Inflammation plays a crucial role in wound healing and the host immune response following pathogenic invasion. However, unresolved chronic inflammation can result in tissue fibrosis and genetic alterations that contribute to the pathogenesis of human diseases such as cancer. Recent scientific advancements exploring the underlying mechanisms of malignant cellular transformations and cancer progression have exposed significant disparities between pediatric and adult-onset cancers. For instance, pediatric cancers tend to have lower mutational burdens and arise in actively developing tissues, where cell-cycle dysregulation leads to gene, chromosomal, and fusion gene development not seen in adult-onset counterparts. As such, scientific findings in adult cancers cannot be directly applied to pediatric cancers, where unique mutations and inherent etiologies remain poorly understood. Here, we review the role of chronic inflammation in processes of genetic and chromosomal instability, the tumor microenvironment, and immune response that result in pediatric tumorigenesis transformation and explore current and developing therapeutic interventions to maintain and/or restore inflammatory homeostasis.
炎症在伤口愈合及病原体入侵后的宿主免疫应答中起着关键作用。然而，未缓解的慢性炎症可能导致组织纤维化和基因改变，进而促进癌症等人类疾病的发生发展。近期关于恶性细胞转化与癌症进展机制的研究揭示了儿童与成人癌症间的显著差异。例如，儿童癌症通常具有较低的突变负荷，且多发生于活跃发育的组织中，其细胞周期失调会导致基因、染色体及融合基因的异常变化，这些特征在成人癌症中较为罕见。因此，成人癌症的研究成果不能直接应用于儿童癌症，后者独特的突变模式和内在病因机制仍不明确。本文综述了慢性炎症在基因与染色体不稳定性、肿瘤微环境及免疫应答中的作用，探讨其如何导致儿童肿瘤发生转化，并评述当前及新兴的旨在维持或恢复炎症稳态的治疗策略。
肿瘤(癌症)患者之家