Evidence map›Paper›PMID 38969731›Full record

ArticleLeukemia2024

Oncogenic dependency on SWI/SNF chromatin remodeling factors in T-cell acute lymphoblastic leukemia.

Hyoju Kim, Tze King Tan, Dean Zi Yang Lee, Xiao Zi Huang, Jolynn Zu Lin Ong, Michelle A Kelliher, Allen Eng Juh Yeoh, Takaomi Sanda, Shi Hao Tan

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
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

9 authors.

Hyoju KimCancer Science Institute of Singapore, National University of, Singapore, 117599, Singapore.
Tze King TanCancer Science Institute of Singapore, National University of, Singapore, 117599, Singapore.ORCID 0000-0003-1623-615X
Dean Zi Yang LeeCancer Science Institute of Singapore, National University of, Singapore, 117599, Singapore.
Xiao Zi HuangCancer Science Institute of Singapore, National University of, Singapore, 117599, Singapore.ORCID 0009-0008-5413-086X
Jolynn Zu Lin OngCancer Science Institute of Singapore, National University of, Singapore, 117599, Singapore.
Michelle A KelliherDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, 01605, USA.ORCID 0000-0001-9211-3659
Allen Eng Juh YeohCancer Science Institute of Singapore, National University of, Singapore, 117599, Singapore.
Takaomi SandaCancer Science Institute of Singapore, National University of, Singapore, 117599, Singapore. Takaomi_Sanda@u.nus.edu.ORCID 0000-0003-1621-4954
Shi Hao TanCancer Science Institute of Singapore, National University of, Singapore, 117599, Singapore.

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) 18K19960Ministry of Education - Singapore (MOE) MOE-000061Ministry of Health -Singapore (MOH) MOH-000208-00Ministry of Health -Singapore (MOH) MOH-001225-00
6 · The paper itself

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is a hematological malignancy arising from immature thymocytes. Unlike well-known oncogenic transcription factors, such as NOTCH1 and MYC, the involvement of chromatin remodeling factors in T-ALL pathogenesis is poorly understood. Here, we provide compelling evidence on how SWI/SNF chromatin remodeling complex contributes to human T-ALL pathogenesis. Integrative analysis of transcriptomic and ATAC-Seq datasets revealed high expression of SMARCA4, one of the subunits of the SWI/SNF complex, in T-ALL patient samples and cell lines compared to normal T cells. Loss of SMARCA protein function resulted in apoptosis induction and growth inhibition in multiple T-ALL cell lines. ATAC-Seq analysis revealed a massive reduction in chromatin accessibility across the genome after the loss of SMARCA protein function. RUNX1 interacts with SMARCA4 protein and co-occupies the same genomic regions. Importantly, the NOTCH1-MYC pathway was primarily affected when SMARCA protein function was impaired, implicating SWI/SNF as a novel therapeutic target.

Indexed as

Chromatin Assembly and DisassemblyDNA HelicasesNuclear ProteinsPrecursor T-Cell Lymphoblastic Leukemia-LymphomaTranscription FactorsApoptosisCell Line, TumorChromosomal Proteins, Non-HistoneCore Binding Factor Alpha 2 SubunitGene Expression Regulation, LeukemicHumansProto-Oncogene Proteins c-mycReceptor, Notch1Chromosomal Proteins, Non-HistoneCore Binding Factor Alpha 2 SubunitDNA HelicasesNOTCH1 protein, humanNuclear ProteinsProto-Oncogene Proteins c-mycReceptor, Notch1RUNX1 protein, humanSMARCA4 protein, humanSWI-SNF-B chromatin-remodeling complexTranscription Factors

Identifiers

PMID38969731

What OpenQuestion holds

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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.