Oxidative Stress and Inflammation in B-Cell Lymphomas

Abstract

Mature lymphoid neoplasms arise de novo or by the transformation of more indolent lymphomas in a process that relies on the stepwise accumulation of genomic and transcriptomic alterations. The microenvironment and neoplastic precursor cells are heavily influenced by pro-inflammatory signaling, regulated in part by oxidative stress and inflammation. Reactive oxygen species (ROSs) are by-products of cellular metabolism able to modulate cell signaling and fate. Moreover, they play a crucial role in the phagocyte system, which is responsible for antigen presentation and the selection of mature B and T cells under normal conditions. Imbalances in pro-oxidant and antioxidant signaling can lead to physiological dysfunction and disease development by disrupting metabolic processes and cell signaling. This narrative review aims to analyze the impact of reactive oxygen species on lymphomagenesis, specifically examining the regulation of microenvironmental players, as well as the response to therapy for B-cell-derived non-Hodgkin lymphomas. Further research is needed to investigate the involvement of ROS and inflammation in the development of lymphomas, which may unravel disease mechanisms and identify innovative therapeutic targets.