Evidence map›Paper›PMID 36780103›Full record

ReviewCurrent hematologic malignancy reports2023

The Bone Marrow Immune Microenvironment in CML: Treatment Responses, Treatment-Free Remission, and Therapeutic Vulnerabilities.

Shaun David Patterson, Mhairi Copland

Open access · hybridAbstract readReview
In one paragraph

Review in Current hematologic malignancy reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

24 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. 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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  11. Targeting Lysosomes for Enhanced Anti-Cancer Therapeutics and Immune Response.International journal of biological sciences · 2026
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  18. Modelling Cancer in Drosophila: Exploration to Personalised Medicine.Advances in experimental medicine and biology · 2025
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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

2 authors at 1 institution in 1 country.

Shaun David PattersonSchool of Cancer Sciences, College of Medical, Veterinary and Life Sciences, Paul O'Gorman Leukaemia Research Centre, University of Glasgow, 21 Shelley Road, Glasgow, G12 0ZD, UK. shaun.patterson@glasgow.ac.uk.ORCID 0000-0001-7131-1533
Mhairi CoplandSchool of Cancer Sciences, College of Medical, Veterinary and Life Sciences, Paul O'Gorman Leukaemia Research Centre, University of Glasgow, 21 Shelley Road, Glasgow, G12 0ZD, UK. Mhairi.Copland@glasgow.ac.uk.ORCID 0000-0002-7655-016X
University of Glasgow · GB

Funding

Cancer Research UK
6 · The paper itself

Abstract

purpose of reviewTyrosine kinase inhibitors (TKIs) are very successful for the treatment of chronic myeloid leukaemia (CML) but are not curative in most patients due to persistence of TKI-resistant leukaemia stem cells (LSCs). The bone marrow immune microenvironment (BME) provides protection to the LSC through multidimensional interactions, driving therapy resistance, and highlighting the need to circumvent these protective niches therapeutically. This review updates the evidence for interactions between CML cells and the immune microenvironment with a view to identifying targetable therapeutic vulnerabilities and describes what is known about the role of immune regulation in treatment-free remission (TFR). RECENT

findingsIntracellular signalling downstream of the chemotactic CXCL12-CXCR4 axis, responsible for disrupted homing in CML, has been elucidated in LSCs, highlighting novel therapeutic opportunities. In addition, LSCs expressing CXCL12-cleaving surface protein CD26 were highly correlated with CML burden, building on existing evidence. Newer findings implicate the adhesion molecule CD44 in TKI resistance, while JAK/STAT-mediated resistance to TKIs may occur downstream of extrinsic signalling in the BME. Exosomal BME-LSC cross-communication has also been explored. Finally, further detail on the phenotypes of natural killer (NK) cells putatively involved in maintaining successful TFR has been published, and NK-based immunotherapies are discussed. Recent studies highlight and build on our understanding of the BME in CML persistence and TKI resistance, pinpointing therapeutically vulnerable interactions. Repurposing existing drugs and/or the development of novel inhibitors targeting these relationships may help to overcome these issues in TKI-resistant CML and be used as adjuvant therapy for sustained TFR.

Indexed as

Bone MarrowLeukemia, Myelogenous, Chronic, BCR-ABL PositiveHumansNeoplastic Stem CellsProtein Kinase InhibitorsSignal TransductionTumor MicroenvironmentProtein Kinase InhibitorsBone marrow immune microenvironmentChronic myeloid leukaemiaLeukaemia stem cellsNK cellsTreatment-free remissionTyrosine kinase inhibitor

Identifiers

PMID36780103
PMCPMC9995533
OpenAlexW4320489868

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.