• Journal of Chest Surgery
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• 제43권1호
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• pp.117-119
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• 2010

맥락막 흑색종은 성인에서 가장 빈번한 안구 내 종양이다. 간, 폐, 뼈로 전이를 잘하며 그 예후는 나쁜 것으로 알려져 있다. 본 논문에서 저자들은 늑골 및 기관지에 전이된 맥락막 흑색종에 대하여 수술적 절제를 하였으며 이를 보고하고자 한다.

• 한방안이비인후피부과학회지
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• 제21권1호
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• pp.55-69
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• 2008

Objective : This study was designed to investigated effects of Gleditsia spina (GS) on human derived melanoma cells Methods : The genetic profile for the effect of medicine on human derived melanoma cells of SK-MEL-2, was measured by using microarray technique, and the functional analysis on these genes was conducted. The network of total protein interactions was measured by using cytoscape program. Results : Total 253 genes were up-regulated and 439 genes down-regulated in cells treated with GS. Genes induced or suppressed by GS were all mainly concerned with metabolic process, regulation of biological process and protein binding. Conclusion : Suggest the possibility of GS as anti-cancer drug and cosmetic agent, and also suggest that related mechanisms are involved in regulation of intra-cellular metabolism in melanoma cells.

• 한국식품위생안전성학회지
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• 제34권2호
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• pp.183-190
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• 2019

우르솔릭산은 항암, 항산화, 항염증 작용과 같은 다양한 효과를 지니고 있다. 본 연구에서는 우르솔릭산이 인간 흑색종 암세포인 A375SM과 A375P 세포에 항암효과가 있는지 확인하였다. 두 세포의 생존율은 MTT assay를 통하여 확인하였으며 증식률은 Wound healing assay로 확인하였다. 두 세포의 apoptotic body와 apoptosis 비율의 확인을 위한 DAPI 염색과 유세포 분석을 진행하였다. 그리고 웨스턴 블로팅을 통하여 흑색종 세포의 우르솔릭산의 농도에 따른 apoptosis 단백질의 유도를 조사하였다. 우르솔릭산의 처리 농도에 따라 흑색종 세포의 생존율 감소와 증식률 감소를 확인하였다. DAPI 염색을 통하여 우르솔릭산의 농도가 증가함에 따라 흑색종 세포의 염색체 응축이 농도 의존적으로 증가하였고, 유세포 분석을 통하여 우르솔릭산에 대하여 농도 의존적으로 흑색종 세포의 apoptosis 비율의 증가를 확인하였다. 그리고 웨스턴 블로팅을 통해 흑색종 세포 A375SM과 A375P의 우르솔릭산 $12{\mu}M$ 농도에서 cleaved-PARP와 Bax의 증가와 Bcl-2의 감소를 확인하였다. 본 연구는 우르솔릭산의 농도를 0 에서 $20{\mu}M$ 수준의 저농도에서 진행하였으며, 물질 처리 후 24 시간 뒤 결과를 가지고 분석하였다. 본 연구의 결과로 보아 우르솔릭산은 흑색종 세포 A375SM과 A375P에서 apoptosis 관련 단백질들의 조절을 통해 항암효과를 일으키는 것으로 사료된다.

• Asian Pacific Journal of Cancer Prevention
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• 제15권23호
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• pp.10451-10456
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• 2015

Background: We defined melanoma distribution in a large series of Turkish patients and evaluated the prognostic parameters of melanomas. Materials and Methods: A total of 1574 patients' data was retrospectively collected at 18 centers in Turkey. Demographic characteristics were questioned and noted. Prognostic parametres were evaluated based on sentinel lymph node involvement. Results: Mean age was 56.7 (4-99) years. While 844 (53.6%) cases were male, 730 (46.4%) cases were female. One thousand four hundred forty-seven (92%) cases were invasive melanoma and 127 (8%) cases were in-situ melanoma. The most common histopathological form was the superficial spreading melanoma (SSM) which was found in 549 patients (37.9%). It was followed by nodular melanoma in 379 (26.2%), acral lentiginous melanoma (ALM) in 191 (13.2%) and lentigo maligna melanoma in 132 (9.1%), respectively. On univariate analysis, lymphovascular invasion (p<0.001), tumor thickness (p<0.001), histopathological subtype (p<0.001), Clark level (p=0.001), ulceration (p<0.001), ${\geq}6/mm^2$ mitosis (p=0.005), satellite formation (p=0.001) and gender (p=0.03) were found to be associated with sentinel lymph node positivity. Regression was associated with sentinel lymph node negativity (p=0.017). According to multivariate analysis, lymphovascular invasion and tumor thickness were significant independent predictive factors of SLN positivity. Patient age, tumor localization, precursor lesions, lymphocytic infiltration and neurotropism were not related with sentinel lymph node involvement. Conclusions: In this retrospective analysis, it was found that the prevalence of SSM is at a lower rate while the prevalence of ALM is at a higher rate when compared to western countries. According to Breslow index; most of the melanoma lesions' thickness were greater than 2 mm, corresponding Clark IV. Vascular invasion and tumor thickness are the most important factors for sentinel lymph node involvement.

• Asian Pacific Journal of Cancer Prevention
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• 제16권2호
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• pp.699-705
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• 2015

Vemurafenib has recently been used as drug for treatment of melanomas with $BRAF^{V600E}$ mutation. Unfortunately, treatment with only vemurafenib has not been sufficiently effective, with recurrence after a short period. In this study, three vemurafenib-resistant $BRAF^{V600E}$ melanoma cell lines, $A375P^R$, $A375M^R$ and SKMEL-$28^R$, were established from the original A375P, A375M and SKMEL-28 cell lines. Examination of the molecular mechanisms showed that the phosphorylation levels of MEK and ERK, which play key roles in the RAS/RAF/MEK/ERK signaling pathway, were reduced in these three cell lines, with increased phosphorylation levels of pAKTs limited to SKMEL-$28^R$ cells. Treatment of SKMEL-$28^R$ cells with 100 nM paclitaxel resulted in increased apoptosis and decreased cellular proliferation, invasion and colony formation via reduction of expression levels of EGFR and pAKTs. Moreover, vemurafenib-induced pAKTs in SKMEL-$28^R$ were decreased by treatment with an AKT inhibitor, MK-2206. Taken together, our results revealed that resistance mechanisms of $BRAF^{V600E}$-mutation melanoma cells to vemurafenib depended on the cell type. Our results suggested that paclitaxel should be considered as a drug in combination with vemurafenib to treat melanoma cells.

• Journal of Gastric Cancer
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• 제14권4호
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• pp.279-283
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• 2014

We report a case of primary gastric malignant melanoma that was diagnosed after curative resection but initially misdiagnosed as adenocarcinoma. A 68-year-old woman was referred to our department for surgery for gastric adenocarcinoma presenting as a polypoid lesion with central ulceration located in the upper body of the stomach. The preoperative diagnosis was confirmed by endoscopic biopsy. We performed laparoscopic total gastrectomy, and the final pathologic evaluation led to the diagnosis of primary gastric malignant melanoma without a primary lesion detected in the body. To the best of our knowledge, primary gastric malignant melanoma is extremely rare, and this is the first case reported in our country. According to the literature, it has aggressive biologic activity compared with adenocarcinoma, and curative resection is the only promising treatment strategy. In our case, the patient received an early diagnosis and underwent curative gastrectomy with radical lymphadenectomy, and no recurrence was noted for about two years.

• Asian Pacific Journal of Cancer Prevention
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• 제13권8호
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• pp.3795-3802
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• 2012

Cochinchina momordica seeds (CMS) have been widely used due to antitumor activity by Mongolian tribes of China. However, the details of the underlying mechanisms remain unknown. In the present study, we found that an EtOAc (ethyl ester) extract of CMS (CMSEE) induced differentiation and caused growth inhibition of melanoma B16 F1 cells. CMSEE at the concentration of $5-200{\mu}g/ml$ exhibited strongest anti-proliferative effects on B16 F1 cells among other CMS fractions (water or petroleum ether). Moreover, CMSEE induced melanoma B16 F1 cell differentiation, characterized by dendrite-like outgrowth, increasing melanogenesis production, as well as enhancing tyrosinase activity. Western blot analysis showed that sustained phosphorylation of p38 MAP accompanied by decrease in ERK1/2 and JNK dephosphorylation were involved in CMSEE-induced B16 F1 cell differentiation. Notably, 6 compounds that were isolated and identified may be responsible for inducing differentiation of CMSEE. These results indicated that CMSEE contributes to the differentiation of B16 F1 cells through modulating MAPKs activity, which may throw some light on the development of potentially therapeutic strategies for melanoma treatment.

• Asian Pacific Journal of Cancer Prevention
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• 제17권12호
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• pp.5281-5285
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• 2016

Background: Brachytherapy is the most commonly used conservative treatment for the uveal melanoma. The aim of this study was to evaluate therapeutic results of Ruthenium-106 plaque brachytherapy in the management of localized uveal melanoma cases. Methods: We reviewed retrospectively the clinical records of all patients treated in our department for an uveal melanoma, undergoing Ruthenium-106 plaque brachytherapy, from January 1996 to December 2015. We focused on clinical features, therapeutic characteristics, local and distant tumor control and side effects. Results: Nineteen patients were enrolled in our study. Mean age was 56.2 years (28-79) and the sex ratio was 1.37:1 males to females. Diagnosis was made on the basis of ophthalmological clinical examination, angiography, ultrasound and/or magnetic resonance. Median tumor diameter was 9.7 mm (6-13) and median thickness 4.4 mm (2.5-8). The dose of Ruthenium-106 plaque brachytherapy prescribed to the apex of each tumor was 70 Gy in all cases. The median radiation dose to the sclera surface was 226.4 Gy (range: 179.6-342.3) and the median total application time 115.2 hours (range: 27 to 237). After a median follow-up of 61.5 months, local control was achieved in 17 patients (89%): 16 demonstrated a partial tumor response and 1 tumor stabilization. Two patients suffered local progression leading to enucleation, one dying of hepatic metastasis. Radiation-induced complications were cataracts in 3 cases and vitreal hemorrhage in 2. Conclusion: Ruthenium-106 plaque brachytherapy is an efficient treatment for localized uveal melanoma, offering good local control with low toxicity.

• International Journal of Oral Biology
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• 제37권4호
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• pp.189-195
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• 2012

Resistance to the induction of apoptosis is a possible mechanism by which tumor cells can survive anti-neoplastic treatments. Melanoma is notoriously resistant to anti-neoplastic therapy. Previous studies have demonstrated focal adhesion kinase (FAK) overexpression in melanoma cell lines. Given its probable role in mediating resistance to apoptosis, many researchers have sought to determine whether the downregulation of FAK in melanoma cells would confer a greater sensitivity to anti-neoplastic agents. Genistein is a known inhibitor of protein-tyrosine kinase (PTK), which may attenuate the growth of cancer cells by inhibiting the PTK-mediated signaling pathway. This present study was undertaken to investigate the effect of genistein on the expression of FAK and cell cycle related proteins in the G361 melanoma cell line. Genistein was found to have a preferential cytotoxic effect on G361 melanoma cells over HaCaT normal keratinocytes. Genistein decreased the expression of 125 kDa phosphotyrosine kinase and the FAK protein in particular. Genistein treatment did not affect the expression of p53 in G361 cells in which p21 is upregulated. The expression of cyclin B and cdc2 was downregulated by genistein treatment. Taken together, our data indicate that genistein induces the decreased proliferation of G361 melanoma cells via the inhibition of FAK expression and regulation of cell cycle genes. This suggests that the use of genistein may be a viable approach to future melanoma treatments.

• BMB Reports
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• 제54권12호
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• pp.608-613
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• 2021

Melanoma, the most serious type of skin cancer, exhibits a high risk of metastasis. Although chemotherapeutic treatment for metastatic melanoma improves disease outcome and patient survival, some patients exhibit resistance or toxicity to the drug treatment regime. OTUB1 is a deubiquitinating enzyme overexpressed in several cancers. In this study, we investigated the effects of inhibiting OTUB1 expression on melanoma-cell proliferation and viability and identified the underlying molecular mechanism of action of OTUB1. We did endogenous OTUB1 knockdown in melanoma cells using short interfering RNA, and assessed the resulting phenotypes via MTT assays, Western blotting, and cell-cycle analysis. We identified differentially expressed genes between OTUB1-knockdown cells and control cells using RNA sequencing and confirmed them via Western blotting and reverse transcription polymerase chain reaction. Furthermore, we investigated the involvement of apoptotic and cell survival signaling pathways upon OTUB1 depletion. OTUB1 depletion in melanoma cells decreased cell viability and caused simultaneous accumulation of cells in the sub-G1 phase, indicating an increase in the apoptotic-cell population. RNA sequencing of OTUB1-knockdown cells revealed an increase in the levels of the apoptosis-inducing protein TRAIL. Additionally, OTUB1-knockdown cells exhibited increased sensitivity to PLX4032, a BRAF inhibitor, implying that OTUB1 and BRAF act collectively in regulating apoptosis. Taken together, our findings show that OTUB1 induces apoptosis of melanoma cells in vitro, likely by upregulating TRAIL, and suggest that approaches targeting OTUB1 can be developed to provide novel therapeutic strategies for treating melanoma.