ArticleCancer discovery2015
The genetics of splicing in neuroblastoma.
Article in Cancer discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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
16 citing papers in PubMed, 22 citations in OpenAlex.
- Targeting TRIM59 impairs RNA splicing and promotes neuroblastoma differentiation and therapeutic responses.Journal of experimental & clinical cancer research : CR · 2025Article
- CAMKV Kinase Signaling Is a Novel Therapeutic Avenue with Prognostic Relevance in Neuroblastoma.bioRxiv : the preprint server for biology · 2024Article
- Investigating SH-SY5Y Neuroblastoma Cell Surfaceome as a Model for Neuronal-Targeted Novel Therapeutic Modalities.International journal of molecular sciences · 2022Article
- Targeting the spliceosome through RBM39 degradation results in exceptional responses in high-risk neuroblastoma models.Science advances · 2021Article
- Clonal evidence for the development of neuroblastoma with extensive copy-neutral loss of heterozygosity arising in a mature teratoma.Cancer science · 2021Article
- Aberrant splicing in neuroblastoma generates RNA-fusion transcripts and provides vulnerability to spliceosome inhibitors.Nucleic acids research · 2021Article
- Fusion genes as biomarkers in pediatric cancers: A review of the current state and applicability in diagnostics and personalized therapy.Cancer letters · 2021Review
- Splice variants of RAS-translational significance.Cancer metastasis reviews · 2020Review
- Identification of RNA-Binding Proteins as Targetable Putative Oncogenes in Neuroblastoma.International journal of molecular sciences · 2020Article
- Increased plasma concentration of cell-free DNA precedes disease recurrence in children with high-risk neuroblastoma.BMC cancer · 2020Article
- The master regulator FUBP1: its emerging role in normal cell function and malignant development.Cellular and molecular life sciences : CMLS · 2019Review
- Transcriptome 3'end organization by PCF11 links alternative polyadenylation to formation and neuronal differentiation of neuroblastoma.Nature communications · 2018Article
- Whole exome sequencing reveals novel somatic alterations in neuroblastoma patients with chemotherapy.Cancer cell international · 2018Article
- CTD2 Dashboard: a searchable web interface to connect validated results from the Cancer Target Discovery and Development Network.Database : the journal of biological databases and curation · 2017Article
- Distinct splicing signatures affect converged pathways in myelodysplastic syndrome patients carrying mutations in different splicing regulators.RNA (New York, N.Y.) · 2016Article
- The "neuro" of neuroblastoma: Neuroblastoma as a neurodevelopmental disorder.Annals of neurology · 2016Review
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 3 countries.
Funding
Abstract
unlabelledRegulation of mRNA splicing, a critical and tightly regulated cellular function, underlies the majority of proteomic diversity and is frequently disrupted in disease. Using an integrative genomics approach, we combined both genomic data and exon-level transcriptome data in two somatic tissues (cerebella and peripheral ganglia) from a transgenic mouse model of neuroblastoma, a tumor that arises from the peripheral neural crest. Here, we describe splicing quantitative trait loci associated with differential splicing across the genome that we use to identify genes with previously unknown functions within the splicing pathway and to define de novo intronic splicing motifs that influence splicing from hundreds of bases away. Our results show that these splicing motifs represent sites for functional recurrent mutations and highlight novel candidate genes in human cancers, including childhood neuroblastoma. SIGNIFICANCE: Somatic mutations with predictable downstream effects are largely relegated to coding regions, which comprise less than 2% of the human genome. Using an unbiased in vivo analysis of a mouse model of neuroblastoma, we have identified intronic splicing motifs that translate into sites for recurrent somatic mutations in human cancers.
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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.