ArticleMolecular and cellular biology2006
Mutation of the murine Bloom's syndrome gene produces global genome destabilization.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Induced somatic mutation accumulation during skeletal muscle regeneration reduces muscle strength.Nature aging · 2025Article
- Functions of BLM Helicase in Cells: Is It Acting Like a Double-Edged Sword?Frontiers in genetics · 2021Review
- Heterozygous germlineProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Break-induced replication promotes fragile telomere formation.Genes & development · 2020Article
- DNA repair fidelity in stem cell maintenance, health, and disease.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- DNA repair and cell cycle checkpoint defects in a mouse model of 'BRCAness' are partially rescued by 53BP1 deletion.Cell cycle (Georgetown, Tex.) · 2018Article
- BLM helicase regulates DNA repair by counteracting RAD51 loading at DNA double-strand break sites.The Journal of cell biology · 2017Article
- Repair of Meiotic DNA Breaks and Homolog Pairing in Mouse Meiosis Requires a Minichromosome Maintenance (MCM) Paralog.Genetics · 2017Article
- BLM promotes the activation of Fanconi Anemia signaling pathway.Oncotarget · 2016Article
- Manipulation of DNA Repair Proficiency in Mouse Models of Colorectal Cancer.BioMed research international · 2016Review
- NSMCE2 suppresses cancer and aging in mice independently of its SUMO ligase activity.The EMBO journal · 2015Article
- Cooperation of Blm and Mus81 in development, fertility, genomic integrity and cancer suppression.Oncogene · 2015Article
- TRF1 negotiates TTAGGG repeat-associated replication problems by recruiting the BLM helicase and the TPP1/POT1 repressor of ATR signaling.Genes & development · 2014Article
- Human RecQ helicases in DNA repair, recombination, and replication.Annual review of biochemistry · 2014Review
- BLM and RAD51 genes polymorphism and susceptibility to breast cancer.Pathology oncology research : POR · 2013Article
- Mechanism of DNA resection during intrachromosomal recombination and immunoglobulin class switching.The Journal of experimental medicine · 2013Article
- Synergic and opposing activities of thermophilic RecQ-like helicase and topoisomerase 3 proteins in Holliday junction processing and replication fork stabilization.The Journal of biological chemistry · 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
- Tumor hypoxia and genetic alterations in sporadic cancers.The journal of obstetrics and gynaecology research · 2011Review
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Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bloom's syndrome (BS) is a genetic disorder characterized cellularly by increases in sister chromatid exchanges (SCEs) and numbers of micronuclei. BS is caused by mutation in the BLM DNA helicase gene and involves a greatly enhanced risk of developing the range of malignancies seen in the general population. With a mouse model for the disease, we set out to determine the relationship between genomic instability and neoplasia. We used a novel two-step analysis to investigate a panel of eight cell lines developed from mammary tumors that appeared in Blm conditional knockout mice. First, the panel of cell lines was examined for instability. High numbers of SCEs were uniformly seen in members of the panel, and several lines produced chromosomal instability (CIN) manifested by high numbers of chromosomal structural aberrations (CAs) and chromosome missegregation events. Second, to see if Blm mutation was responsible for the CIN, time-dependent analysis was conducted on a tumor line harboring a functional floxed Blm allele. The floxed allele was deleted in vitro, and mutant as well as control subclones were cultured for 100 passages. By passage 100, six of nine mutant subclones had acquired high CIN. Nine mutant subclones produced 50-fold more CAs than did nine control subclones. Finally, chromosome loss preceded the appearance of CIN, suggesting that this loss provides a potential mechanism for the induction of instability in mutant subclones. Such aneuploidy or CIN is a universal feature of neoplasia but has an uncertain function in oncogenesis. Our results show that Blm gene mutation produces this instability, strengthening a role for CIN in the development of human cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.