Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Genetic Events Inhibiting Apoptosis in Diffuse Large B-cell Lymphoma

Version 1 : Received: 13 April 2021 / Approved: 14 April 2021 / Online: 14 April 2021 (12:32:31 CEST)

A peer-reviewed article of this Preprint also exists.

Leveille, E.; Johnson, N.A.A. Genetic Events Inhibiting Apoptosis in Diffuse Large B Cell Lymphoma. Cancers 2021, 13, 2167. Leveille, E.; Johnson, N.A.A. Genetic Events Inhibiting Apoptosis in Diffuse Large B Cell Lymphoma. Cancers 2021, 13, 2167.

Journal reference: Cancers 2021, 13, 2167
DOI: 10.3390/cancers13092167

Abstract

Diffuse large B cell lymphoma (DLBCL) is curable with chemoimmunotherapy in ~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 discuss their implication for the future of DLBCL therapy.

Keywords

Diffuse large B cell lymphoma; non-Hodgkin lymphoma; apoptosis; genetics; BCL2; NF-kB; TP53; mutations; translocations; amplifications

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