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Melanoma invasion - current knowledge and future directions

机译：黑色素瘤入侵-当前的知识和未来的方向

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The acquisition of invasive behaviour is the key transition in the progression of benign melanocyte hyperplasia to life threatening melanoma. Understanding this transition and the mechanisms of invasion are the key to understanding why malignant melanoma is such a devastating disease and will aid treatment strategies. Underlying the invasive behaviour is increased cell motility caused by changes in cytoskeletal organization and altered contacts with the extra-cellular matrix (ECM). In addition, changes in the interactions of melanoma cells with keratinocytes and fibroblasts enable them to survive and proliferate outside their normal epidermal location. Proteomic and genomic initiatives are greatly increasing our knowledge of which gene products are deregulated in invasive and metastatic melanoma; however, the next challenge is to understand how these genes promote the invasion of melanoma cells. In recent years new models have been developed that more closely recapitulate the conditions of melanoma invasion in vivo. It is hoped that these models will give us a better understanding of how the genes implicated in melanoma progression affect the motility of melanoma cells and their interactions with the ECM, stromal cells and blood vessels. This review will summarise our current understanding of melanoma invasion and focus on the new model systems that can be used to study melanoma.
机译：侵袭性行为的获得是良性黑素细胞增生向威胁生命的黑色素瘤发展的关键转变。了解这种转变和侵袭的机制是理解为什么恶性黑色素瘤如此具有破坏性的疾病并将有助于治疗策略的关键。侵袭行为的根本是由于细胞骨架组织的变化和与细胞外基质（ECM）的接触改变引起的细胞运动性增强。另外，黑素瘤细胞与角质形成细胞和成纤维细胞相互作用的变化使它们能够在正常表皮位置之外生存和增殖。蛋白质组学和基因组学计划极大地增加了我们对哪些基因产物在侵袭性和转移性黑色素瘤中失活的认识。然而，下一个挑战是了解这些基因如何促进黑色素瘤细胞的侵袭。近年来，已经开发出了新的模型，该模型可以更紧密地概括体内黑色素瘤的入侵情况。希望这些模型能够使我们更好地理解与黑色素瘤进展有关的基因如何影响黑色素瘤细胞的运动以及它们与ECM，基质细胞和血管的相互作用。这篇综述将总结我们目前对黑色素瘤侵袭的理解，并将重点放在可用于研究黑色素瘤的新模型系统上。

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