ArticleJournal of biomedical science2024
BUB1B monoallelic germline variants contribute to prostate cancer predisposition by triggering chromosomal instability.
Article in Journal of biomedical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- BUB signaling in cancer and molecular insights into targeted therapies.Communications biology · 2026Review
- BUB1B is a novel prognostic-related biomarker and correlated with immune infiltrates in lung adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Translational evaluation of BUB1B as a precision medicine biomarker for hepatocellular carcinoma.Scientific reports · 2026Article
- Whole genome sequencing-based analysis of genetic predisposition to adult glioblastoma.NPJ genomic medicine · 2025Article
- Integrated transcriptomic and immunoinformatics analysis identifies tpx2, bub1b, and ube2c as diagnostic biomarkers and therapeutic targets in endometrial carcinoma.Discover oncology · 2025Article
- BubR1 and SIRT2: Insights into aneuploidy, aging, and cancer.Seminars in cancer biology · 2024Review
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20 authors.
Funding
Abstract
backgroundProstate cancer (PrCa) is the most frequently diagnosed cancer in men. Variants in known moderate- to high-penetrance genes explain less than 5% of the cases arising at early-onset (< 56 years) and/or with familial aggregation of the disease. Considering that BubR1 is an essential component of the mitotic spindle assembly checkpoint, we hypothesized that monoallelic BUB1B variants could be sufficient to fuel chromosomal instability (CIN), potentially triggering (prostate) carcinogenesis.
methodsTo unveil BUB1B as a new PrCa predisposing gene, we performed targeted next-generation sequencing in germline DNA from 462 early-onset/familial PrCa patients and 1,416 cancer patients fulfilling criteria for genetic testing for other hereditary cancer syndromes. To explore the pan-cancer role of BUB1B, we used in silico BubR1 molecular modeling, in vitro gene-editing, and ex vivo patients' tumors and peripheral blood lymphocytes.
resultsRare BUB1B variants were found in ~ 1.9% of the early-onset/familial PrCa cases and in ~ 0.6% of other cancer patients fulfilling criteria for hereditary disease. We further show that BUB1B variants lead to decreased BubR1 expression and/or stability, which promotes increased premature chromatid separation and, consequently, triggers CIN, driving resistance to Taxol-based therapies.
conclusionsOur study shows that different BUB1B variants may uncover a trigger for CIN-driven carcinogenesis, supporting the role of BUB1B as a (pan)-cancer predisposing gene with potential impact on genetic counseling and treatment decision-making.
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