ArticleeLife2017
Copy-number and gene dependency analysis reveals partial copy loss of wild-type SF3B1 as a novel cancer vulnerability.
Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 83 citations in OpenAlex.
- Impact of Chromosomal Instability and Aneuploidy in Cancer Development.Annual review of cancer biology · 2026Article
- Modeling and targeting general and chromosome-specific aneuploidy in cancer.Genes & development · 2025Review
- SF3A3 Drives Tumorigenesis in Endometrial Cancer by Enhancing c-FOS Expression and Represents a Potential Therapeutic Target.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Bio-primed machine learning to enhance discovery of relevant biomarkers.NPJ precision oncology · 2025Article
- SF3B1K700E mutation in human embryonic stem cells causes aberrant expression of immune-related genes.PloS one · 2025Article
- Aneuploidy as a driver of human cancer.Nature genetics · 2024Review
- Expression of GNAQ, BAP1, SF3B1, and EIF1AX Proteins in the Aqueous Humor of Eyes Affected by Uveal Melanoma.Investigative ophthalmology & visual science · 2024Article
- Gene essentiality in cancer is better predicted by mRNA abundance than by gene regulatory network-inferred activity.NAR cancer · 2023Article
- Partial gene suppression improves identification of cancer vulnerabilities when CRISPR-Cas9 knockout is pan-lethal.Genome biology · 2023Article
- Alternative mRNA Splicing and Promising Therapies in Cancer.Biomolecules · 2023Review
- Predicting gene knockout effects from expression data.BMC medical genomics · 2023Article
- Article
- Systematic illumination of druggable genes in cancer genomes.Cell reports · 2022Article
- Co-occurrence of BAP1 and SF3B1 mutations in uveal melanoma induces cellular senescence.Molecular oncology · 2022Article
- A synthetic small molecule stalls pre-mRNA splicing by promoting an early-stage U2AF2-RNA complex.Cell chemical biology · 2021Article
- Targeting the transcription cycle and RNA processing in cancer treatment.Current opinion in pharmacology · 2021Review
- Probing Isoform Switching Events in Various Cancer Types: Lessons From Pan-Cancer Studies.Frontiers in molecular biosciences · 2021Review
- Determination of Genetic and Epigenetic Modifications-Related Prognostic Biomarkers of Breast Cancer: Genome High-Throughput Data Analysis.Journal of oncology · 2021Article
- Defining eligible patients for allele-selective chemotherapies targeting NAT2 in colorectal cancer.Scientific reports · 2020Article
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Authors and funding
27 authors at 4 institutions in 1 country.
Funding
Abstract
Genomic instability is a hallmark of human cancer, and results in widespread somatic copy number alterations. We used a genome-scale shRNA viability screen in human cancer cell lines to systematically identify genes that are essential in the context of particular copy-number alterations (copy-number associated gene dependencies). The most enriched class of copy-number associated gene dependencies was CYCLOPS (Copy-number alterations Yielding Cancer Liabilities Owing to Partial losS) genes, and spliceosome components were the most prevalent. One of these, the pre-mRNA splicing factor
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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.