ArticleBritish journal of haematology2016
Effects of pharmacological and genetic disruption of CXCR4 chemokine receptor function in B-cell acute lymphoblastic leukaemia.
Article in British journal of haematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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.
Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Trial
- Expression of the CXCR4 S338X Variant Improves Anti-Leukemia Efficacy of Anti-CD19 CAR-T Cells.Cancer science · 2026Article
- Novel molecular mechanisms of FLT3 deregulation: from the acute myeloid leukemia experience to therapeutic insights in acute lymphoblastic leukemia.Molecular cancer · 2025Review
- Glucocorticoids paradoxically promote steroid resistance in B cell acute lymphoblastic leukemia through CXCR4/PLC signaling.Nature communications · 2024Article
- CRISPR-Cas9 in basic and translational aspects of cancer therapy.BioImpacts : BI · 2024Review
- Review
- Bone Marrow Aging and the Leukaemia-Induced Senescence of Mesenchymal Stem/Stromal Cells: Exploring Similarities.Journal of personalized medicine · 2022Review
- Fast H3K9 methylation promoted by CXCL12 contributes to nuclear changes and invasiveness of T-acute lymphoblastic leukemia cells.Oncogene · 2022Article
- Targeting chemokines for acute lymphoblastic leukemia therapy.Journal of hematology & oncology · 2021Review
- Analysis of acute lymphoblastic leukemia drug sensitivity by changes in impedance via stromal cell adherence.PloS one · 2021Article
- Bone marrow MSC from pediatric patients with B-ALL highly immunosuppress T-cell responses but do not compromise CD19-CAR T-cell activity.Journal for immunotherapy of cancer · 2020Article
- The Biology of B-Progenitor Acute Lymphoblastic Leukemia.Cold Spring Harbor perspectives in medicine · 2020Review
- New Insights on the Emerging Genomic Landscape of CXCR4 in Cancer: A Lesson from WHIM.Vaccines · 2020Review
- CXC Chemokine Receptors in the Tumor Microenvironment and an Update of Antagonist Development.Reviews of physiology, biochemistry and pharmacology · 2020Review
- Support of acute lymphoblastic leukemia cells by nonmalignant bone marrow stromal cells.Oncology letters · 2019Article
- Notch/CXCR4 Partnership in Acute Lymphoblastic Leukemia Progression.Journal of immunology research · 2019Review
- Targeted genome editing in acute lymphoblastic leukemia: a review.BMC biotechnology · 2018Review
- A novel orally available Syk/Src/Jak2 inhibitor, SKLB-850, showed potent anti-tumor activities in B cell lymphoma (BCL) models.Oncotarget · 2017Article
- Novel AIDS therapies based on gene editing.Cellular and molecular life sciences : CMLS · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
B cell acute lymphoblastic leukaemia (B-ALL) cells express high levels of CXCR4 chemokine receptors for homing and retention within the marrow microenvironment. Bone marrow stromal cells (BMSC) secrete CXCL12, the ligand for CXCR4, and protect B-ALL cells from cytotoxic drugs. Therefore, the therapeutic use of CXCR4 antagonists has been proposed to disrupt cross talk between B-ALL cells and the protective stroma. Because CXCR4 antagonists can have activating agonistic function, we compared the genetic and pharmacological deletion of CXCR4 in B-ALL cells, using CRISPR-Cas9 gene editing and CXCR4 antagonists that are in clinical use (plerixafor, BKT140). Both genetic and pharmacological CXCR4 inhibition significantly reduced B-ALL cell migration to CXCL12 gradients and beneath BMSC, and restored drug sensitivity to dexamethasone, vincristine and cyclophosphamide. NOD/SCID/IL-2rγnull mice injected with CXCR4 gene-deleted B-ALL cells had significant delay in disease progression and superior survival when compared to control mice injected with CXCR4 wild-type B-ALL cells. These findings indicate that anti-leukaemia activity of CXCR4 antagonists is primarily due to CXCR4 inhibition, rather than agonistic activity, and corroborate that CXCR4 is an important target to overcome stroma-mediated drug resistance in B-ALL.
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What OpenQuestion holds
Registered trials
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.