Evidence map›Paper›PMID 36627445›Full record

ReviewNature reviews. Cancer2023

RNA splicing dysregulation and the hallmarks of cancer.

Robert K Bradley, Olga Anczuków

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 391 papers.

0numbers the graph read from it
0cells of the map it votes in
391citing papers in PubMed
82.5field-weighted citation impact, top 1% 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

391 citing papers in PubMed, 502 citations in OpenAlex.

  1. Article
  2. Article
  3. 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
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Estimating protein isoform abundances with [Formula: see text].Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. TargetingGenes & development · 2026
    Article

331 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 2 institutions in 1 country.

Robert K BradleyComputational Biology Program, Public Health Sciences Division and Basic Sciences Division, Fred Hutchinson Cancer Center, Seattle, WA, USA. rbradley@fredhutch.org.ORCID http://orcid.org/0000-0002-8046-1063
Olga AnczukówThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA. olga.anczukow@jax.org.ORCID http://orcid.org/0000-0003-0516-2677
Fred Hutch Cancer Center · USJackson Laboratory · US

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI Paul Robson · 1985 to 2026
$61.9M
Genetic and molecular basis for SRSF2 mutations in myelodysplasiaR01HL128239 · NHLBI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Omar Abdel-Wahab, Robert K Bradley · 2015 to 2026
$8.0M
Functional and molecular consequences of SF3B1 mutations in human hematopoietic stem cellsR01HL151651 · NHLBI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Robert K Bradley, Sergei Doulatov · 2020 to 2026
$4.0M
Interrogating the minor spliceosome to understand and treat leukemiaR01CA251138 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI ABDEL-WAHAB, OMAR, BRADLEY, ROBERT K · 2020 to 2024
$3.3M
MYC-regulated RNA Binding Protein Networks and Spliced Isoforms Driving CancerR01CA248317 · NCI · JACKSON LABORATORY · PI ANCZUKOW-CAMARDA, OLGA · 2021 to 2025
$2.7M
Mechanisms of post-transcriptional regulation of splicing factorsR01GM138541 · NIGMS · JACKSON LABORATORY · PI ANCZUKOW-CAMARDA, OLGA · 2020 to 2024
$2.1M
NCI NIH HHS P30 CA034196NCI NIH HHS R01 CA248317NCI NIH HHS R01 CA251138NHLBI NIH HHS R01 HL128239NHLBI NIH HHS R01 HL151651NIGMS NIH HHS R01 GM138541
6 · The paper itself

Abstract

Dysregulated RNA splicing is a molecular feature that characterizes almost all tumour types. Cancer-associated splicing alterations arise from both recurrent mutations and altered expression of trans-acting factors governing splicing catalysis and regulation. Cancer-associated splicing dysregulation can promote tumorigenesis via diverse mechanisms, contributing to increased cell proliferation, decreased apoptosis, enhanced migration and metastatic potential, resistance to chemotherapy and evasion of immune surveillance. Recent studies have identified specific cancer-associated isoforms that play critical roles in cancer cell transformation and growth and demonstrated the therapeutic benefits of correcting or otherwise antagonizing such cancer-associated mRNA isoforms. Clinical-grade small molecules that modulate or inhibit RNA splicing have similarly been developed as promising anticancer therapeutics. Here, we review splicing alterations characteristic of cancer cell transcriptomes, dysregulated splicing's contributions to tumour initiation and progression, and existing and emerging approaches for targeting splicing for cancer therapy. Finally, we discuss the outstanding questions and challenges that must be addressed to translate these findings into the clinic.

Indexed as

Alternative SplicingNeoplasmsCarcinogenesisCell Transformation, NeoplasticHumansProtein IsoformsRNA SplicingProtein Isoforms

Identifiers

PMID36627445
PMCPMC10132032
OpenAlexW4315475728

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.