Genetic Events Inhibiting Apoptosis in Diffuse Large B Cell Lymphoma

Diffuse large B cell lymphoma (DLBCL) is curable with chemoimmunotherapy in similar to 65% of patients. One of the hallmarks of the pathogenesis and resistance to therapy in DLBCL is inhibition of apoptosis, which allows malignant cells to survive and acquire further alterations. Inhibition of apoptosis can be the result of genetic events inhibiting the intrinsic or extrinsic apoptotic pathways, as well as their modulators, such as the inhibitor of apoptosis proteins, P53, and components of the NF-kB pathway. Mechanisms of dysregulation include upregulation of anti-apoptotic proteins and downregulation of pro-apoptotic proteins via point mutations, amplifications, deletions, translocations, and influences of other proteins. Understanding the factors contributing to resistance to apoptosis in DLBCL is crucial in order to be able to develop targeted therapies that could improve outcomes by restoring apoptosis in malignant cells. This review describes the genetic events inhibiting apoptosis in DLBCL, provides a perspective of their interactions in lymphomagenesis, and discusses their implication for the future of DLBCL therapy.

Automated summary

Diffuse large B cell lymphoma (DLBCL) can be cured in around 65% of patients with chemoimmunotherapy. Inhibition of apoptosis is a key factor in the pathogenesis and resistance to therapy in DLBCL, involving genetic events that suppress apoptotic pathways and their regulators like inhibitor of apoptosis proteins, P53, and NF-kB pathway components. Understanding and targeting these factors is crucial for developing improved therapies for DLBCL.