文章：

甲状腺滤泡细胞衍生的癌症发病机制

Pathogenesis of cancers derived from thyroid follicular cells

原文发布日期：2023-07-12

DOI: 10.1038/s41568-023-00598-y

类型: Review Article

开放获取: 否

英文摘要：

The genomic simplicity of differentiated cancers derived from thyroid follicular cells offers unique insights into how oncogenic drivers impact tumour phenotype. Essentially, the main oncoproteins in thyroid cancer activate nodes in the receptor tyrosine kinase–RAS–BRAF pathway, which constitutively induces MAPK signalling to varying degrees consistent with their specific biochemical mechanisms of action. The magnitude of the flux through the MAPK signalling pathway determines key elements of thyroid cancer biology, including differentiation state, invasive properties and the cellular composition of the tumour microenvironment. Progression of disease results from genomic lesions that drive immortalization, disrupt chromatin accessibility and cause cell cycle checkpoint dysfunction, in conjunction with a tumour microenvironment characterized by progressive immunosuppression. This Review charts the genomic trajectories of these common endocrine tumours, while connecting them to the biological states that they confer.

摘要翻译： 

源自甲状腺滤泡细胞的分化型癌症在基因组上的简单性，为我们理解致癌驱动因子如何影响肿瘤表型提供了独特视角。本质上，甲状腺癌中的主要癌蛋白通过激活受体酪氨酸激酶-RAS-BRAF通路中的关键节点，以与其特定生化作用机制相符的程度持续诱导MAPK信号传导。MAPK信号通路的活性强度决定了甲状腺癌生物学的关键要素，包括分化状态、侵袭特性以及肿瘤微环境的细胞组成。疾病进展源于驱动永生化、破坏染色质可及性并导致细胞周期检查点功能障碍的基因组损伤，同时伴随着以进行性免疫抑制为特征的肿瘤微环境。本综述描绘了这些常见内分泌肿瘤的基因组演变轨迹，并将其与所对应的生物学状态相联系。

原文链接：

Pathogenesis of cancers derived from thyroid follicular cells