Department of Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, International University of Sarajevo, Hrasnička cesta 15, 71000 Sarajevo, Bosnia and Herzegovina.
PanTherapeutics, Route de Lavaux 49, CH1095 Lutry, Switzerland.
Viruses. 2022 Sep 22;14(10):2105. doi: 10.3390/v14102105.
Among numerous causative agents recognized as oncogenic drivers, 13% of total cancer cases occur as a result of viral infections. The intricacy and diversity of carcinogenic processes, however, raise significant concerns about the mechanistic function of viruses in cancer. All tumor-associated viruses have been shown to encode viral oncogenes with a potential for cell transformation and the development of malignancies, including diffuse large B-cell lymphoma (DLBCL). Given the difficulties in identifying single mechanistic explanations, it is necessary to combine ideas from systems biology and viral evolution to comprehend the processes driving viral cancer. The potential for more efficient and acceptable therapies lies in targeted medicines that aim at viral proteins or trigger immune responses to either avoid infection or eliminate infected or cancerous cells. In this review, we aim to describe the role of viral infections and their mechanistic approaches in DLBCL tumorigenesis. To the best of our knowledge, this is the first review summarizing the oncogenic potential of numerous viral agents in DLBCL development.
在被认为致癌的众多因素中,有 13%的癌症是由病毒感染引起的。然而,致癌过程的复杂性和多样性引发了人们对病毒在癌症中作用的机制功能的高度关注。所有与肿瘤相关的病毒都被证明编码具有潜在细胞转化和恶性肿瘤发展能力的病毒癌基因,包括弥漫性大 B 细胞淋巴瘤 (DLBCL)。鉴于确定单一机制解释存在困难,有必要结合系统生物学和病毒进化的观点来理解驱动病毒致癌的过程。更有效和可接受的治疗方法的潜力在于靶向药物,这些药物针对病毒蛋白或触发免疫反应,以避免感染或消除感染或癌变细胞。在这篇综述中,我们旨在描述病毒感染及其在 DLBCL 肿瘤发生中的机制方法的作用。据我们所知,这是第一篇总结众多病毒因子在 DLBCL 发展中的致癌潜力的综述。