type II receptor. To determine whether pertussis toxin affects EMT via the TGF Type II receptor pathway, we compared AV cultures treated with pertussis toxin and TGF Type II receptor blocking antibody. Pertussis toxin inhibited several elements of EMT. At all stages tested, pertussis toxin blocked endothelial cell-cell separation, cell hypertrophy, and the cellular polarization associated with endothelial activation. These activities were unaffected by TGF Type II receptor anti-bodies. Pertussis toxin also reduced transformed mesenchymal cell migration by 61%. The expression patterns of several proteins (as markers of EMT) were analyzed in untreated, pertussis toxin-treated, and TGF Type II receptor blocking antibody-treated cultures. These markers were-smooth muscle actin, Mox-1, fibrillin 2, tenas-cin, cell surface 1,4 galactosyltransferase (GalT-ase), and integrin 6. Clear differences in marker expression were found between the two inhibi-tors. For example, in all cells, pertussis toxin inhibited expression of-smooth muscle actin and GalTase while TGF Type II receptor anti-body treatment increased expression of these two proteins. These data suggest that G protein-mediated signaling is required for several elements of EMT. Furthermore, distinct G protein and TGF signal transduction pathways mediate discrete components of EMT. Dev Dyn 1999;214: 81-91.