ArticlePLoS computational biology2008
Entropy measures quantify global splicing disorders in cancer.
Article in PLoS computational biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 61 citations in OpenAlex.
- Single-cell splice isoform usage reveals distinct axes of cellular identity and senescence.bioRxiv : the preprint server for biology · 2026Article
- Single-base resolution atlas reveals moderate conservation and regulatory diversity of m6A modifications across mammals.Nucleic acids research · 2026Article
- Perplexity as a Metric for Isoform Diversity in the Human Transcriptome.bioRxiv : the preprint server for biology · 2025Article
- Epigene functional diversity: isoform usage, disordered domain content, and variable binding partners.Epigenetics & chromatin · 2025Article
- Quantifying transcriptome diversity: a review.Briefings in functional genomics · 2024Review
- Aire-dependent transcripts escape Raver2-induced splice-event inclusion in the thymic epithelium.EMBO reports · 2022Article
- Splicing is an alternate oncogenic pathway activation mechanism in glioma.Nature communications · 2022Article
- Article
- TranscriptAchilles: a genome-wide platform to predict isoform biomarkers of gene essentiality in cancer.GigaScience · 2019Article
- Transcriptional fates of human-specific segmental duplications in brain.Genome research · 2018Article
- Article
- Analysis of distribution of DNA methylation in kidney-renal-clear-cell-carcinoma specific genes using entropy.Genomics data · 2016Article
- Extensive RNA editing and splicing increase immune self-representation diversity in medullary thymic epithelial cells.Genome biology · 2016Article
- Article
- Significance of duon mutations in cancer genomes.Scientific reports · 2016Article
- Entropy, complexity, and Markov diagrams for random walk cancer models.Scientific reports · 2014Article
- Cachexia: a problem of energetic inefficiency.Journal of cachexia, sarcopenia and muscle · 2014Article
- Alternative splicing regulation of telomerase: a new paradigm?Trends in genetics : TIG · 2014Article
- An integrative framework identifies alternative splicing events in colorectal cancer development.Molecular oncology · 2014Article
- Splicing factor SRSF6 promotes hyperplasia of sensitized skin.Nature structural & molecular biology · 2014Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most mammalian genes are able to express several splice variants in a phenomenon known as alternative splicing. Serious alterations of alternative splicing occur in cancer tissues, leading to expression of multiple aberrant splice forms. Most studies of alternative splicing defects have focused on the identification of cancer-specific splice variants as potential therapeutic targets. Here, we examine instead the bulk of non-specific transcript isoforms and analyze their level of disorder using a measure of uncertainty called Shannon's entropy. We compare isoform expression entropy in normal and cancer tissues from the same anatomical site for different classes of transcript variations: alternative splicing, polyadenylation, and transcription initiation. Whereas alternative initiation and polyadenylation show no significant gain or loss of entropy between normal and cancer tissues, alternative splicing shows highly significant entropy gains for 13 of the 27 cancers studied. This entropy gain is characterized by a flattening in the expression profile of normal isoforms and is correlated to the level of estimated cellular proliferation in the cancer tissue. Interestingly, the genes that present the highest entropy gain are enriched in splicing factors. We provide here the first quantitative estimate of splicing disruption in cancer. The expression of normal splice variants is widely and significantly disrupted in at least half of the cancers studied. We postulate that such splicing disorders may develop in part from splicing alteration in key splice factors, which in turn significantly impact multiple target genes.
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