Evidence map›Paper›PMID 21041405›Full record

ReviewGenes & development2010

Alternative pre-mRNA splicing regulation in cancer: pathways and programs unhinged.

Charles J David, James L Manley

Abstract readReview
In one paragraph

Review in Genes & development, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 497 papers.

0numbers the graph read from it
0cells of the map it votes in
497citing papers in PubMed
–field-weighted citation impact
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

497 citing papers in PubMed.

  1. SRSF3 plays a key role in liver cancer sex disparity by facilitating hepatocyte expression of ERα and FOXA.Proceedings of the National Academy of Sciences of the United States of America · 2026
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437 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.

Charles J DavidDepartment of Biological Sciences, Columbia University, New York, New York 10027, USA.
James L Manley

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alternative splicing of mRNA precursors is a nearly ubiquitous and extremely flexible point of gene control in humans. It provides cells with the opportunity to create protein isoforms of differing, even opposing, functions from a single gene. Cancer cells often take advantage of this flexibility to produce proteins that promote growth and survival. Many of the isoforms produced in this manner are developmentally regulated and are preferentially re-expressed in tumors. Emerging insights into this process indicate that pathways that are frequently deregulated in cancer often play important roles in promoting aberrant splicing, which in turn contributes to all aspects of tumor biology.

Indexed as

Alternative SplicingAnimalsGene Expression ProfilingGene Expression Regulation, NeoplasticHumansModels, GeneticNeoplasmsProtein IsoformsRNA PrecursorsSignal TransductionProtein IsoformsRNA Precursors

Identifiers

PMID21041405
PMCPMC2964746

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.