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P181 : The expression of c-Jun in various skin tumors
( Bum Joon Ko ),( Hong Ki Cho ),( Kyung O Kim ),( Han Eul Lee ),( Young Lip Park ),( Jong Suk Lee ),( Kyu Uang Whang ) 대한피부과학회 2013 대한피부과학회 학술발표대회집 Vol.65 No.2
Background: c-Jun, along with JunB, JunD and Fos group proteins, comprises the core members of the activator protein 1(AP1) family of transcription factors. Recent many studies have demonstrated that AP1 has key roles in regulating a wide spectrum of biological processes, including tumorigenesis. So We hypothesized that c-Jun has influence on differentiation and malignant change of various skin tumors. Objectives: This study was investigate to measure the expression of c-Jun in different skin tumors. Methods: The expression of c-Jun was examined by immunohistochemical staining of 46 specimens of skin tumors including 2 cases of pigmented nevus, 2 cases of dysplastic nevus, 4 case of seborrheic keratosis, 4 case of keratoacanthoma, 4 cases of actinic keratosis, 4 cases of bowen disease, 16 cases of squamous cell carcinoma, 4 case of basal cell carcinoma and 6 cases of malignant melanoma. Results: Immunohistochemical analysis of the skin tumor tissue samples revealed a significantly higher expression of c-Jun in malignant melanoma than other skin tumors. Conclusion: These findings showed that c-Jun have a positive association with the malignancies of the skin tumors and suggested the role of c-Jun in the protection of malignant changes including loss of differentiation and dysplasia in skin tumors.
FC 1-13 : Expression of extracellular superoxide dismutase protein in diabetes
( Bum Joon Ko ),( Han Eul Lee ),( Gang Mo Lee ),( Je Min An ),( You In Bae ),( Sung Yul Lee ),( Moon Kyun Cho ) 대한피부과학회 2013 대한피부과학회 학술발표대회집 Vol.65 No.2
Background: Diabetes is characterized by chronic hyperglycemia, which can increase reactive oxygen species (ROS) production by the mitochondrial electron transport chain. The formation of ROS induces oxidative stress and activates oxidative damage-inducing genes in cells. No research has been published on oxidative damage-related extracellular superoxide dismutase (EC-SOD) protein levels in human diabetic skin. We investigated the expression of EC-SOD in diabetic skin compared with normal skin tissue in vivo. Objectives: To compare the expression of EC-SOD in normal skin versus diabetic skin. Methods: The expression of EC-SOD protein was evaluated by western blotting in 6 diabetic skin tissue samples and 6 normal skin samples. Immunohistochemical staining was also carried out to confirm the EC-SOD expression level in the 6 diabetic skin tissue samples. Results: The western blotting showed significantly lower EC-SOD protein expression in the diabetic skin tissue than in the normal tissue. Immunohistochemical examination of EC-SOD protein expression supported the western blotting analysis. Conclusion: Diabetic skin tissues express a relatively small amount of EC-SOD protein and may not be protected against oxidative stress. We believe that EC-SOD is related to the altered metabolic state in diabetic skin, which elevates ROS production.
( Bum Joon Ko ),( Seung Il Choi ),( Sang Jin Oh ),( Kyung O Kim ),( Jong Suk Lee ),( Sang Hoon Lee ),( Moon Kyun Cho ) 대한피부과학회 2013 대한피부과학회 학술발표대회집 Vol.65 No.2
Background: Diabetes is characterized by chronic hyperglycemia, and hyperglycemia could Increase Reactive Oxygen Species (ROS) production from the mitochondrial electron transport chain. The formation of ROS in cells induces oxidative stress and activates oxidative damage-inducing genes. There is no research on oxidative damage-related genes AKR1C3 protein levels in human diabetic skin. We explored the expression of AKR1C3 in diabetic skin compared with normal skin tissue. Objectives: To compare the expression of AKR1C3 in normal skin versus diabetic skin. Methods: AKR1C3 expression was evaluated by western blotting in 6 diabetic skin tissue samples and 6 normal skin samples. Immunohistochemical staining was carried out to analyze AKR1C3 expression in the 6 diabetic skin tissue samples. Results: The western blotting showed a significant reduction in AKR1C3 protein expression in diabetic skin tissue compared to normal tissue. Immunohistochemical examination of AKR1C3 showed that it was weakly expressed in all diabetic skin samples. Conclusion: We believe that AKR1C3 is related to diabetic skin in an altered metabolic state which elevates ROS production.
( Bum Joon Ko ),( Ga Hee Jung ),( Yung Lip Park ),( Jong Suk Lee ),( Kyu Uang Whang ),( Sung Yul Lee ) 대한피부과학회 2014 대한피부과학회지 Vol.52 No.10
Melasma is a relatively common skin disorder associated with dark, brown, symmetrical patches of hyperpigmentation involving the sun-exposed areas of the face. While various treatments are currently being used, there is no treatment regarded as entirely satisfactory1,2. Recently, the low-fluence 1064 nm Q-switched Nd:YAG (QSNY) laser has bee shown to be an effective and safe treatment option for patients with melasma1. Additionally, topical, intralesional tranexamic acid administration has been reported to improve clinical efficacy in melasma treatment2. Therefore, we attempted to treat patients with melasma using oral tranexamic acid and QSNY laser combination therapy. Two female patients, aged 38 and 43 years (Fitzpatrick skin type IV), were observed to have symmetric, multi-size, brown-colored patches on the malar area that had onset several weeks prior to examination (Fig. 1A, 2A). They both had normal menstruation with no significant past medical history. They were diagnosed with melasma based upon clinical appearance. The severity of the melasma was assessed using the modified Melasma Area and Severity Index (mMASI), with scores of 7.5 and 7.8. We began to treat for melasma with a combination of oral tranexamic acid (500 mg twice daily) and once-weekly use of the QSNY laser (Revlite®, HOYA ConBio, USA) set at 1,064 nm wavelength, 8 mm spot size, and 2.8 J/cm2. After 12 weeks, their melasma lesions greatly improved without complications, and mMASI scores decreased to 4.8 and 5.0 (Fig. 1B, 2B). Melasma may be treated using various therapeutic methods including topical or oral agents, chemical peeling, or laser treatment. These methods have been used alone or together as a form of combination therapy1. However, a satisfactory treatment regimen has yet to be found for patients with melasma and dark skin. QSNY treatment is based on photothermal and photomechanical interactions induced by selective photothermolysis. The 1064 nm QSNY laser can cause dermal and epidermal melanosome rupture in melanocytes and destructionof dermal melanophages1. Recently, the use of the 1064 nm QSNY laser has become increasingly referred to as “laser toning” for melasma in Asian countries. Although multiple passes of the low-fluence laser are delivered to obtain clinical improvement with less downtime in laser toning, it is possible to cause painful swelling and post- inflammatory hyper- or hypo-pigmentation1. Tranexamic acid is used as a hemostatic agent due to its selective antifibrolytic action. More recently, tranexamic acid has been used in the treatment of hyperpigmentation. Ultraviolet irradiation induces plasminogen activator synthesis and increases plasmin activity in keratinocytes and stimulates the release of arachidonic acid. Free arachidonic acid stimulates melanogenesis via its metabolite, prostaglandin. Tranexamic acid attaches to the lysine-binding site of plasminogen activator, which inhibits the plasminogen/ plasmin system. This results in interference with keratinocyte- melanocyte interactions and lower arachidonic acid and prostaglandin levels2,3. This mechanism down-regulates the tyrosine activity of melanocytes, resulting in improvement in patients with melasma hyperpigmentation lesions. Karn et al.4 reported that the addition of oral tranexamic acid provided rapid and sustained improvement in the treatment of melasma as compared to routine topical therapies only. Histologically, tranexamic acid decreases the epidermal pigmentation associated with melasma and also reverses melasma-related dermal changes, such as increased numbers of vessels and mast cells3. Side effects of tranexamic acid, such as gastrointestinal discomfort and hypomenorrhea, were observed in 5.4-8.1%of patients in 1 study; however, no severe complications were found until 6 months had passed, and the recurrence of melasma was observed in only a small portion of treated patients3. Currently, there are no long-term follow-up studies regarding this combination therapy. A 4-week follow-up study showed that in combination with low- fluence QSNY, oral tranexamic acid enhanced the efficacy of laser treatments, and reduced the risk of laser side effects by allowing for longer laser treatment intervals5. However, the treatment of melasma remains challenging due to its frequent recurrence, even after successful removal of lesions. Therefore, a long-term follow-up study of ongoing treatment is needed.We observed improvement in our patients with melasma after oral tranexamic acid and QSNY laser treatment. Therefore, we suggest that combination therapy using tranexamic acid and the QSNY laser should be considered as an effective modality for the treatment of melasma.
다양한 피부 종양에서 c-Jun과 JunB 발현에 관한 연구
고범준 ( Bum Joon Ko ),조문균 ( Moon Kyun Cho ),박영립 ( Young Lip Park ),이종석 ( Jong Suk Lee ),이증훈 ( Jeung Hoon Lee ),황규왕 ( Kyu Uang Whang ) 대한피부과학회 2014 大韓皮膚科學會誌 Vol.52 No.4
Background: c-Jun along with JunB, JunD, and the Fos group proteins comprise the core members of the activatorprotein 1 (AP1) family of transcription factors. Recently, many studies have demonstrated the key roles of AP1 inregulating a wide spectrum of biological processes, including tumorigenesis. We therefore hypothesized that c-Junand JunB influence the differentiation and malignant change of various skin tumors. Objective: We measured the expression levels of c-Jun and JunB in different skin tumors. Methods: The expressions of c-Jun and JunB were examined by performing the immunohistochemical staining of 55specimens of skin tumors, including 13 cases of seborrheic keratosis, 4 cases of keratoacanthoma, 9 cases of actinickeratosis, 4 cases of Bowen’s disease, 4 cases of basal cell carcinoma, 16 cases of squamous cell carcinoma, and5 cases of malignant melanoma. Results: Immunohistochemical analysis of the skin tumor tissue samples revealed a significantly higher expressionof c-Jun in malignant skin tumors (basal cell carcinoma, squamous cell carcinoma, malignant melanoma) than inbenign (seborrheic keratosis, keratoacanthoma) or premalignant skin tumors (actinic keratosis, Bowen``s disease). Theexpression of JunB, however, was significantly lower in malignant skin tumors than in benign skin tumors. Conclusion: These findings showed that c-Jun has a positive association with skin malignancies, while JunB has anegative association with skin malignancies. The role of AP1 as key regulators of cell proliferation and epidermaltumor progression is suggested.