AI Article Synopsis
- The TP53 gene and its pathway play a critical role in the development of various cancers, notably diffuse large B cell lymphoma (DLBCL), by regulating key processes like DNA repair and apoptosis.
- Dysfunction in TP53, caused by mutations and alterations, significantly contributes to the initiation and progression of lymphoma.
- Recent research has focused on understanding TP53's mechanisms in DLBCL and exploring new therapeutic strategies to address TP53 inactivation.
Article Abstract
The aberrations of TP53 gene and dysregulation of the TP53 pathway are important in the pathogenesis of many human cancers, including malignant lymphomas, especially for diffuse large B cell lymphoma (DLBCL). By regulating many downstream target genes or molecules, TP53 governs major defenses against tumor growth and promotes cellular DNA repair, apoptosis, autophagy, cell cycle arrest, signaling, transcription, immune or inflammatory responses and metabolism. Dysfunction of TP53, including microRNA regulations, copy number alterations of TP53 pathway and TP53 itself, dysregulation of TP53 regulators, and somatic mutations by abnormal TP53 function modes, play an important role in lymphoma generation, progression and invasion. The role of TP53 in DLBCL has been widely explored recently. In this review, we summarized recent advances on different mechanisms of TP53 in DLBCL and new therapeutic approaches to overcome TP53 inactivation.
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| http://dx.doi.org/10.1016/j.critrevonc.2015.08.006 | DOI Listing |
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