Schwann Cell Features in Neurotropic Melanoma

Schwann cell features were found on ultrastructural examination of a neurotropic melanoma ( de novo type) of the lip. A neurotropic pattern of growth was retained in metastatic tumors in lymph nodes and lung. Melanin was not demonstrable in extra-epidermal tumor cells.     

白消一号方对黑素瘤细胞与角质形成细胞混合培养模型中黑素合成的影响

目的 体外构建黑素瘤细胞与角质形成细胞直接接触的混合培养模型,观察白消一号方对此模型中黑素瘤细胞的影响,探讨其治疗白癜风的药理作用.方法 分别培养角质形成细胞、黑素瘤细胞;体外构建黑素瘤细胞与角质形成细胞直接接触的混合培养模型,大鼠中药灌胃后不同时间取血清加入此模型中,用MTT法、多巴氧化法、及NaOH法.检测含药血清对黑素瘤细胞增殖、酪氧酸酶活性以及黑素合成的影响.结果 含药血清可促进黑素瘤细胞增殖,上调酪氨酸酶活性.增加黑素合成.结论 成功构建了黑素瘤细胞与角质形成细胞直接接触的混合培养模型,白消一号方作用于此模型对黑素瘤细胞增殖、酪氨酸酶活性及黑素的合成均呈促进作用.     

ERK在黑素瘤细胞和人正常黑色素细胞中的表达

目的:研究ERK1/2和P-ERK1/2在人正常黑色素细胞和黑素瘤细胞A375中表达强度的差异,并分析其意义。方法:从健康青年人阴茎包皮中分离并培养原代黑色素细胞;传代培养黑素瘤细胞A375;Western-blot检测两种细胞中ERK1/2和P-ERK1/2的表达强度,并进行统计比较。结果:ERK1/2、P-ERK1/2在黑素瘤细胞A375的表达强度均明显高于人正常黑色素细胞,差异均具有统计学意义(t值分别为17.75、104.39,P值均<0.01)。结论:黑素瘤的发生、发展可能与MAPK/ERK通路有关。     

麦冬皂苷B通过抑制PI3K/Akt/mTOR通路诱导人黑色素瘤A375细胞凋亡

目的探讨麦冬皂苷B对人黑色素瘤(Melanoma)A375细胞增殖,凋亡和细胞周期的影响以及相关机制。方法麦冬皂苷B处理A375细胞后,采用CCK-8法检测细胞活力;流式细胞仪检测A375细胞周期变化及细胞凋亡水平;Hoechst33258荧光染色法观察细胞凋亡形态;免疫印迹法检测麦冬皂苷B对A375细胞PI3K,p-PI3K,AKT,p-AKT蛋白以及通路下游凋亡相关蛋白Bcl-2,Bax,Cleaved-caspase3表达的影响。结果麦冬皂苷B能抑制A375细胞增殖活力及PI3K/Akt/mTOR通路的活化;麦冬皂苷B促进了A375细胞内Bax和Cleaved-caspase 3的表达,抑制Bcl-2表达,诱导人黑色素瘤细胞发生凋亡;麦冬皂苷B阻滞了A375细胞细胞周期,G0/G1期细胞比例明显升高;PI3K/Akt/mTOR通路活化剂IGF-1处理A375细胞后抑制了麦冬皂苷B的上述作用。结论麦冬皂苷B能抑制A375细胞的增殖,诱导细胞发生凋亡,阻滞细胞周期于G0/G1期。     

Pathologic Features of Pediatric Head and Neck Melanoma

Although malignant melanoma is rare in children, its incidence is steadily increasing, and it is potentially lethal. Few studies have examined head and neck melanoma in children, and even fewer have focused on the histopathologic features of melanoma within this anatomic region. To further the understanding of this entity, we examined pathology specimens from nine subjects age 18 years and younger with an original diagnosis of head or neck melanoma. The anatomic locations of these primary melanomas were the face and nose (n = 4), scalp and neck (n = 4), and ear (n = 1). The cases included seven superficial spreading melanomas, one unclassified (possible nodular) melanoma, and one melanoma in situ. No melanomas demonstrating desmoplastic or spindle cell morphologies were noted upon review. Breslow depth ranged from 0 to 2.9 mm (mean 1.3 mm, median 0.6 mm), with Clark level ranging from I to V. Pagetoid scatter was found in eight cases. Other notable features included regression (n = 5), ulceration (n = 1), and associated melanocytic nevus (n = 4). We did not observe any small cell variants; all nine cases had an epithelioid appearance. Nor was any melanoma‐associated mortality observed at last follow‐up (mean 60.4 mos, median 48 mos, range 2–174 mos). These histopathologic features were consistent with adult‐type melanoma, which is in agreement with other histopathologic studies of melanoma in children.