Evidence map›Paper›PMID 42547267›Full record

ArticleGenes & development2026

Targeting

Md Rafikul Islam, Preeti Nagar, Naomi McNaughton, Shabiha Afroj Heeamoni, Md Mahbub Hasan, Shila Kandel, Israt Jahan Mukta, Panagiotis Tsakiroglou, William Brian Dalton, Omar Abdel-Wahab and 2 more

Abstract read
In one paragraph

Article in Genes & development, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Md Rafikul Islam *Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
Preeti Nagar *Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
Naomi McNaughtonDepartment of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
Shabiha Afroj HeeamoniDepartment of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
Md Mahbub HasanDepartment of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
Shila KandelDepartment of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
Israt Jahan MuktaDepartment of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
Panagiotis TsakiroglouDivision of Hematologic Malignancies and Bone Marrow Transplantation, Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA.
William Brian DaltonDivision of Hematologic Malignancies and Bone Marrow Transplantation, Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA.ORCID http://orcid.org/0000-0002-1314-0534
Omar Abdel-WahabMolecular Pharmacology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center (MSK), New York, New York 10065, USA.
Adrian R KrainerCold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.
Mohammad Alinoor RahmanDepartment of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA; marahman@uams.edu.

Funding

Unraveling DNA Polymerase Double-Strand Break Repair Strategies in CancerP20GM152281 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI Eric Enemark · 2024 to 2026
$9.2M
Decoding Mechanisms of Nonsense-mediated mRNA Decay through Alternative SplicingR35GM154991 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI MOHAMMAD ALINOOR RAHMAN · 2024 to 2026
$1.1M
NIGMS NIH HHS P20 GM152281NIGMS NIH HHS R35 GM154991
6 · The paper itself

Abstract

Recurrent mutations in splicing factors (SFs) have been established as crucial drivers of tumorigenesis in several types of blood cancer and are also common in a variety of solid tumors. Mutations change the RNA-binding preferences of SFs, promote global splicing alterations, and often generate erroneous mRNAs that are then degraded by nonsense-mediated mRNA decay (NMD). Consequently, several critical genes linked to hematopoiesis are dysregulated, leading to blood cancer. Although the field has progressed considerably in identifying aberrant genes and affected pathways, effective therapies have not yet emerged. To address this key gap, we instigated a gene-specific targeted strategy by unlocking the regulatory network. As a proof of concept, we scrutinized a tumor suppressor gene,

Indexed as

Enhancer of Zeste Homolog 2 ProteinGene Regulatory NetworksOligonucleotides, AntisenseRNA SplicingAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceMutationNonsense Mediated mRNA DecaySerine-Arginine Splicing FactorsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanOligonucleotides, AntisenseSerine-Arginine Splicing Factorsantisense oligonucleotide therapycancergene expressionnonsense-mediated mRNA decayRNA splicing

Identifiers

PMID42547267
PMCPMC13474417

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.