DNA repair is an important defense mechanism that faces the difficult task of protecting the genome from the constant assaults caused by endogenous and exogenous agents. Since DNA repair mechanisms are responsible for correcting DNA damage and preserving genomic integrity, it is obvious that abnormalities of these mechanisms may result in neoplastic transformation. Hematological malignancies are characterized by genomic instability that is possibly related to underlying defects in DNA repair. The purpose of this review is to summarize the existing knowledge concerning abnormalities in DNA repair components and their influence on common hematological malignancies.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.3109/10428194.2010.551155 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Flap endonuclease 1 repairs DNA-protein cross-links via ADP-ribosylation-dependent mechanisms.
Sci Adv
January 2025
Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, National Institute of Health, Bethesda, MD 20892, USA.
DNA-protein cross-links (DPCs) are among the most detrimental genomic lesions. They are ubiquitously produced by formaldehyde (FA), and failure to repair FA-induced DPCs blocks chromatin-based processes, leading to neurodegeneration and cancer. The type, structure, and repair of FA-induced DPCs remain largely unknown.
View Article and Find Full Text PDFFunctions of the Bloom Syndrome Helicase N-terminal Intrinsically Disordered Region.
Genetics
January 2025
Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Bloom Syndrome helicase (Blm) is a RecQ family helicase involved in DNA repair, cell-cycle progression, and development. Pathogenic variants in human BLM cause the autosomal recessive disorder Bloom Syndrome, characterized by predisposition to numerous types of cancer. Prior studies of Drosophila Blm mutants lacking helicase activity or protein have shown sensitivity to DNA damaging agents, defects in repairing DNA double-strand breaks (DSBs), female sterility, and improper segregation of chromosomes in meiosis.
View Article and Find Full Text PDFPreclinical evaluation of the potential PARP-imaging probe [carbonyl-C]DPQ.
EJNMMI Radiopharm Chem
January 2025
Division of Nuclear Medicine, Department of Biomedical Imaging and Image-Guided Therapy, Medical University of Vienna, Vienna, Austria.
Background: Poly (ADP-ribose) polymerase (PARP) enzymes are crucial for the repair of DNA single-strand breaks and have become key therapeutic targets in homologous recombination-deficient cancers, including prostate cancer. To enable non-invasive monitoring of PARP-1 expression, several PARP-1-targeting positron emission tomography (PET) tracers have been developed. Here, we aimed to preclinically investigate [carbonyl-C]DPQ as an alternative PARP-1 PET tracer as it features a strongly distinct chemotype compared to the frontrunners [F]FluorThanatrace and [F]PARPi.
View Article and Find Full Text PDFThe M1/M2 Macrophage Polarization and Hepatoprotective Activity of Quercetin in Cyclophosphamide-Induced Experimental Liver Toxicity.
Vet Med Sci
January 2025
Department of Medical Biology, Faculty of Medicine, Dicle University, Diyarbakir, Turkey.
Background: Chemotherapy drugs may lead to hepatic injury, which is considered one of the limitations of these drugs.
Objectives: The aim of this study was to evaluate the effect of quercetin (QUE) on M1/M2 macrophage polarization and hepatoprotective effect in cyclophosphamide (CTX)-induced liver toxicity.
Methods: Twenty-four mice were divided into four groups (Control, QUE, CTX, CTX + QUE).
Strategies to Overcome Intrinsic and Acquired Resistance to Chemoradiotherapy in Head and Neck Cancer.
Cells
December 2024
Radiotherapy Department, Institut Jules Bordet, Université Libre de Bruxelles (ULB), 1070 Brussels, Belgium.
Definitive chemoradiotherapy (CRT) is a cornerstone of treatment for locoregionally advanced head and neck cancer (HNC). Research is ongoing on how to improve the tumor response to treatment and limit normal tissue toxicity. A major limitation in that regard is the growing occurrence of intrinsic or acquired treatment resistance in advanced cases.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!