Johansson Magnus, Tan Tingting, de Visser Karin E, Coussens Lisa M
Department of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
J Cell Biochem. 2007 Jul 1;101(4):918-26. doi: 10.1002/jcb.21230.
Chronic inflammation is a contributing factor to overall cancer risk as well as cancer promotion and progression; however, pathways regulating onset of cancer-promoting inflammatory responses are still poorly understood. Clinical data suggest that deficient anti-tumor cell-mediated immunity, in combination with enhanced pro-tumor humoral and/or innate immunity (inflammation), are significant factors influencing malignant outcome. Here, we discuss therapeutic implications from clinical data and experimental studies using de novo immune-competent mouse models of cancer development that together are revealing molecular and cellular mechanisms underlying interactions between immune cells and evolving neoplastic cells that regulate cancer outcome. Understanding the functionally significant links between adaptive and innate immunity that regulate cancer development will open new therapeutic opportunities to manipulate aspects of immunobiology and minimize lethal effects of cancer development.
慢性炎症是导致整体癌症风险以及癌症促进和进展的一个因素;然而,调节促癌炎症反应发生的途径仍知之甚少。临床数据表明,抗肿瘤细胞介导的免疫缺陷,与增强的促肿瘤体液和/或先天免疫(炎症)相结合,是影响恶性结局的重要因素。在此,我们讨论临床数据和使用癌症发生的从头免疫活性小鼠模型的实验研究的治疗意义,这些研究共同揭示了免疫细胞与不断演变的肿瘤细胞之间相互作用的分子和细胞机制,这些机制调节癌症结局。了解调节癌症发生的适应性免疫和先天免疫之间功能上的重要联系,将为操纵免疫生物学方面并将癌症发展的致命影响降至最低带来新的治疗机会。