Untangling the Epigenetic Imbalance in B cell Lymphoma
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EPIGENETICS (ATY LAU, SECTION EDITOR)
Untangling the Epigenetic Imbalance in B cell Lymphoma Rui Wu 1
# Springer Nature Switzerland AG 2020
Abstract Purpose of the Review Structural and functional genomics of B cell lymphoma identified several recurrent lesions in epigenetic machinery that drive disease pathogenesis. However, the functional relationship between these lesions and disease phenotype has not been well studied. This review is crafted with the aim to delineate pathologic derangements in the epigenetic system that underlies the imbalance and to identify opportunities for strategic design of novel therapeutic interventions by restoring the balance in epigenetic signaling of B cell lymphoma. Recent Findings Selective gain or loss of epigenetic machinery components at the genetic or proteomic level through various regulatory cues including genetic lesions and transcriptional or post-translational regulations often bring regulatory system functional imbalance. This also impinges upon our understanding of consequences when epigenetic regulation goes awry leading to loss of cellular identity and unchecked cellular proliferation, a hallmark of cancer. Such deregulations prompted by epigenetic imbalance are prone to spuriously activate proto-oncogene and/or cripple the tumor suppressor function to gain growthpromoting advantages, particularly in B cell lymphomagenesis. Often, the restoration of epigenetic balance through pharmacologic approaches caused synthetic lethality to neoplastic cells. Therefore, a detailed understanding needed to utilize these phenomena as novel therapeutic interventions targeting B cell lymphoma. Summary This review illustrates the previously underrepresented importance of epigenetic imbalance caused by genetic lesions and restoration of functional epigenetic balance as a novel treatment strategy for B cell lymphoma. Keywords Epigenetic . Lymphoma . Chromatin remodeling . Synthetic lethality . Polycomb . Trithorax
B cell lymphomas are the type of lymphoma affecting B cells at different stages of maturation. B cell lymphomas mostly originate from histological structures called germinal centers that develop during immune reaction for the generation and selection of B cells that produce high-affinity antibodies. B cells are particularly vulnerable to neoplastic transformation. The mechanisms that are utilized B cells for diversification of antibody can also spuriously generate genetic lesions in the form of chromosomal translocation or oncogenic mutations. These genetic lesions endow B cells with the relentless capacity of proliferation and survival. The development of sequencing approaches and their functional validation in recent years This article is part of the Topical Collection on Epigenetics * Rui Wu [email protected] 1
Department of Pathology and Laboratory Medicine, University of Pennsylvania, 610 Stellar-Chance, 422 Curie Blvd, Philadelphia, PA 19104, USA
identified several genetic lesions in epigenetic modulators that participate significantly in B cell lymphoma
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