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Progress in understanding melanoma propagation

机译:黑色素瘤扩散的了解进展

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摘要

Melanoma, like most cancers, is a disease that wreaks havoc mostly through its propensity to spread and establish secondary tumors at sites that are anatomically distant from the primary tumor. The consideration of models of cancer progression is therefore important to understand the essence of this disease. Previous work has suggested that melanoma may propagate according to a cancer stem cell (CSC) model in which rare tumorigenic and bulk non‐tumorigenic cells are organized into stable hierarchies within tumors. However, recent studies using assays that are more permissive for revealing tumorigenic potential indicate that it will not be possible to cure patients by focusing research and therapy on rare populations of cells within melanoma tumors. Studies of the nature of tumorigenic melanoma cells reveal that these cells may gain a growth, metastasis and/or therapy resistance advantage by acquiring new genetic mutations and by reversible epigenetic mechanisms. In this light, efforts to link the phenotypes, genotypes and epigenotypes of melanoma cells with differences in their in vivo malignant potential provide the greatest hope of advancing the exciting progress finally being made against this disease.
机译:像大多数癌症一样,黑色素瘤是一种造成破坏的疾病,主要是因为它倾向于在解剖上远离原发肿瘤的部位扩散和建立继发性肿瘤。因此,对癌症进展模型的考虑对于理解这种疾病的实质很重要。先前的研究表明,黑色素瘤可能会按照癌症干细胞(CSC)模型传播,在这种模型中,稀有的致瘤细胞和大量非致瘤细胞被组织成稳定的肿瘤层次。但是,最近的研究使用更宽松的方法来揭示致瘤潜力,表明不可能通过将研究和治疗集中于黑色素瘤肿瘤内的稀有细胞群来治愈患者。对致瘤性黑色素瘤细胞性质的研究表明,这些细胞可通过获得新的基因突变和通过可逆的表观遗传机制获得生长,转移和/或治疗耐药性优势。有鉴于此,将黑素瘤细胞的表型,基因型和表型与体内恶性潜能的差异联系起来的努力提供了最大的希望,以推动针对这种疾病的激动人心的进展。

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