Francuz Tomasz, Czajka-Francuz Paulina, Cisoń-Jurek Sylwia, Wojnar Jerzy
Klinika Chorób Wewnętrznych i Chemioterapii Onkologicznej, Śląski Uniwersytet Medyczny w Katowicach.
Katedra i Zakład Biochemii, Śląski Uniwersytet Medyczny w Katowicach.
Postepy Hig Med Dosw (Online). 2016 Apr 27;70:360-6. doi: 10.5604/17322693.1200551.
The results of the latest research more and more bind development of neoplasms with the chronic inflammation. Inflammatory process creates microenvironment promoting development of neoplasms; as a result, malignant process start to develop in places, where chronic inflammation proceeds or regeneration of tissues takes place. Inflammatory cells not only create suitable microenvironment for development of neoplasms, but also excrete number of cytokines and growth factors promoting survival of a neoplasmatic cell and avoiding its apoptosis, promoting neoangiogenesis and metastases formation. Moreover, cytokines and other pro-inflammatory factors modulate expression of genes important in cancerogenesis, they also activate NFκB-dependent signaling pathways, which favor neoplasmatic cells to avoid apoptosis. On the other hand, oxidative stress accompanying chronic inflammation may promote mutagenesis, enabling that way the neoplasm development. The same cells and metabolic pathways are engaged in inflammatory and neoplasmatic processes, and development of cancer may be a consequence of loss of control over tissue regeneration during resolution of chronic inflammation. The role of most important cells and metabolic pathways in inflammatory process, which may lead to colon cancer, was discussed in this paper.
最新研究结果越来越多地将肿瘤的发展与慢性炎症联系起来。炎症过程创造了促进肿瘤发展的微环境;因此,恶性过程开始在慢性炎症发生或组织再生的部位发展。炎症细胞不仅为肿瘤的发展创造了适宜的微环境,还分泌多种细胞因子和生长因子,促进肿瘤细胞的存活并避免其凋亡,促进新血管生成和转移形成。此外,细胞因子和其他促炎因子调节癌症发生过程中重要基因的表达,它们还激活NFκB依赖性信号通路,这有利于肿瘤细胞避免凋亡。另一方面,伴随慢性炎症的氧化应激可能促进诱变,从而促进肿瘤发展。相同的细胞和代谢途径参与炎症和肿瘤过程,癌症的发展可能是慢性炎症消退过程中对组织再生失去控制的结果。本文讨论了炎症过程中可能导致结肠癌的最重要细胞和代谢途径的作用。