In non-AIDS individuals, the cutaneous lesions from CMV infection showed similar clinical and histopathological features to those of patients with AIDS. However, skin lesions may not be highly associated with HSV, and CMV does seem to contribute to lesion development as a cutaneous manifestation among the CMV infected, non-AIDS, immunocompromised patients.

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Histone deacetylase (HDAC) inhibitors are promising anticancer drugs, but these exert differential responses depending on the cell types. Here, we demonstrate a new mechanism for activation of nuclear factor-jB (NF-jB) by HDAC inhibitor apicidin and the role of NF-jB signaling pathway for mediating differential cellular responses, especially, apoptosis. Treatment of HeLa cells with apicidin increases transcriptional activity of NF-jB and its target gene IL-8 and cIAP-1 induction, which involves the activation of IKK-IjBa signaling pathway through Sp1-dependent de novo protein synthesis. In parallel, apicidin treatment leads to histone hyperacetylation in the IL-8 promoter region independent of NF-jB signaling pathway, which is not sufficient for full transcription of IL-8 gene. This NF-jB activation contributes to resistance of HeLa cells to apoptotic potential of apicidin. Collectively, our results suggest that activation of NF-jB signaling cascade functions as a critical modulator to determine cell fate on apoptosis in response to HDAC inhibitors.

Serum OPN levels were significantly higher in patients with advanced HCC. In addition, HCC patients with low pretreatment serum OPN levels and those for whom serum OPN declined following TACE exhibited better tumor responses and survived for longer.