ArticlePancreas2011
Characterization of alternative spliceoforms and the RNA splicing machinery in pancreatic cancer.
Article in Pancreas, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Single-Cell Transcriptomics and Mendelian Randomization Analysis Reveal Key Genes in Atrial Fibrillation.Journal of cardiovascular electrophysiology · 2026Article
- Spliceosomic dysregulation in pancreatic cancer uncovers splicing factors PRPF8 and RBMX as novel candidate actionable targets.Molecular oncology · 2024Article
- Article
- Splicing alterations in pancreatic ductal adenocarcinoma: a new molecular landscape with translational potential.Journal of experimental & clinical cancer research : CR · 2023Review
- Article
- Dysregulated splicing factor SF3B1 unveils a dual therapeutic vulnerability to target pancreatic cancer cells and cancer stem cells with an anti-splicing drug.Journal of experimental & clinical cancer research : CR · 2021Article
- Alternative Splicing Events in Tumor Immune Infiltration in Colorectal Cancer.Frontiers in oncology · 2021Article
- Splice variants as novel targets in pancreatic ductal adenocarcinoma.Scientific reports · 2017Article
- Genome-wide Profiling of RNA splicing in prostate tumor from RNA-seq data using virtual microarrays.Journal of clinical bioinformatics · 2012Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
OBJECTIVES AND
methodsAlternative splicing provides proteomic diversity that can have profound effects. The extent, pattern, and roles of alternative splicing in pancreatic cancer have not been systematically investigated. We have utilized a spliceoform-specific microarray and polymerase chain reaction to evaluate all known splice variants in human pancreatic cancer cell lines representing a spectrum of differentiation, from near-normal HPDE6 to Capan-1 and poorly differentiated MiaPaCa2 cells. Validation of altered spliceoforms was verified in primary cancer specimens and normal pancreatic ductal cells. In addition, expression of 92 spliceosomal genes was examined to better understand the mechanism for observed differences in mRNA splicing.
resultsA statistically significant reduction in alternative splicing was found in the pancreatic cancer cell lines compared with HPDE6 cells. Many splice variants identified in Capan-1 and MiaPaCa2 cells were observed in grades 3 and 4 tumors. Analysis of genes encoding spliceosomal proteins revealed that 28 of 92 genes had significantly decreased expression in cancer compared with normal pancreas.
conclusionsPancreatic cancer has reduced alternative splicing diversity compared with normal pancreas. This is demonstrated in both cell lines and primary tumors, with the loss in splicing diversity correlated with relative reduction in expression of spliceosomal genes.
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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.