ArticleThe Journal of experimental medicine2013
MIP-1α/CCL3-mediated maintenance of leukemia-initiating cells in the initiation process of chronic myeloid leukemia.
Article in The Journal of experimental medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- Oncogenic and microenvironmental signals drive cell type specific apoptosis resistance in juvenile myelomonocytic leukemia.Cell death & disease · 2025Article
- Serologic IL-18 increase with B-cell IL-18R loss characterizes selective IgA deficiency.Frontiers in immunology · 2025Article
- Basophils may as a risk factor for upper gastrointestinal cancer: a Mendelian randomization (MR) study.Ecancermedicalscience · 2024Article
- Predictive nonlinear modeling of malignant myelopoiesis and tyrosine kinase inhibitor therapy.eLife · 2023Article
- Persistent DNA damage and oncogenic stress-induced Trem1 promotes leukemia in mice.Haematologica · 2022Article
- Basophils from allergy to cancer.Frontiers in immunology · 2022Review
- Regulation of emergency granulopoiesis during infection.Frontiers in immunology · 2022Review
- From the niche to malignant hematopoiesis and back: reciprocal interactions between leukemia and the bone marrow microenvironment.JBMR plus · 2021Article
- New routes to eradicating chronic myelogenous leukemia stem cells by targeting metabolism.International journal of hematology · 2021Review
- Article
- Reduction of leukemic burden via bone-targeted nanoparticle delivery of an inhibitor of C-chemokine (C-C motif) ligand 3 (CCL3) signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Cytoplasmic DNA accumulation preferentially triggers cell death of myeloid leukemia cells by interacting with intracellular DNA sensing pathway.Cell death & disease · 2021Article
- Cancer non-stem cells as a potent regulator of tumor microenvironment: a lesson from chronic myeloid leukemia.Molecular biomedicine · 2021Review
- Expansion of senescent megakaryocyte-lineage cells maintains CML cell leukemogenesis.Blood advances · 2020Article
- Involvement of a Transcription factor,Cancers · 2020Article
- CC Chemokines in a Tumor: A Review of Pro-Cancer and Anti-Cancer Properties of Receptors CCR5, CCR6, CCR7, CCR8, CCR9, and CCR10 Ligands.International journal of molecular sciences · 2020Review
- CCL3-CCR5 axis contributes to progression of esophageal squamous cell carcinoma by promoting cell migration and invasion via Akt and ERK pathways.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Oxidative resistance of leukemic stem cells and oxidative damage to hematopoietic stem cells under pro-oxidative therapy.Cell death & disease · 2020Review
- Is There a Role for Basophils in Cancer?Frontiers in immunology · 2020Review
- Loss of FGFR3 Delays Acute Myeloid Leukemogenesis by Programming Weakly Pathogenic CD117-Positive Leukemia Stem-Like Cells.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the initiation process of chronic myeloid leukemia (CML), a small number of transformed leukemia-initiating cells (LICs) coexist with a large number of normal hematopoietic cells, gradually increasing thereafter and eventually predominating in the hematopoietic space. However, the interaction between LICs and normal hematopoietic cells at the early phase has not been clearly delineated because of the lack of a suitable experimental model. In this study, we succeeded in causing a marked leukocytosis resembling CML from restricted foci of LICs in the normal hematopoietic system by direct transplantation of BCR-ABL gene-transduced LICs into the bone marrow (BM) cavity of nonirradiated mice. Herein, we observed that BCR-ABL(+)lineage(-)c-kit(-) immature leukemia cells produced high levels of an inflammatory chemokine, MIP-1α/CCL3, which promoted the development of CML. Conversely, ablation of the CCL3 gene in LICs dramatically inhibited the development of CML and concomitantly reduced recurrence after the cessation of a short-term tyrosine kinase inhibitor treatment. Finally, normal hematopoietic stem/progenitor cells can directly impede the maintenance of LICs in BM in the absence of CCL3 signal.
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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.