Evidence map›Paper›PMID 31334570›Full record

ReviewGenes, chromosomes & cancer2019

Mutations in spliceosome genes and therapeutic opportunities in myeloid malignancies.

Justin Taylor, Stanley C Lee

Open access · hybridAbstract readReview
In one paragraph

Review in Genes, chromosomes & cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Alternative splicing and cancer: a systematic review.Signal transduction and targeted therapy · 2021
    Pooled it
  2. Article
  3. Phase I Study of Rogocekib in Patients with Advanced, Relapsed, or Refractory Malignant Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  4. Article
  5. Review
  6. The cancer-associated SF3B1Cell death & disease · 2025
    Article
  7. Review
  8. ADAR1: from basic mechanisms to inhibitors.Trends in cell biology · 2025
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
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  17. Article
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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.

Justin TaylorHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York.ORCID 0000-0003-4407-6325
Stanley C LeeHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York.ORCID 0000-0001-7110-2416
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Defining the Biological and Mechanistic Implications of XPO1 Mutations in Hematologic MalignanciesK08CA230319 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI TAYLOR, JUSTIN · 2018 to 2023
$1.2M
Defining Novel Genetic Dependencies in Spliceosome Mutant LeukemiaK99CA218896 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI LEE, STANLEY CHUN-WEI · 2017 to 2018
$297k
NCI NIH HHS K08 CA230319NCI NIH HHS K99 CA218896NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Since the discovery of RNA splicing more than 40 years ago, our comprehension of the molecular events orchestrating constitutive and alternative splicing has greatly improved. Dysregulation of pre-mRNA splicing has been observed in many human diseases including neurodegenerative diseases and cancer. The recent identification of frequent somatic mutations in core components of the spliceosome in myeloid malignancies and functional analysis using model systems has advanced our knowledge of how splicing alterations contribute to disease pathogenesis. In this review, we summarize our current understanding on the mechanisms of how mutant splicing factors impact splicing and the resulting functional and pathophysiological consequences. We also review recent advances to develop novel therapeutic approaches targeting splicing catalysis and splicing regulatory proteins, and discuss emerging technologies using oligonucleotide-based therapies to modulate pathogenically spliced isoforms.

Indexed as

HumansLeukemia, MyeloidMutationMyelodysplastic SyndromesMyeloproliferative DisordersNeoplasmsRibonucleoproteins, Small NuclearRibonucleoprotein, U2 Small NuclearRNA PrecursorsRNA SplicingRNA Splicing FactorsSpliceosomesSplicing Factor U2AFRibonucleoproteins, Small NuclearRibonucleoprotein, U2 Small NuclearRNA PrecursorsRNA Splicing FactorsSplicing Factor U2AFmyeloid leukemiaRNA splicingSF3B1SRSF2U2AF1

Identifiers

PMID31334570
PMCPMC6852509
OpenAlexW2963943817

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.