ArticleScientific reports2020
Pathogenic impact of transcript isoform switching in 1,209 cancer samples covering 27 cancer types using an isoform-specific interaction network.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Switches in alternatively spliced isoforms impact protein and drug interactions in melanoma, ovarian cancer, and acute myeloid leukemia.British journal of cancer · 2026Article
- The splice of life: an isoform-centric view of disease, technology, and therapeutics.The Journal of clinical investigation · 2026Review
- Variant-resolved prediction of context-specific isoform variation with a graph-based attention model.Cell genomics · 2026Article
- Proteoform medicine: characterizing and targeting protein forms in human disease.Nature reviews. Genetics · 2026Review
- Potential shared neoantigens from pan-cancer transcript isoforms.Scientific reports · 2025Article
- Heterogeneous and novel transcript expression in single cells of patient-derived clear cell renal cell carcinoma organoids.Genome research · 2025Article
- Global profiling of alternative splicing in non-small cell lung cancer reveals novel histological and population differences.Oncogene · 2025Article
- RNA-Based Strategies for Cancer Therapy: In Silico Design and Evaluation of ASOs for Targeted Exon Skipping.International journal of molecular sciences · 2023Article
- High throughput single cell long-read sequencing analyses of same-cell genotypes and phenotypes in human tumors.Nature communications · 2023Article
- Quantitative Analysis of Isoform Switching in Cancer.International journal of molecular sciences · 2023Article
- ASCancer Atlas: a comprehensive knowledgebase of alternative splicing in human cancers.Nucleic acids research · 2023Article
- CanIsoNet: a database to study the functional impact of isoform switching events in diseases.Bioinformatics advances · 2023Article
- EXPANSION: a webserver to explore the functional consequences of protein-coding alternative splice variants in cancer genomics.Bioinformatics advances · 2023Article
- Isoform switching leads to downregulation of cytokine producing genes in estrogen receptor positive breast cancer.Frontiers in genetics · 2023Article
- Characterizing isoform switching events in esophageal adenocarcinoma.Molecular therapy. Nucleic acids · 2022Article
- Multi-omics approach to identifying isoform variants as therapeutic targets in cancer patients.Frontiers in oncology · 2022Review
- Editorial: Alternative Splicing in Health and Disease.Frontiers in molecular biosciences · 2022Article
- Identification of an mRNA isoform switch for HNRNPA1 in breast cancers.Scientific reports · 2021Article
- Global mapping of cancers: The Cancer Genome Atlas and beyond.Molecular oncology · 2021Review
- Review
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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
Under normal conditions, cells of almost all tissue types express the same predominant canonical transcript isoform at each gene locus. In cancer, however, splicing regulation is often disturbed, leading to cancer-specific switches in the most dominant transcripts (MDT). To address the pathogenic impact of these switches, we have analyzed isoform-specific protein-protein interaction disruptions in 1,209 cancer samples covering 27 different cancer types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) project of the International Cancer Genomics Consortium (ICGC). Our study revealed large variations in the number of cancer-specific MDT (cMDT) with the highest frequency in cancers of female reproductive organs. Interestingly, in contrast to the mutational load, cancers arising from the same primary tissue had a similar number of cMDT. Some cMDT were found in 100% of all samples in a cancer type, making them candidates for diagnostic biomarkers. cMDT tend to be located at densely populated network regions where they disrupted protein interactions in the proximity of pathogenic cancer genes. A gene ontology enrichment analysis showed that these disruptions occurred mostly in protein translation and RNA splicing pathways. Interestingly, samples with mutations in the spliceosomal complex tend to have higher number of cMDT, while other transcript expressions correlated with mutations in non-coding splice-site and promoter regions of their genes. This work demonstrates for the first time the large extent of cancer-specific alterations in alternative splicing for 27 different cancer types. It highlights distinct and common patterns of cMDT and suggests novel pathogenic transcripts and markers that induce large network disruptions in cancers.
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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 Socratic graph.