Disruption of tissue function activates cellular stress which triggers a number of mechanisms that protect the tissue from further damage. These mechanisms involve a number of homeostatic modules, which are regulated at the level of gene expression by the transactivator NF-κB. This transcription factor shifts between activation and repression of discrete, cell-dependent gene expression clusters. Some of its target genes provide feedback to NF-κB itself, thereby strengthening the inflammatory response of the tissue and later terminating inflammation to facilitate restoration of tissue homeostasis. Disruption of key feedback modules for NF-κB in certain cell types facilitates the survival of clones with genomic aberrations, and protects them from being recognized and eliminated by the immune system, to enable thereby carcinogenesis.

中文翻译：

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炎症和组织稳态：生理和恶性进展中的NF-κB系统。

组织功能的破坏会激活细胞应力，从而触发许多保护组织免受进一步损害的机制。这些机制涉及许多稳态模块，其由反式激活因子NF-κB在基因表达水平上调节。该转录因子在离散的细胞依赖性基因表达簇的激活和抑制之间转移。其某些靶基因向NF-κB本身提供反馈，从而增强组织的炎症反应，并随后终止炎症以促进组织稳态的恢复。某些细胞类型中NF-κB关键反馈模块的破坏促进了具有基因组异常的克隆的存活，并保护了它们免于被免疫系统识别和消除，从而实现了癌变。