Abstract
DNA repair plays an essential role in protecting cells that are repeatedly exposed to endogenous or exogenous insults that can induce varying degrees of DNA damage. Any defect in DNA repair mechanisms results in multiple genomic changes that ultimately may result in mutation, tumor growth, and/or cell apoptosis. Furthermore, impaired repair mechanisms can also lead to genomic instability, which can initiate tumorigenesis and development of hematological malignancy. This review discusses recent findings and highlights the importance of DNA repair components and the impact of their aberrations on hematological malignancies.
Highlights
DNA damage leads to changes in the DNA double-helical structure [1]
These components are stimulated by double strand breaks (DSB) and replication protein A (RPA) that attach to single-stranded DNA [30]
This study indicates that MK-8776 treatment is more potent when combined with a histone deacetylase (HDAC) inhibitor (HDACI) in acute myeloid leukemia (AML) cell lines and AML primary cells [121]
Summary
DNA damage leads to changes in the DNA double-helical structure [1]. Under normal physiological conditions, the DNA repair mechanism is activated in response to DNA damage in an attempt to correct the defected DNA and restore normal cell function [2]. It is important to note that lymphoma is associated with hereditary diseases such as ataxia-telangiectasia (A-T), Nijmegen breakage syndrome (NBS), and bloom syndrome, which exhibit genomic instability Particular mutations such as ataxia telangiectasia mutated (ATM) gene are associated with the defects in DNA repair mechanisms and are present in various cancers including acute leukemia [11]. Several hematological cancers such as CLL and AML have a poor prognosis and the use of PARP1 inhibitor, an inhibitor of the DNA repair pathway, has shown promising results in chemosensitization when treating with cytotoxic agents [12,13]. We have discussed and summarized the use of new and emerging therapeutic agents in this field
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