Moon Kyun Cho

Expression of heat shock protein 105 and 70 in malignant melanoma and benign melanocytic nevi

Background:u2002 Heat shock proteins (HSPs) restore immature proteins or denatured proteins, thus protecting cells. Also, the expression of some HSPs is elevated substantially in malignant tumors, but the expression of HSPs in association with melanoma has yet to be studied. Therefore, we examined the expression patterns of HSP 70 and 105 in melanoma, benign melanocytic nevi and normal human skin.

A case of zoster duplex bilateralis.

The skin lesions of herpes zoster are classically limited to a single dermatome and most cases of multidermatomal herpes zoster have contiguous skin lesions. Simultaneous involvement of two noncontiguous dermatomes is very rare and it has been referred to as zoster duplex unilateralis or bilateralis, depending whether one or both halves of the body are involved. A 67-year-old woman presented with a group of painful vesicles on the right buttock and thigh, and left anterior chest and back. The Tzanck smear and skin biopsy were consistent with a herpetic infection. We report a rare case of zoster duplex bilateralis.

Vulvar Skin Metastasis of Lung Squamous Cell Carcinoma

In this study, we examined a case where lung cancer metastasized to the vulvar area. A 79-year-old woman that was a heavy smoker was referred to our department with a short (two-week) history of dyspnea, and with a painful nodule on her right labium majora, which she had noticed almost three years earlier. Histopathologically, the specimen appeared as a poorly differentiated squamous cell carcinoma. The chest X-ray, chest computerized tomography scan, and percutaneous transthoracic needle biopsy via bronchoscopy revealed squamous cell carcinoma in the right upper lobe of the lung. Based on these clinical and histopathological findings, we concluded that her condition was skin metastasis at the right labium majora from the lung cancer, which occurs very rarely.

Pro-oxidant status and Nrf2 levels in psoriasis vulgaris skin tissues and dimethyl fumarate-treated HaCaT cells

Reactive oxygen species (ROS) contribute to pathogenesis of many inflammatory skin diseases, including psoriasis. The aim of this study is to compare antioxidant protein expression in psoriasis vulgaris (PV) skin tissues with that in normal skin tissues in vivo and to evaluate the effects of dimethyl fumarate (DMF), used for the treatment of psoriasis, on ROS generation and apoptosis in a human keratinocyte cell line HaCaT. Compared with normal skin tissues, PV skin tissues showed increased protein oxidation as well as down-regulation of Nrf2 and its regulatory proteins such as HO-1 and AKR1C3. Using HaCaT cells to model DMF-induced pro-oxidant effects in the skin cells, we found that DMF treatment induced increased ROS levels and apoptotic cell death, as signified by increased proportion of cells with Annexin V-PE(+) staining and a sub-G0/G1 peak in the cell cycle. Preceding these changes, DMF treatment resulted in up-regulation of Nrf2, HO-1, and AKR1C3 proteins in these cells. Collectively, increased oxidative stress and impaired cellular anti-oxidant enzyme systems may participate in the pathogenesis of PV. DMF may exert an additive therapeutic efficacy in PV by attenuating the redox burden and subsequent oxidative damage to normal keratinocytes through activation of Nrf2 pathway relative to PV.

Abstract 3460: Reactive oxygen species generated by cadmium play a role in the upregulation of aldo-keto reductase 1C3 in RPMI 2630 nasal carcinoma cells

Cadmium (Cd) is a carcinogenic metal which induces oxidative stress through the generation of reactive oxygen species (ROS). Therefore, the ability of cells to up-regulate their antioxidant enzymes is fundamental in the protection of cells and tissues from oxidative damage. In probing the possible survival mechanism of cancer cells to Cd-induced oxidative stress, we examined the ability of Cd to regulate the level of aldo-keto reductase 1C3 (AKR1C3), which has an anti-oxidative role that catalyzes the reductive detoxification of reactive aldehydes and ketones. Exposure of cells to Cd induced a dose- and time-dependent increase in the AKR1C3 expression in the RPMI 2640 nasal septum carcinoma cells, and this up-regulation was blocked by the free radical scavenger N-acetylcysteine (NAC). Additionally, we confirmed that Cd triggered a rapid increase in the intracellular ROS levels, and this increase was inhibited by pretreatment with NAC, which suggests that the up-regulation of AKR1C3 expression involves ROS signaling. Furthermore, pretreatment of cells with LY294002, a pharmacologic inhibitor of phosphatidylinositol-3-kinase (PI3K), suppressed the Cd-augmented AKR1C3 expression; however, inhibition of PKC or MEK1/2 signaling with Go6976 or PD98059, respectively, did not alter Cd-induced AKR1C3 expression. Collectively, these data suggest that Cd can modulate the expression of the AKR1C3 by activation of PI3K via the generation of ROS in RPMI2640 cells, which would contribute to adaptive response to oxidative stress. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3460.