Jutzi Jonas S, Pahl Heike L
Division of Molecular Hematology, University Hospital Freiburg, Center for Clinical Research, Breisacher Straße 66, 79106 Freiburg, Germany ; Spemann Graduate School of Biology and Medicine (SGBM), University of Freiburg, Albertstraße 19A, 79104 Freiburg, Germany ; Faculty of Biology, University of Freiburg, Schänzlestraße 1, 79104 Freiburg, Germany.
Division of Molecular Hematology, University Hospital Freiburg, Center for Clinical Research, Breisacher Straße 66, 79106 Freiburg, Germany.
Mediators Inflamm. 2015;2015:101987. doi: 10.1155/2015/101987. Epub 2015 Oct 12.
It has been known for some time that solid tumors, especially gastrointestinal tumors, can arise on the basis of chronic inflammation. However, the role of inflammation in the genesis of hematological malignancies has not been extensively studied. Recent evidence clearly shows that changes in the bone marrow niche can suffice to induce myeloid diseases. Nonetheless, while it has been demonstrated that myeloproliferative neoplasms (MPN) are associated with a proinflammatory state, it is not clear whether inflammatory processes contribute to the induction or maintenance of MPN. More provocatively stated: which comes first, the hen or the egg, inflammation or MPN? In other words, can chronic inflammation itself trigger an MPN? In this review, we will describe the evidence supporting a role for inflammation in initiating and promoting MPN development. Furthermore, we will compare and contrast the data obtained in gastrointestinal tumors with observations in MPN patients and models, pointing out the opportunities provided by novel murine MPN models to address fundamental questions regarding the role of inflammatory stimuli in the molecular pathogenesis of MPN.
一段时间以来,人们已经知道实体瘤,尤其是胃肠道肿瘤,可在慢性炎症的基础上发生。然而,炎症在血液系统恶性肿瘤发生中的作用尚未得到广泛研究。最近的证据清楚地表明,骨髓微环境的变化足以诱发髓系疾病。尽管如此,虽然已经证明骨髓增殖性肿瘤(MPN)与促炎状态有关,但尚不清楚炎症过程是否有助于MPN的诱导或维持。更具启发性地说:是先有鸡还是先有蛋,是炎症还是MPN?换句话说,慢性炎症本身能否引发MPN?在这篇综述中,我们将描述支持炎症在启动和促进MPN发展中起作用的证据。此外,我们将比较和对比在胃肠道肿瘤中获得的数据与在MPN患者及模型中的观察结果,指出新型小鼠MPN模型为解决关于炎症刺激在MPN分子发病机制中作用的基本问题所提供的机会。