Viral Agents as Potential Drivers of Diffuse Large B-Cell Lymphoma Tumorigenesis
Esma Bilajac,
Lejla Mahmutović,
Kenneth Lundstrom,
Una Glamočlija,
Jasmin Šutković,
Abas Sezer,
Altijana Hromić-Jahjefendić
Affiliations
Esma Bilajac
Department of Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, International University of Sarajevo, Hrasnička cesta 15, 71000 Sarajevo, Bosnia and Herzegovina
Lejla Mahmutović
Department of Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, International University of Sarajevo, Hrasnička cesta 15, 71000 Sarajevo, Bosnia and Herzegovina
Kenneth Lundstrom
PanTherapeutics, Route de Lavaux 49, CH1095 Lutry, Switzerland
Una Glamočlija
Department of Pharmaceutical Biochemistry and Laboratory Diagnostics, University of Sarajevo, Faculty of Pharmacy, Zmaja od Bosne 8, 71 000 Sarajevo, Bosnia and Herzegovina
Jasmin Šutković
Department of Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, International University of Sarajevo, Hrasnička cesta 15, 71000 Sarajevo, Bosnia and Herzegovina
Abas Sezer
Department of Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, International University of Sarajevo, Hrasnička cesta 15, 71000 Sarajevo, Bosnia and Herzegovina
Altijana Hromić-Jahjefendić
Department of Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, International University of Sarajevo, Hrasnička cesta 15, 71000 Sarajevo, Bosnia and Herzegovina
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.
