ArticleBlood2012
Effects of plerixafor in combination with BCR-ABL kinase inhibition in a murine model of CML.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- Review
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- Targeting Abnormal Hematopoietic Stem Cells in Chronic Myeloid Leukemia and Philadelphia Chromosome-Negative Classical Myeloproliferative Neoplasms.International journal of molecular sciences · 2021Review
- Review
- Kindlin-3 loss curbs chronic myeloid leukemia in mice by mobilizing leukemic stem cells from protective bone marrow niches.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Redistribution, homing and organ-invasion of neoplastic stem cells in myeloid neoplasms.Seminars in cancer biology · 2020Review
- Bone marrow microenvironment: The guardian of leukemia stem cells.World journal of stem cells · 2019Review
- Chemokines as a Conductor of Bone Marrow Microenvironment in Chronic Myeloid Leukemia.International journal of molecular sciences · 2017Review
- Cellular and Molecular Networks in Chronic Myeloid Leukemia: The Leukemic Stem, Progenitor and Stromal Cell Interplay.Current drug targets · 2017Review
- Chronic myelogenous leukaemia exosomes modulate bone marrow microenvironment through activation of epidermal growth factor receptor.Journal of cellular and molecular medicine · 2016Article
- Survival regulation of leukemia stem cells.Cellular and molecular life sciences : CMLS · 2016Review
- A hostel for the hostile: the bone marrow niche in hematologic neoplasms.Haematologica · 2015Review
- A derivative of epigallocatechin-3-gallate induces apoptosis via SHP-1-mediated suppression of BCR-ABL and STAT3 signalling in chronic myelogenous leukaemia.British journal of pharmacology · 2015Article
- Cancer stem cells in basic science and in translational oncology: can we translate into clinical application?Journal of hematology & oncology · 2015Review
- Chronic myeloid leukemia-derived exosomes promote tumor growth through an autocrine mechanism.Cell communication and signaling : CCS · 2015Article
- Cytokine Regulation of Microenvironmental Cells in Myeloproliferative Neoplasms.Mediators of inflammation · 2015Review
- Toward a therapeutic reduction of imatinib refractory myeloproliferative neoplasm-initiating cells.Oncogene · 2014Article
- Antagonism of SET using OP449 enhances the efficacy of tyrosine kinase inhibitors and overcomes drug resistance in myeloid leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Sequestration in the bone marrow niche may allow leukemic stem cells to evade exposure to drugs. Because the CXCR4/SDF-1 axis is an important mechanism of leukemic stem cell interaction with marrow stroma, we tested whether plerixafor, an antagonist of CXCR4, may dislodge chronic myeloid leukemia (CML) cells from the niche, sensitizing them to tyrosine kinase inhibitors. We initially treated mice with retrovirally induced CML-like disease with imatinib plus plerixafor. Plerixafor mobilized CXCR4(+) cells, but no difference was observed in leukemia burden, possibly reflecting insufficient disease control by imatinib. In a second series of experiments, we tested the combination of plerixafor with dasatinib in the same as well as an attenuated CML model. Despite much improved leukemia control, plerixafor failed to reduce leukemia burden over dasatinib alone. In addition, mice receiving plerixafor had an increased incidence of neurologic symptoms in association with CNS infiltration by BCR-ABL-expressing cells. We conclude that plerixafor is ineffective in reducing leukemia burden in this model but promotes CNS infiltration. Beneficial effects of combining tyrosine kinase inhibitors with plerixafor may be observed in a situation of minimal residual disease, but caution is warranted when disease control is incomplete.
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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.