ReviewWiley interdisciplinary reviews. RNA2018
Alternative-splicing defects in cancer: Splicing regulators and their downstream targets, guiding the way to novel cancer therapeutics.
Review in Wiley interdisciplinary reviews. RNA, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 251 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
251 citing papers in PubMed, 414 citations in OpenAlex.
- Validation of next‑generation sequencing‑derived circulating mRNA variants as potential diagnostic tools in hepatocellular carcinoma and cholangiocarcinoma.Oncology reports · 2026Article
- Multiplex RT-PCR-Based Sequencing Assay to Detect Kidney Cancer-Specific Splice Variants in Tumor Tissues and Plasma Cell-Free RNAs.Molecular diagnosis & therapy · 2026Article
- Deconvoluting the multi-faceted roles of alternative splicing events in cancer: From underlying mechanisms to innovative therapeutics.Acta pharmaceutica Sinica. B · 2026Review
- Genome-Wide Analysis of Alternative Splicing Identifies a Prognostic Signature in ER-Positive Breast Cancer.Genes · 2026Article
- Review
- The Role of Splicing Machinery as a Promising Potential Therapeutic Target for Pituitary Neuroendocrine Tumors (PitNETs).Cancers · 2026Review
- Matricellular Proteins in Bladder Cancer: Context-Dependent Roles in Tumor Promotion and Suppression.International journal of molecular sciences · 2026Review
- Bclaf1 drives heart failure by recruiting Srsf2 to enhance Hand2 pre-mRNA splicing and pathological hypertrophy.Nature communications · 2026Article
- Neurochondrin promotes U5 snRNP maturation by regulating AAR2 release from PRPF8.Nucleic acids research · 2026Article
- Global landscape of protein-coding and long non-coding RNA alternative splicing and regulation in the human esophageal squamous cell carcinoma.Cancer cell international · 2026Article
- Splicing of ultraconserved poison exons controls mitotic fidelity and stem cell viability.bioRxiv : the preprint server for biology · 2026Article
- U2AF2-regulated alternative splicing of UPP1 promotes NSCLC progression by enhancing glycolysis.Cell communication and signaling : CCS · 2026Article
- SRSF10 promotes cisplatin resistance in bladder cancer via BIN1 Exon 12 retention and ANXA1 activation.Oncogene · 2026Article
- Landscape of splicing factors in early-onset gastric cancer reveals SRSF1 as a key driver of oxaliplatin resistance.The Journal of biological chemistry · 2026Article
- Improving isoform-level eQTL and integrative genetic analyses of breast cancer risk with long-read RNA transcript assemblies.bioRxiv : the preprint server for biology · 2026Article
- Extracellular Vesicle-Mediated U1 snRNA Delivery Restores Aberrant Pre-mRNA Splicing in Human Cells.Biomolecules · 2026Article
- Alternative splicing events show high prognostic values and indicate potential core genes in acute myeloid leukemia.Clinical and experimental medicine · 2026Article
- Beyond counting: how single-cell long-read sequencing turns transcriptome complexity into precision targets.Frontiers in oncology · 2026Review
- RNA Splicing as a Therapeutic Target in Cancer.Annual review of pharmacology and toxicology · 2026Review
- ESRP2 constrains EMT plasticity associated with ZEB1 expression in bladder cancer.Frontiers in oncology · 2026Article
191 more citing papers are in PubMed but not listed here.
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
Abstract
Defects in alternative splicing are frequently found in human tumors and result either from mutations in splicing-regulatory elements of specific cancer genes or from changes in the regulatory splicing machinery. RNA splicing regulators have emerged as a new class of oncoproteins and tumor suppressors, and contribute to disease progression by modulating RNA isoforms involved in the hallmark cancer pathways. Thus, dysregulation of alternative RNA splicing is fundamental to cancer and provides a potentially rich source of novel therapeutic targets. Here, we review the alterations in splicing regulatory factors detected in human tumors, as well as the resulting alternatively spliced isoforms that impact cancer hallmarks, and discuss how they contribute to disease pathogenesis. RNA splicing is a highly regulated process and, as such, the regulators are themselves tightly regulated. Differential transcriptional and posttranscriptional regulation of splicing factors modulates their levels and activities in tumor cells. Furthermore, the composition of the tumor microenvironment can also influence which isoforms are expressed in a given cell type and impact drug responses. Finally, we summarize current efforts in targeting alternative splicing, including global splicing inhibition using small molecules blocking the spliceosome or splicing-factor-modifying enzymes, as well as splice-switching RNA-based therapeutics to modulate cancer-specific splicing isoforms. This article is categorized under: RNA in Disease and Development > RNA in Disease RNA Processing > Splicing Regulation/Alternative Splicing.
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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.