ArticleJournal of medical genetics2002
Genetic variants of NHEJ DNA ligase IV can affect the risk of developing multiple myeloma, a tumour characterised by aberrant class switch recombination.
Article in Journal of medical genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Relevance of LIG4 gene polymorphisms with cancer susceptibility: evidence from a meta-analysis.Scientific reports · 2014Pooled it
- The Converging Roles of DNA Damage Resolution and Redox Dysregulation in Plasma Cell Transformation During the Evolution of Multiple Myeloma.International journal of molecular sciences · 2026Article
- Signals in Peripheral Blood: Tracking Redox Status and DNA Damage Response During the Progression of Multiple Myeloma.International journal of molecular sciences · 2026Article
- The Interplay between the DNA Damage Response (DDR) Network and the Mitogen-Activated Protein Kinase (MAPK) Signaling Pathway in Multiple Myeloma.International journal of molecular sciences · 2024Review
- Disruption of theJournal of fungi (Basel, Switzerland) · 2023Article
- Current perspectives on interethnic variability in multiple myeloma: Single cell technology, population pharmacogenetics and molecular signal transduction.Translational oncology · 2022Article
- The Role of DNA Repair in Genomic Instability of Multiple Myeloma.International journal of molecular sciences · 2022Review
- Review
- Targeting the Interplay between HDACs and DNA Damage Repair for Myeloma Therapy.International journal of molecular sciences · 2021Review
- Review
- Review
- Ligase 1 is a predictor of platinum resistance and its blockade is synthetically lethal in XRCC1 deficient epithelial ovarian cancers.Theranostics · 2021Article
- Genetic predisposition for multiple myeloma.Leukemia · 2020Review
- Treatment May Be Harmful: Mechanisms/Prediction/Prevention of Drug-Induced DNA Damage and Repair in Multiple Myeloma.Frontiers in genetics · 2019Review
- Genetic intersection of male infertility and cancer.Fertility and sterility · 2018Review
- Review
- The spatial organization of non-homologous end joining: from bridging to end joining.DNA repair · 2014Article
- Inherited genetic susceptibility to multiple myeloma.Leukemia · 2014Review
- DNA damage response genes and the development of cancer metastasis.Radiation research · 2014Review
- DNA repair pathways in human multiple myeloma: role in oncogenesis and potential targets for treatment.Cell cycle (Georgetown, Tex.) · 2013Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The DNA double stranded break (DSB) repair mechanism, non-homologous end joining (NHEJ) represents an essential step in antigen receptor gene rearrangement mechanisms, processes believed to be intimately involved in the aetiology of lymphoproliferative disease. We investigated the potential impact that previously undescribed polymorphisms identified within NHEJ DNA ligase IV (LIG4) have upon predisposition to several lymphoproliferative disorders, including leukaemia, lymphoma, and multiple myeloma. Two LIG4 polymorphisms were examined, both C>T transitions, which result in the amino acid substitutions A3V and T9I. Inheritance of the LIG4 A3V CT genotype was found to be significantly associated with a two-fold reduction in risk of developing multiple myeloma (OR 0.49, 95% CI 0.27 to 0.89). Similarly, inheritance of the LIG4 T9I CT and the T9I TT genotypes were found to associate with a 1.5-fold reduction (OR 0.77, 95% CI 0.51 to 1.17) and a four-fold reduction (OR 0.22, 95% CI 0.07 to 0.70) in risk of developing multiple myeloma respectively, suggesting a gene dosage effect for this polymorphism. The LIG4 A3V and T9I variant alleles are in linkage disequilibrium (D'=0.95, p<0.0001), and the protective effect associated with these polymorphisms was found to be the result of inheritance of the A3V-T9I CT and A3V-T9I TT haplotypes. These data suggest that genetic variants of NHEJ LIG4 may modulate predisposition to multiple myeloma, a tumour characterised by aberrant immunoglobulin (Ig) class switch recombination.
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Registered trials
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