Twenty-one Japanese cases of subungual malignant melanoma were investigated clinically and histologically. In the majority of the cases, the initial sign of the disease was confirmed to be melanonychia striata. Five cases of Clark's Level I melanoma were found in the series. Melanonychia striata had appeared as the initial sign in these five cases. Melanonychia striata is frequently observed in persons who are not white and is attributed to various local and systemic causes. Detailed clinical analysis of the five cases of early subungual melanoma showed that melanonychia striata with the following characteristics may increase the risk of early subungual melanoma developing: it is noticed during adulthood, it is broader than 6 mm, it is brownish with variegated shades or homogenously black, and it is accompanied by periungual pigmentation (Hutchinson's sign). Detection of early lesions of subungual melanoma is beneficial not only for the improvement of prognosis, but also for the preservation of the affected phalanx.

We investigated the effects of histone deacetylase (HDAC) inhibitors such as sodium butyrate (SB) and trichostatin A (TSA) on the expression of vascular endothelial growth factor (VEGF) by human glioblastoma T98G, U251MG, and U87MG cells. The glioblastoma cells secreted three VEGF isoforms, VEGF (189), (165), and (121), although the expression levels of VEGF differed between the cell types. Treatment with either 5mM SB or 100 ng/ml TSA reduced VEGF secretion in conditioned media and reduced VEGF mRNA expression. We also studied the expression of VEGF-B, -C, and -D mRNA in human glioblastoma cells and their modulation by HDAC inhibitors. The PCR products of VEGF-B (357bp), VEGF-C (501bp), and VEGF-D (484bp) were amplified in all glioblastoma cells examined. Treatment with SB reduced the expression of VEGF-D mRNA in U251MG cells and the expression of VEGF-B mRNA in U87MG cells. TSA treatment reduced the expression of VEGF-D in U251MG cells. These results suggest that HDAC inhibitors reduce VEGF secretion and modulate the expression of the other VEGF family members, and therefore may inhibit angiogenesis in glioblastoma tissues.

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