Viral Agents as Potential Drivers of Diffuse Large B-Cell Lymphoma Tumorigenesis.
Esma BilajacLejla MahmutovićKenneth LundstromUna GlamočlijaJasmin ŠutkovićAbas SezerAltijana Hromić-JahjefendićPublished in: Viruses (2022)
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.
Keyphrases
- diffuse large b cell lymphoma
- sars cov
- epstein barr virus
- papillary thyroid
- immune response
- healthcare
- oxidative stress
- squamous cell carcinoma
- young adults
- stem cells
- mesenchymal stem cells
- induced apoptosis
- human health
- cancer therapy
- drug delivery
- lymph node metastasis
- bone marrow
- cell therapy
- inflammatory response
- signaling pathway
- climate change
- childhood cancer
- cell cycle arrest