Evidence map›Paper›PMID 42065040›Full record

ArticleOncology research2026

Data Mining for Identification of Targets and Repurposed Drugs to Eliminate Persistent Chronic Myeloid Leukaemia Stem Cells: Targeting RAS/RAF Signalling.

I Made Bayu Anggriawan, Heather G Jørgensen

Abstract read
In one paragraph

Article in Oncology research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

I Made Bayu AnggriawanSchool of Medicine, Dentistry and Nursing, College of MVLS, University of Glasgow, Glasgow, UK.
Heather G JørgensenSchool of Cancer Sciences, College of MVLS, University of Glasgow, Glasgow, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Persistent leukaemic stem cells (LSCs) in chronic myeloid leukaemia (CML) are insensitive to targeted tyrosine kinase inhibitors (TKIs). Identifying alternative molecular vulnerabilities may offer new therapeutic opportunities. This study aimed to identify active RAS/RAF signalling pathway components in persistent CML-LSCs using publicly available datasets to propose a novel drug combination that could synergise with TKI therapy. Methods: EMBL-EBI Single Cell Expression Atlas and Stemformatics were used to analyse gene expression within the chosen signalling pathway using DESeq2 analysis in R Studio. Genes that showed statistically significant differences across three comparisons (CML vs. normal; post vs. pre TKI; post TKI vs. normal) were evaluated for gene dependency (Chronos scores), expression profiles, and inhibitor sensitivity using the DepMap platform, with a focus on CML cell lines. Candidate inhibitors were identified using DrugBank. Results: Conclusion:

Indexed as

Antineoplastic AgentsData MiningDrug RepositioningLeukemia, Myelogenous, Chronic, BCR-ABL PositiveNeoplastic Stem Cellsraf Kinasesras ProteinsCell Line, TumorHumansProtein Kinase InhibitorsSignal TransductionAntineoplastic AgentsProtein Kinase Inhibitorsraf Kinasesras Proteinsand drug repurposing/combination therapyChronic myeloid leukaemia (CML)leukaemic stem cells (LSCs)PPP2CARAS/RAF signalling pathwaytyrosine kinase inhibitors (TKIs)

Identifiers

PMID42065040
PMCPMC13126564

What OpenQuestion holds

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Registered trials

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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.