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Seborrheic keratosis is a benign condition that can mimic many different non-melanoma and melanoma neoplasms. There have been several case reports of underlying squamous cell carcinomas or intraepidermal carcinomas appearing within lesions that look analogous to seborrheic keratoses. We present a patient with a verrucous melanoma that could be mistaken for a benign skin tumor like an inflamed seborrheic keratosis. In our patient's case, her verrucous plaque was initially clinically suggestive of a benign seborrheic keratosis. However, given the patient's complaint of pain associated with the lesion, a biopsy was performed and revealed a verrucous-keratotic malignant melanoma, which was subsequently removed through surgical excision. It is important to remain vigilant of this diagnosis, as treatment for inflamed seborrheic keratosis often includes a trial of cryotherapy, which potentially could lead to a delayed diagnosis of an underlying malignant lesion.

Prenatal stress, psychologically and metabolically, increases the risk of obesity and diabetes in the progeny. However, the mechanisms of the pathogenesis remain unknown. In adult mice, stress activates NPY and its Y2R in a glucocorticoid-dependent manner in the abdominal fat. This increased adipogenesis and angiogenesis, leading to abdominal obesity and metabolic syndrome which were inhibited by intra-fat Y2R inactivation. To determine whether stress elevates NPY system and accelerates adipogenic potential of embryo, here we ''stressed'' murine embryonic stem cells (mESCs) in vitro with epinephrine (EPI) during their adipogenic differentiation. EPI was added during the commitment stage together with insulin, and followed by dexamethasone in the standard adipogenic differentiation medium. Undifferentiated embryonic bodies (EBs) showed no detectable expression of NPY. EPI markedly up-regulated the expression NPY and the Y1R at the commitment stage, followed by increased Y2R mRNA at the late of the commitment stage and the differentiation stage. EPI significantly increased EB cells proliferation and expression of the preadipocyte marker Pref-1 at the commitment stage. EPI also accelerated and amplified adipogenic differentiation detected by increasing the adipocyte markers FABP4 and PPARc mRNAs and Oil-red O-staining at the end of the differentiation stage. EPI-induced adipogenesis was completely prevented by antagonists of the NPY receptors (Y1R+Y2R+Y5R), indicating that it was mediated by the NPY system in mESC's. Taken together, these data suggest that stress may play an important role in programing ESCs for accelerated adipogenesis by altering the stress induced hormonal regulation of the NPY system. [ABSTRACT FROM AUTHOR]