Evidence map›Paper›PMID 38177125›Full record

ArticleOncogenesis2024

Transcriptomic analysis identifies B-lymphocyte kinase as a therapeutic target for desmoplastic small round cell tumor cancer stem cell-like cells.

Justin W Magrath, Dane A Flinchum, Alifiani B Hartono, Shruthi Sanjitha Sampath, Tina M O'Grady, Melody Baddoo, Liang Haoyang, Xiaojiang Xu, Erik K Flemington, Sean B Lee

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. 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

10 authors at 1 institution in 1 country.

Justin W MagrathDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, USA.
Dane A FlinchumDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, USA.
Alifiani B HartonoDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, USA.
Shruthi Sanjitha SampathDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, USA.
Tina M O'GradyDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, USA.ORCID http://orcid.org/0000-0002-1283-0293
Melody BaddooDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, USA.ORCID http://orcid.org/0000-0001-8501-9728
Liang HaoyangDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, USA.ORCID http://orcid.org/0009-0003-5246-8406
Xiaojiang XuDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, USA.
Erik K FlemingtonDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, USA.
Sean B LeeDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA, USA. slee30@tulane.edu.ORCID http://orcid.org/0000-0001-6211-3498
Tulane University · US

Funding

Programmed splicing derangement as new EBV host cell shut-off mechanismR01CA262090 · NCI · WAYNE STATE UNIVERSITY · PI ERIK K FLEMINGTON · 2022 to 2026
$2.1M
EBV reactivation causes widespread host de novo promoter transcription and transcriptional interferenceR01CA272142 · NCI · WAYNE STATE UNIVERSITY · PI ERIK K FLEMINGTON · 2022 to 2026
$2.1M
RPMS1 circular RNAs in EBV malignanciesR01CA243793 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI FLEMINGTON, ERIK K · 2019 to 2023
$1.8M
An Integrative Approach to Identify Vulnerabilities in Pediatric Cancer DSRCTR01CA222856 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI LEE, SEAN B. · 2019 to 2024
$1.7M
NCI NIH HHS R01 CA222856NCI NIH HHS R01 CA243793NCI NIH HHS R01 CA262090NCI NIH HHS R01 CA272142
6 · The paper itself

Abstract

Desmoplastic small round cell tumor (DSRCT) is an aggressive pediatric cancer caused by the EWSR1-WT1 fusion oncoprotein. The tumor is refractory to treatment with a 5-year survival rate of only 15-25%, necessitating the development of novel therapeutics, especially those able to target chemoresistant subpopulations. Novel in vitro cancer stem cell-like (CSC-like) culture conditions increase the expression of stemness markers (SOX2, NANOG) and reduce DSRCT cell line susceptibility to chemotherapy while maintaining the ability of DSRCT cells to form xenografts. To gain insights into this chemoresistant model, RNA-seq was performed to elucidate transcriptional alterations between DSRCT cells grown in CSC-like spheres and normal 2-dimensional adherent state. Commonly upregulated and downregulated genes were identified and utilized in pathway analysis revealing upregulation of pathways related to chromatin assembly and disassembly and downregulation of pathways including cell junction assembly and extracellular matrix organization. Alterations in chromatin assembly suggest a role for epigenetics in the DSRCT CSC-like state, which was further investigated with ATAC-seq, identifying over 10,000 differentially accessible peaks, including 4444 sphere accessible peaks and 6,120 adherent accessible peaks. Accessible regions were associated with higher gene expression, including increased accessibility of the CSC marker SOX2 in CSC-like culture conditions. These analyses were further utilized to identify potential CSC therapeutic targets, leading to the identification of B-lymphocyte kinase (BLK) as a CSC-enriched, EWSR1-WT1-regulated, druggable target. BLK inhibition and knockdown reduced CSC-like properties, including abrogation of tumorsphere formation and stemness marker expression. Importantly, BLK knockdown reduced DSRCT CSC-like cell chemoresistance, making its inhibition a promising target for future combination therapy.

Identifiers

PMID38177125
PMCPMC10767073
OpenAlexW4390580509

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.