Nazarbayev University, 53 Kabanbay Batyr Avenue, Astana 010000, Kazakhstan.
Infect Agent Cancer. 2012 Aug 8;7(1):18. doi: 10.1186/1750-9378-7-18.
The regulation of cancerous tumor development is converged upon by multiple pathways and factors. Besides environmental factors, gastrointestinal (GI) tract cancer can be caused by chronic inflammation, which is generally induced by bacteria, viruses, and parasites. The role of these inducers in cancer development, cell differentiation and transformation, cell cycle deregulation, and in the expression of tumor-associated genes cannot be ignored. Although Helicobacter pylori activates many oncogenic pathways, particularly those in gastric and colorectal cancers, the role of viruses in tumor development is also significant. Viruses possess significant oncogenic potential to interfere with normal cell cycle control and genome stability, stimulating the growth of deregulated cells. An increasing amount of recent data also implies the association of GI cancers with bacterial colonization and viruses. This review focuses on host-cell interactions that facilitate primary mechanisms of tumorigenesis and provides new insights into novel GI cancer treatments.
癌症肿瘤的发展受到多种途径和因素的调节。除了环境因素外,胃肠道(GI)癌症还可能由慢性炎症引起,这种炎症通常是由细菌、病毒和寄生虫引起的。这些诱导物在癌症发展、细胞分化和转化、细胞周期失控以及肿瘤相关基因表达中的作用不容忽视。虽然幽门螺杆菌激活了许多致癌途径,特别是在胃癌和结直肠癌中,但病毒在肿瘤发展中的作用也很重要。病毒具有显著的致癌潜力,可以干扰正常的细胞周期控制和基因组稳定性,刺激不受调节的细胞生长。越来越多的最新数据也暗示了 GI 癌症与细菌定植和病毒之间的关联。本综述重点关注促进肿瘤发生的主要机制的宿主细胞相互作用,并为新型 GI 癌症治疗提供新的见解。