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首页> 外文期刊>The Journal of investigative dermatology. >BRAF Kinase Gene V599E Mutation in Growing Melanocytic Lesions.
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BRAF Kinase Gene V599E Mutation in Growing Melanocytic Lesions.

机译：生长中的黑素细胞病变中的BRAF激酶基因V599E突变。

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Mutations in the BRAF-gene are found in benign and malignant melanocytic lesions, >90% being a V599E mutation. This mutation results in constitutively active kinase function and increased colony formation in vitro. The biological impact of this mutation in vivo is still debated. To address this question, we used our digital epiluminescence image archive and retrospectively selected 49 melanocytic lesions, which did not meet the criteria of melanoma at the initial presentation. Mean 12 months later these lesions were excised because of increased size or changed structure and BRAF(V599E) mutations were analyzed. Among 36 growing lesions, BRAF(V599E) mutations were found in 16 (11 melanomas and 5 nevi). Among 13 lesions with structural changes, BRAF(V599E) mutations were found in 4 (3 melanomas and 1 nevus). Thirty-five randomly selected additional lesions with no changes during follow-up served as controls, all nevi by histology, and two of them showed a BRAF(V599E) mutation. Statistics revealed odds forthe presence of the BRAF(V599E) mutation being seven times higher in lesions with structural changes and 13 times higher in growing lesions as compared with lesions without changes. This raises the question if the V599E mutation determines lesions at risk developing into melanoma and if not, what are the mechanisms controlling growth stop in benign lesions?
机译：在良性和恶性黑素细胞病变中发现了BRAF基因的突变，其中> 90％是V599E突变。该突变导致组成型活性激酶功能并增加体外菌落形成。这种突变在体内的生物学影响尚有争议。为了解决这个问题，我们使用了我们的数字荧光发光图像档案，并回顾性地选择了49个黑色素细胞病变，这些病变在最初出现时不符合黑色素瘤的标准。平均12个月后，由于大小增加或结构改变而切除了这些病变，并分析了BRAF（V599E）突变。在36个正在生长的病变中，发现16个（11个黑色素瘤和5个痣）BRAF（V599E）突变。在13个结构改变的病变中，在4个（3个黑色素瘤和1个痣）中发现了BRAF（V599E）突变。在随访过程中无变化的35个随机选择的附加病变作为对照，根据组织学均显示为痣，其中两个显示出BRAF（V599E）突变。统计数据显示，与无变化的病变相比，存在结构变化的病变中存在BRAF（V599E）突变的几率高出7倍，在生长的病变中高出13倍。这就提出了一个问题，即V599E突变是否确定有风险发展为黑色素瘤的病灶，如果不是，控制良性病灶生长停止的机制是什么？

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