The immunohistochemical profile of Spitz nevi and conventional (non-Spitzoid) melanomas: a baseline study.

Several isolated markers have been proposed to aid in differential diagnostic of difficult melanocytic lesions, albeit none has been shown to be definitive in differentiating Spitz nevus from melanoma. This study proposes a wide panel of 22 markers having important functions in different biological functions (cell cycle, apoptosis, DNA repair proteins and membranous receptors) to provide a combination of proteins associated with either benign or malignant phenotype. Using tissue microarrays, we compared protein expression profiles in 28 typical Spitz nevi and 62 primary vertical growth phase non-spitzoid melanomas. Most of the significant differences were linked to cell-cycle deregulation such as overexpression of cyclin D1 and p21 in Spitz nevi compared with non-spitzoid melanomas (74 vs 16% and 91 vs 27%, respectively) and mitotic rate including Ki-67, highly expressed in deep areas of non-spitzoid melanomas (37%), whereas it is not expressed in Spitz nevi (0%), topoisomerase IIalpha (79% in non-spitzoid melanomas vs 15% in Spitz nevi) and nuclear survivin (69% in melanomas vs 0% in Spitz nevi). A combination of biological markers differentially expressed in Spitz nevi from non-spitzoid melanomas is defined, thus providing a potential tool for histopathological differential diagnostic between Spitz nevus and melanoma. Nevertheless, more studies including atypical Spitz nevi and spitzoid melanomas are necessary to further establish a reliable panel to differentiate among difficult cases.

Lichenoid sarcoidosis: a case with clinical and histopathological lichenoid features.

Sarcoidosis is a chronic multisystemic granulomatous disease of unknown etiology, characterized by the formation of noncaseating granulomas in the involved organs. Cutaneous involvement is about 25% with different clinical expressions, the lichenoid pattern being one of the rarest types of cutaneous sarcoidosis. Lichenoid sarcoidosis clinically manifests with multiple scale papules involving extensive skin areas, especially the trunk, limbs, and face mimicking a lichen planus. Although diverse histologic patterns have been previously related, a lichenoid granulomatous infiltrate involving the dermo-epidermal junction has never been reported in lichenoid sarcoidosis. We report a case of a 43-year-old woman presenting with skin-colored pruritic papules, slightly scaling in trunk, extremities, and ears. These symptoms condition continued to expand and worsen for several years. The patient was otherwise in good health with no lymphadenopathies. Histopathologic examination of a skin biopsy showed an upper dermal granulomatous infiltrate of epithelioid cells, without necrosis, distributed in a lichenoid pattern with many cytoid bodies. We consider this may be the first case presenting a characteristic microscopic granulomatous lichen-like pattern in the setting of a clinically lichenoid type of sarcoidosis.

Mycosis fungoides shows concurrent deregulation of multiple genes involved in the TNF signaling pathway: an expression profile study.

Mycosis fungoides (MF) is the most frequent type of cutaneous T-cell lymphoma, whose diagnosis and study is hampered by its morphologic similarity to inflammatory dermatoses (ID) and the low proportion of tumoral cells, which often account for only 5% to 10% of the total tissue cells. cDNA microarray studies using the CNIO OncoChip of 29 MF and 11 ID cases revealed a signature of 27 genes implicated in the tumorigenesis of MF, including tumor necrosis factor receptor (TNFR)-dependent apoptosis regulators, STAT4, CD40L, and other oncogenes and apoptosis inhibitors. Subsequently a 6-gene prediction model was constructed that is capable of distinguishing MF and ID cases with unprecedented accuracy. This model correctly predicted the class of 97% of cases in a blind test validation using 24 MF patients with low clinical stages. Unsupervised hierarchic clustering has revealed 2 major subclasses of MF, one of which tends to include more aggressive-type MF cases including tumoral MF forms. Furthermore, signatures associated with abnormal immunophenotype (11 genes) and tumor stage disease (5 genes) were identified.