ArticleHuman molecular genetics2011
Increased levels of noisy splicing in cancers, but not for oncogene-derived transcripts.
Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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Who cites it
32 citing papers in PubMed, 40 citations in OpenAlex.
- Pervasive noise in human pre-mRNA splice site selection.Molecular cell · 2026Article
- RNA Splicing as a Therapeutic Target in Cancer.Annual review of pharmacology and toxicology · 2026Review
- Aberrant pre-mRNA processing in cancer.The Journal of experimental medicine · 2024Review
- Article
- Expression of circular RNAs in myelodysplastic neoplasms and their association with mutations in the splicing factor gene SF3B1.Molecular oncology · 2023Article
- Sonic hedgehog signaling: Alternative splicing and pathogenic role in medulloblastoma.Genes & diseases · 2023Review
- Alternative mRNA Splicing and Promising Therapies in Cancer.Biomolecules · 2023Review
- Targeted splicing therapy: new strategies for colorectal cancer.Frontiers in oncology · 2023Review
- The Heterochromatin protein 1 is a regulator in RNA splicing precision deficient in ulcerative colitis.Nature communications · 2022Article
- Dysregulation and therapeutic targeting of RNA splicing in cancer.Nature cancer · 2022Review
- The role of splicing factor PRPF8 in breast cancer.Technology and health care : official journal of the European Society for Engineering and Medicine · 2022Article
- New GFAP splice isoform (GFAPµ) differentially expressed in glioma translates into 21 kDa N-terminal GFAP protein.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Alternative Splicing: Expanding the Landscape of Cancer Biomarkers and Therapeutics.International journal of molecular sciences · 2020Review
- Revised Exon Structure of l-DOPA Decarboxylase (International journal of molecular sciences · 2020Article
- Mutations in spliceosome genes and therapeutic opportunities in myeloid malignancies.Genes, chromosomes & cancer · 2019Review
- Altered RNA Processing in Cancer Pathogenesis and Therapy.Cancer discovery · 2019Review
- Prognostic index of aberrant mRNA splicing profiling acts as a predictive indicator for hepatocellular carcinoma based on TCGA SpliceSeq data.International journal of oncology · 2019Article
- Events of alternative splicing in head and neck cancer via RNA sequencing - an update.BMC genomics · 2019Article
- Exploiting differential RNA splicing patterns: a potential new group of therapeutic targets in cancer.Expert opinion on therapeutic targets · 2018Review
- Depletion of somatic mutations in splicing-associated sequences in cancer genomes.Genome biology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent genome-wide analyses have detected numerous cancer-specific alternative splicing (AS) events. Whether transcripts containing cancer-specific AS events are likely to be translated into functional proteins or simply reflect noisy splicing, thereby determining their clinical relevance, is not known. Here we show that consistent with a noisy-splicing model, cancer-specific AS events generally tend to be rare, containing more premature stop codons and have less identifiable functional domains in both the human and mouse. Interestingly, common cancer-derived AS transcripts from tumour suppressor and oncogenes show marked changes in premature stop-codon frequency; with tumour suppressor genes exhibiting increased levels of premature stop codons whereas oncogenes have the opposite pattern. We conclude that tumours tend to have faithful oncogene splicing and a higher incidence of premature stop codons among tumour suppressor and cancer-specific splice variants showing the importance of considering splicing noise when analysing cancer-specific splicing changes.
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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.