ABSTRACT
Anetoderma is a rare cutaneous disorder characterized by a loss of normal elastic tissue that presents clinically as atrophic patches located mainly on the upper trunk. Recent studies suggest immunological mechanisms may play a role in this process. Furthermore, a secondary form of macular atrophy occurs in the course of infectious diseases (e.g. syphilis and tuberculosis) and autoimmune disease (e.g. systemic lupus erythematosus [SLE]). Here, we report the case of a 20-year-old woman previously diagnosed with SLE, who presented with numerous well-circumscribed atrophic macules on the face and upper trunk. Histopathological examination showed decreased elastic tissues in the reticular dermis and mononuclear cells adhering to elastic fibers, consistent with anetoderma. Thus, the eruptive anetoderma localized widely on the face and upper trunk may have been caused by an autoimmune response of SLE.
ABSTRACT
Trastuzumab (Herceptin), a humanized monoclonal antibody, is a cancer drug developed to target the human epidermal receptor (HER) 2, which is overexpressed in some cancer cells. Cutaneous side effects, such as folliculitis, xerosis, and alopecia have not been reported with therapies targeting HER2, in spite of the frequent observances of such with the therapies targeting the epidermal growth factor receptor. We experienced a patient in whom psoriasis was triggered by the trastuzumab treatment for breast cancer. She was a 57-year-old woman with erythematous and scaly plaques occurring a few months after starting trastuzumab, with repeated aggravation after the re-administration of trastuzumab for the breast cancer. Histologic examination showed the typical features of psoriasis with parakeratosis, epidermal hyperplasia, elongation of the rete ridges, and a lymphocytic and polymorphonuclear cell infiltrate in the dermis. To the best of our knowledge, this is the first report of psoriasis triggered by trastuzumab treatment for breast cancer.
ABSTRACT
BACKGROUND: Epigenetic modulation of gene expression occurs by various methods, including DNA methylation and histone modification. DNA methylation of specific genes may affect the chromatin structure, preventing access by the transcriptional machinery. Although gene expression is dramatically changed during keratinocyte differentiation, there is no evidence of epigenetic modulation during the process of epidermal stratification. OBJECTIVE: We investigated whether epigenetic modulation is involved in keratinocyte differentiation-specific gene regulation. METHODS: We used trypsin to produce epidermal fragmentation (named T1-T4) and performed a morphological analysis using hematoxylin-eosin stain and cytokeratin expression based on reverse transcription polymerase chain reaction. We then constructed a DNA methylation microarray. RESULTS: Each epidermal fragment showed morphological features of the epithelial layer. T1 represented the basal layer, T2 was the spinous layer, T3 was the granular layer, and T4 was the cornified layer. The level of the K14 proliferation marker was increased in the T1 fraction, and the level of K10 differentiation marker was increased in the T2-T4 fractions. Using a methylation microarray with the T1 and T4 fractions, we obtained many hypermethylated and hypomethylated genes from differentiated keratinocytes. CONCLUSION: The importance of epigenetic modulation in target gene expression during keratinocyte differentiation is identified.
ABSTRACT
BACKGROUND: The extracellular matrix (ECM) produced by dermal fibroblasts supports skin structure, and degradation and/or reduced production of ECM are the main causes of wrinkle formation. OBJECTIVE: The aim of this study was to identify the active ingredient that enhances ECM production in dermal fibroblasts. METHODS: Polarity-based fractionation was used to isolate the active ingredient from natural extracts, and the effects of cedrol (isolated from Pterocarpus indicusirginia) on ECM production in cultured human dermal fibroblasts was investigated by reverse transcription-polymerase chain reaction, enzyme linked immunosorbent assay, and Western blot analysis. RESULTS: Cedrol accelerated fibroblast growth in a dose-dependent manner and increased the production of type 1 collagen and elastin. Phosphorylation of p42/44 extracellular signal-regulated kinase, p38 mitogen-activated protein kinase, and Akt was markedly increased by cedrol, indicating that enhanced ECM production is linked to activation of intracellular signaling cascades. CONCLUSION: These results indicate that cedrol stimulates ECM production, with possible applications to the maintenance of skin texture.
