ArticleCancer research2012
Common variation at BARD1 results in the expression of an oncogenic isoform that influences neuroblastoma susceptibility and oncogenicity.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 3 of them syntheses 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
64 citing papers in PubMed, 3 syntheses or guidelines pooled it, 97 citations in OpenAlex.
- Summary ofGenes · 2020Pooled it
- LMO1 polymorphisms and the risk of neuroblastoma: Assessment of meta-analysis of case-control studies.Journal of cellular and molecular medicine · 2020Pooled it
- Evaluation of Genetic Predisposition for MYCN-Amplified Neuroblastoma.Journal of the National Cancer Institute · 2017Pooled it
- BARD1: A Friend or Foe in Pancreatic Ductal Adenocarcinoma?International journal of molecular sciences · 2025Review
- Integrative genomic analyses identify neuroblastoma risk genes involved in neuronal differentiation.Human genetics · 2024Article
- CAMKV Kinase Signaling Is a Novel Therapeutic Avenue with Prognostic Relevance in Neuroblastoma.bioRxiv : the preprint server for biology · 2024Article
- Germline pathogenic variants in neuroblastoma patients are enriched in BARD1 and predict worse survival.Journal of the National Cancer Institute · 2024Article
- BARD1 germline variants induce haploinsufficiency and DNA repair defects in neuroblastoma.Journal of the National Cancer Institute · 2024Article
- Clinical Response to a PARP Inhibitor and Chemotherapy in a Child with BARD1-Mutated Refractory Neuroblastoma: A Case Report.Research square · 2023Article
- Article
- BARD1 mystery: tumor suppressors are cancer susceptibility genes.BMC cancer · 2022Review
- Article
- RNA assay identifies a previous misclassification of BARD1 c.1977A>G variant.Scientific reports · 2021Article
- Adoptive transfer of immature myeloid cells lacking NF-κB p50 (p50-IMC) impedes the growth of MHC-matched high-risk neuroblastoma.Molecular oncology · 2021Article
- Molecular Genetics in Neuroblastoma Prognosis.Children (Basel, Switzerland) · 2021Review
- Small-molecule probe reveals a kinase cascade that links stress signaling to TCF/LEF and Wnt responsiveness.Cell chemical biology · 2021Article
- Differential Expression ofGenes · 2021Article
- Article
- Associations betweenTranslational pediatrics · 2021Article
- Identification of novel prognostic markers of survival time in high-risk neuroblastoma using gene expression profiles.Oncotarget · 2020Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
26 authors at 6 institutions in 3 countries.
Funding
Abstract
The mechanisms underlying genetic susceptibility at loci discovered by genome-wide association study (GWAS) approaches in human cancer remain largely undefined. In this study, we characterized the high-risk neuroblastoma association at the BRCA1-related locus, BARD1, showing that disease-associated variations correlate with increased expression of the oncogenically activated isoform, BARD1β. In neuroblastoma cells, silencing of BARD1β showed genotype-specific cytotoxic effects, including decreased substrate-adherence, anchorage-independence, and foci growth. In established murine fibroblasts, overexpression of BARD1β was sufficient for neoplastic transformation. BARD1β stabilized the Aurora family of kinases in neuroblastoma cells, suggesting both a mechanism for the observed effect and a potential therapeutic strategy. Together, our findings identify BARD1β as an oncogenic driver of high-risk neuroblastoma tumorigenesis, and more generally, they illustrate how robust GWAS signals offer genomic landmarks to identify molecular mechanisms involved in both tumor initiation and malignant progression. The interaction of BARD1β with the Aurora family of kinases lends strong support to the ongoing work to develop Aurora kinase inhibitors for clinically aggressive neuroblastoma.
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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.