DNA repair pathways as guardians of the genome: Therapeutic potential and possible prognostic role in hematologic neoplasms

Rahimian, E. and Amini, A. and Alikarami, F. and Pezeshki, S.M.S. and Saki, N. and Safa, M. (2020) DNA repair pathways as guardians of the genome: Therapeutic potential and possible prognostic role in hematologic neoplasms. DNA Repair, 96.

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DNA repair pathways, which are also identified as guardians of the genome, protect cells from frequent damage that can lead to DNA breaks. The most deleterious types of damage are double-strand breaks (DSBs), which are repaired by homologous recombination (HR) and non-homologous end joining (NHEJ). Single strand breaks (SSBs) can be corrected through base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR). Failure to restore DNA lesions or inappropriately repaired DNA damage culminates in genomic instability and changes in the regulation of cellular functions. Intriguingly, particular mutations and translocations are accompanied by special types of leukemia. Besides, expression patterns of certain repair genes are altered in different hematologic malignancies. Moreover, analysis of mutations in key mediators of DNA damage repair (DDR) pathways, as well as investigation of their expression and function, may provide us with emerging biomarkers of response/resistance to treatment. Therefore, defective DDR pathways can offer a rational starting point for developing DNA repair-targeted drugs. In this review, we address genetic alterations and gene/protein expression changes, as well as provide an overview of DNA repair pathways. © 2020

Item Type: Article
Additional Information: cited By 0
Uncontrolled Keywords: biological marker; DNA; DNA glycosyltransferase; DNA ligase; DNA ligase III; DNA mismatch repair protein MSH2; DNA repair protein XRCC1; double strand break repair protein MRE11; excision repair cross complementing protein 1; imatinib; mismatch repair protein; mismatch repair protein PMS1; mismatch repair protein PMS2; MutL protein homolog 1; nibrin; nicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase; nucleic acid binding protein; protein MSH3; protein MSH6; Rad23B protein; Rad50 protein; tinostamustine; transcription factor; unclassified drug; unindexed drug; xeroderma pigmentosum group A protein; xeroderma pigmentosum group B protein; xeroderma pigmentosum group C protein; xeroderma pigmentosum group D protein; xeroderma pigmentosum group F protein; xeroderma pigmentosum group G protein, acute myeloid leukemia; base excision repair; cancer chemotherapy; cancer patient; chronic myeloid leukemia; DNA damage; DNA repair; gene expression; genome; genomic instability; hematologic disease; hematologic malignancy; homologous recombination; human; leukemia; mismatch repair; nonhomologous end joining repair; nonhuman; nucleotide excision repair; priority journal; protein expression; Review; single nucleotide polymorphism
Subjects: WH Hemic and Lymphatic Systems
Depositing User: eprints admin
Date Deposited: 11 May 2021 05:40
Last Modified: 11 May 2021 05:40
URI: http://eprints.iums.ac.ir/id/eprint/33569

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