Evidence map›Paper›PMID 14500827›Full record

ArticleNucleic acids research2003

Discovery of novel splice forms and functional analysis of cancer-specific alternative splicing in human expressed sequences.

Qiang Xu, Christopher Lee

Open access · bronzeAbstract read
In one paragraph

Article in Nucleic acids research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
7.5field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

86 citing papers in PubMed, 183 citations in OpenAlex.

  1. Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025
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  7. Tumor-associated intronic editing ofThe Journal of biological chemistry · 2018
    Article
  8. Indoleamine 2,3-Dioxygenase and Its Therapeutic Inhibition in Cancer.International review of cell and molecular biology · 2018
    Review
  9. "Dicing and Splicing" Sphingosine Kinase and Relevance to Cancer.International journal of molecular sciences · 2017
    Review
  10. Alternative splicing and the evolution of phenotypic novelty.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  11. Article
  12. iTRAQ-based quantitative proteomic analysis of esophageal squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
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  16. Review
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  20. Article

26 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Qiang XuInstitute for Genomics and Proteomics, Molecular Biology Institute and Department of Chemistry & Biochemistry, University of California, Los Angeles, Los Angeles, CA 90095-1570, USA.
Christopher Lee
University of California, Los Angeles · US

Funding

Computional Brain Biology from Genotype to PhenotypeP20MH065166 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TOGA, ARTHUR W · 2002 to 2004
$3.1M
NIMH NIH HHS MH65166NIMH NIH HHS P20 MH065166
6 · The paper itself

Abstract

We report here a genome-wide analysis of alternative splicing in 2 million human expressed sequence tags (ESTs), to identify splice forms that are up-regulated in tumors relative to normal tissues. We found strong evidence (P < 0.01) of cancer-specific splice variants in 316 human genes. In total, 78% of the cancer-specific splice forms we detected are confirmed by human-curated mRNA sequences, indicating that our results are not due to random mis-splicing in tumors; 73% of the genes showed the same cancer-specific splicing changes in tissue-matched tumor versus normal datasets, indicating that the vast majority of these changes are associated with tumorigenesis, not tissue specificity. We have confirmed our EST results in an independent set of experimental data provided by human-curated mRNAs (P-value 10(-5.7)). Moreover, the majority of the genes we detected have functions associated with cancer (P-value 0.0007), suggesting that their altered splicing may play a functional role in cancer. Analysis of the types of cancer-specific splicing shifts suggests that many of these shifts act by disrupting a tumor suppressor function. Sur prisingly, our data show that for a large number (190 in this study) of cancer-associated genes cloned originally from tumors, there exists a previously uncharacterized splice form of the gene that appears to be predominant in normal tissue.

Indexed as

Alternative SplicingExpressed Sequence TagsGene Expression Regulation, NeoplasticGenomeHumansNeoplasmsReproducibility of ResultsRNA, MessengerRNA, NeoplasmTissue DistributionUp-RegulationRNA, MessengerRNA, Neoplasm

Identifiers

PMID14500827
PMCPMC206480
OpenAlexW2134208113

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.