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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.
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
Subject
Medicine and Pharmacology, Immunology and Allergy
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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