Evidence map›Paper›PMID 30206237›Full record

ArticleCell death & disease2018

Chronic myeloid leukaemia cells require the bone morphogenic protein pathway for cell cycle progression and self-renewal.

Parto Toofan, Caroline Busch, Heather Morrison, Stephen O'Brien, Heather Jørgensen, Mhairi Copland, Helen Wheadon

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Oxidative Phosphorylation and Fatty Acid Oxidation Are Central to Mitochondrial Metabolism Rewiring in CML Stem/Progenitor Cell Survival.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
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  6. CRISPR-Cas9 Library Screening Identifies Novel Molecular Vulnerabilities inInternational journal of molecular sciences · 2023
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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

7 authors at 2 institutions in 1 country.

Parto ToofanPaul O'Gorman Leukaemia Research Centre, Institute of Cancer Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, 21 Shelley Road, Glasgow, G12 0XB, UK.
Caroline BuschPaul O'Gorman Leukaemia Research Centre, Institute of Cancer Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, 21 Shelley Road, Glasgow, G12 0XB, UK.
Heather MorrisonWest of Scotland Genetic Department, QEUH, Glasgow, G51 4TF, UK.
Stephen O'BrienNorthern Institute of Cancer Research, University of Newcastle, Newcastle, NE1 7RU, UK.
Heather JørgensenPaul O'Gorman Leukaemia Research Centre, Institute of Cancer Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, 21 Shelley Road, Glasgow, G12 0XB, UK.ORCID 0000-0003-4663-4191
Mhairi CoplandPaul O'Gorman Leukaemia Research Centre, Institute of Cancer Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, 21 Shelley Road, Glasgow, G12 0XB, UK. Mhairi.Copland@glasgow.ac.uk.
Helen WheadonPaul O'Gorman Leukaemia Research Centre, Institute of Cancer Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, 21 Shelley Road, Glasgow, G12 0XB, UK. Helen.Wheadon@glasgow.ac.uk.
University of Glasgow · GBNewcastle University · GB

Funding

Cancer Research UKChief Scientist OfficeNational Centre for the Replacement, Refinement and Reduction of Animals in Research NC/K500331/1
6 · The paper itself

Abstract

Leukaemic stem cell (LSC) persistence remains a major obstacle to curing chronic myeloid leukaemia (CML). The bone morphogenic protein (BMP) pathway is deregulated in CML, with altered expression and response to the BMP ligands shown to impact on LSC expansion and behaviour. In this study, we determined whether alterations in the BMP pathway gene signature had any predictive value for therapeutic response by profiling 60 CML samples at diagnosis from the UK SPIRIT2 trial and correlating the data to treatment response using the 18-month follow-up data. There was significant deregulation of several genes involved in the BMP pathway with ACV1C, INHBA, SMAD7, SNAIL1 and SMURF2 showing differential expression in relation to response. Therapeutic targeting of CML cells using BMP receptor inhibitors, in combination with tyrosine kinase inhibitor (TKI), indicate a synergistic mode of action. Furthermore, dual treatment resulted in altered cell cycle gene transcription and irreversible cell cycle arrest, along with increased apoptosis compared to single agents. Targeting CML CD34

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsApoptosisBone Morphogenetic Protein 4Cell Cycle CheckpointsCell Line, TumorDrug SynergismHumansInduced Pluripotent Stem CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveNeoplastic Stem CellsProtein Kinase InhibitorsSignal TransductionTreatment OutcomeBMP4 protein, humanBone Morphogenetic Protein 4Protein Kinase Inhibitors

Identifiers

PMID30206237
PMCPMC6134087
OpenAlexW2891924810

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.