ArticleBMC cancer2009
Association between polymorphisms in RMI1, TOP3A, and BLM and risk of cancer, a case-control study.
Article in BMC cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 43 citations in OpenAlex.
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- Multiple susceptibility loci for radiation-induced mammary tumorigenesis in F2[Dahl S x R]-intercross rats.PloS one · 2013Article
- Non-Bloom syndrome-associated partial and total loss-of-function variants of BLM helicase.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- A conditional mouse model for measuring the frequency of homologous recombination events in vivo in the absence of essential genes.Molecular and cellular biology · 2011Article
- Pathways for Holliday junction processing during homologous recombination in Saccharomyces cerevisiae.Molecular and cellular biology · 2011Article
- RMI1 attenuates tumor development and is essential for early embryonic survival.Molecular carcinogenesis · 2011Article
- Significant association between polymorphism of the erythropoietin gene promoter and myelodysplastic syndrome.BMC medical genetics · 2010Article
- Human topoisomerase IIIalpha is a single-stranded DNA decatenase that is stimulated by BLM and RMI1.The Journal of biological chemistry · 2010Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMutations altering BLM function are associated with highly elevated cancer susceptibility (Bloom syndrome). Thus, genetic variants of BLM and proteins that form complexes with BLM, such as TOP3A and RMI1, might affect cancer risk as well.
methodsIn this study we have studied 26 tagged single nucleotide polymorphisms (tagSNPs) in RMI1, TOP3A, and BLM and their associations with cancer risk in acute myeloid leukemia/myelodysplatic syndromes (AML/MDS; N = 152), malignant melanoma (N = 170), and bladder cancer (N = 61). Two population-based control groups were used (N = 119 and N = 156).
resultsBased on consistency in effect estimates for the three cancer forms and similar allelic frequencies of the variant alleles in the control groups, two SNPs in TOP3A (rs1563634 and rs12945597) and two SNPs in BLM (rs401549 and rs2532105) were selected for analysis in breast cancer cases (N = 200) and a control group recruited from spouses of cancer patients (N = 131). The rs12945597 in TOP3A and rs2532105 in BLM showed increased risk for breast cancer. We then combined all cases (N = 584) and controls (N = 406) respectively and found significantly increased risk for variant carriers of rs1563634 A/G (AG carriers OR = 1.7 [95%CI 1.1-2.6], AA carriers OR = 1.8 [1.2-2.8]), rs12945597 G/A (GA carriers OR = 1.5 [1.1-1.9], AA carriers OR = 1.6 [1.0-2.5]), and rs2532105 C/T (CT+TT carriers OR = 1.8 [1.4-2.5]). Gene-gene interaction analysis suggested an additive effect of carrying more than one risk allele. For the variants of TOP3A, the risk increment was more pronounced for older carriers.
conclusionThese results further support a role of low-penetrance genes involved in BLM-associated homologous recombination for cancer risk.
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