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BACKGROUND:In patients with multiple primary melanomas (MPM), mean tumor thickness tends to decrease from the first melanoma to the second melanoma, and prognosis may be improved compared with the prognosis for patients who have a single primary melanoma (SPM). In this study, the authors compared the clinicopathologic features of patients with MPM and SPM to better characterize the differences between these 2 groups and to determine whether or not there is an inherent difference in tumor aggression. METHODS: In total, 788 patients with melanoma who were enrolled prospectively in the Interdisciplinary Melanoma Cooperative Group database from 2002 to 2008 were studied. Patients with SPM and with MPM were compared with regard to clinical and primary melanoma characteristics. RESULTS: Of 788 patients with melanoma, 61 patients (7.7%) had 2 or more primary melanomas. The incidence of developing a second primary melanoma 1 year and 5 years after initial melanoma diagnosis was 4.1% and 8.7%, respectively, and most of the risk accumulated within the first year. The incidence of MPM was greater in patients aged !60 years than in those aged 60 years. The absence or presence of mitosis and other tumor characteristics did not differ significantly between patients with SPM and patients with MPM (P ¼ .61). CONCLUSIONS: No difference was observed in the presence or absence of mitoses, a marker of tumor proliferation, in SPM and MPM. Because it has been demonstrated that the presence of mitosis is a powerful prognostic marker, the current findings suggested that the tumors behave similarly in patients with SPM and patients with MPM. The authors concluded that differences in tumor thickness and prognosis between SPM and MPM more likely are caused by factors other than tumor biology, such as increased surveillance. Cancer 2012;118:4184-92.

We report nine examples of a distinct cutaneous plaque-like proliferation of fibroblasts and myofibroblasts. Eight of nine lesions were located in or around the shoulder, including axilla and upper arm. There was a predominance of women to men of 8:1. The lesions measured from 1 to 2 cm in greatest diameter. All patients were young adults (mean age 29.8 yr). All lesions involved the reticular dermis in a plaque-like fashion and extended to the upper part of the subcutaneous septa in seven cases. The lesions consisted of a proliferation of very uniform slender spindle-shaped cells arranged as well-defined elongated and intersecting fascicles with a predominantly parallel arrangement to the skin surface. There was no evidence of cytologic atypia and mitotic figures were infrequent. The spindle-shaped cells were separated by thin collagen fibers. Elastic fibers were preserved and some of them appeared thicker than normal. All adnexal structures were spared. Immunohistochemistry revealed that the cells stained positively for vimentin and muscle actin, but lacked smooth-muscle specific actin, desmin, and S-100 protein. Some dermal dendrocytes stained positively for Factor XIIIa, but the spindle-shaped cells were negative. Electron microscopy studies revealed a mixture of fibroblasts, myofibroblasts, and undifferentiated mesenchymal cells. All lesions were treated by conservative excision; follow-up information revealed no evidence of recurrence. We name this distinct lesion dermatomyofibroma. To the best of our knowledge, this entity has not been previously described in the literature.

Our study supports the finding that in LPP, the inflammatory infiltrate mainly involves the bulge region, where the stem cells reside. Once this area is damaged, the hair loses its potential of regrowth with resulting scarring alopecia. This is in contrast with inflammatory non-scarring alopecias such as alopecia areata, where the bulb region is targeted, sparing the stem cells.

No abstract

Comprehensive clinical, histopathologic, and immunohistochemical criteria for the classification of tumid LE are proposed that differentiate tumid LE from other cutaneous disorders that may be clinically and histologically indistinguishable. The chronic, benign course indicates that tumid LE be classified as a form of chronic cutaneous LE, although it may be a cutaneous feature of systemic LE.

We describe two young children who developed relapsing, pruritic, papulovesicular eruptions in multiple bands along Blaschko lines on the neck, trunk, and extremities. Skin specimens in both revealed spongiotic dermatitis. This represents the first report of "blaschkitis" in children, providing further evidence that lichen striatus and blaschkitis are related acquired Blaschko-linear dermatoses that exist on a spectrum rather than as the childhood and adult form of a single disease entity. We highlight the features that differentiate blaschkitis from lichen striatus, review the potential roles of cutaneous mosaicism, environmental triggers, and background immunologic state in their pathogenesis, and discuss the spectrum of inflammatory dermatoses that can follow Blaschko lines.

Localized autosomal recessive hypotrichosis (LAH) is a recently defined disorder characterized by fragile, short, sparse hairs on the scalp, trunk, and extremities. Mutations in desmoglein 4 (DSG4), a novel member of the desmosomal cadherin family that is expressed in the hair follicle as well as the suprabasal epidermis, have been found to underlie LAH. Thus far, the allelic series includes a recurrent intragenic deletion identified in affected Pakastani kindreds and a missense mutation detected in an Iraqi family. We report three siblings of Iraqi and Iranian origin with LAH that presented with congenital scalp erosions and monilethrix-like hairs, features that have not been previously described in this disorder. Follicular hyperkeratotic papules and marked pruritus were also prominent clinical findings. Novel compound heterozygous DSG4 mutations, including a splice-site mutation and a missense mutation that disrupts a conserved calcium-binding site in the extracellular (EC)2-EC3 interface, were found to underlie the disease in this family. These observations broaden the phenotypic and genotypic spectrum of LAH, further illustrating the consequences of DSG4 dysfunction on epidermal and hair shaft integrity.