ReviewInternational journal of molecular sciences2017
Chemokines as a Conductor of Bone Marrow Microenvironment in Chronic Myeloid Leukemia.
Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- CCL5 exposure promotes acute and transient megakaryopoiesis and hematopoietic progenitor expansion.Stem cell reports · 2026Article
- Cytokines, Signaling and Epigenetic Mechanisms: Shaping the Acute Lymphoblastic Leukemia Microenvironment.Cells · 2026Review
- The tumor microenvironment in hematologic malignancies: immune evasion, metabolic reprogramming, and therapeutic resistance.Blood science (Baltimore, Md.) · 2026Review
- Maraviroc/cisplatin combination inhibits gastric cancer tumoroid growth and improves mice survival.Biological research · 2025Article
- A novel study on CXXC5: unraveling its regulatory mechanisms in hematopoietic stem cell biology through proteomics and gene editing.Genes & genomics · 2024Article
- Identification of Novel Risk Variants of Inflammatory Factors Related to Myeloproliferative Neoplasm: A Bidirectional Mendelian Randomization Study.Global medical genetics · 2024Article
- Identification of ubiquitination-related hub genes in chronic myeloid leukemia cell by bioinformatics analysis.Journal of Cancer · 2024Article
- IGFBP-6 Alters Mesenchymal Stromal Cell Phenotype Driving Dasatinib Resistance in Chronic Myeloid Leukemia.Life (Basel, Switzerland) · 2023Article
- Resistance to Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia-From Molecular Mechanisms to Clinical Relevance.Cancers · 2021Review
- Bone Marrow Soluble Mediator Signatures of Patients With Philadelphia Chromosome-Negative Myeloproliferative Neoplasms.Frontiers in oncology · 2021Article
- Inhibition of CXCR4 ameliorates hypoxia-induced pulmonary arterial hypertension in rats.American journal of translational research · 2021Article
- The CCL5/CCR5 Axis in Cancer Progression.Cancers · 2020Review
- Bone marrow niches in myeloid neoplasms.Pathology international · 2020Review
- Article
- Cadherins, Selectins, and Integrins in CAM-DR in Leukemia.Frontiers in oncology · 2020Review
- Transcriptomics-Based Characterization of the Toxicity of ZnO Nanoparticles Against Chronic Myeloid Leukemia Cells.International journal of nanomedicine · 2020Article
- Cysteine-rich protein 61 regulates the chemosensitivity of chronic myeloid leukemia to imatinib mesylate through the nuclear factor kappa B/Bcl-2 pathway.Cancer science · 2019Article
- HDAC1,2 Knock-Out and HDACi Induced Cell Apoptosis in Imatinib-Resistant K562 Cells.International journal of molecular sciences · 2019Article
- Deciphering the mechanism of Indirubin and its derivatives in the inhibition of Imatinib resistance using a "drug target prediction-gene microarray analysis-protein network construction" strategy.BMC complementary and alternative medicine · 2019Article
- Strategies For Targeting Chronic Myeloid Leukaemia Stem Cells.Blood and lymphatic cancer : targets and therapy · 2019Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
All blood lineage cells are generated from hematopoietic stem cells (HSCs), which reside in bone marrow after birth. HSCs self-renew, proliferate, and differentiate into mature progeny under the control of local microenvironments including hematopoietic niche, which can deliver regulatory signals in the form of bound or secreted molecules and from physical cues such as oxygen tension and shear stress. Among these mediators, accumulating evidence indicates the potential involvement of several chemokines, particularly CXCL12, in the interaction between HSCs and bone marrow microenvironments. Fusion between breakpoint cluster region (BCR) and Abelson murine leukemia viral oncogene homolog (ABL)-1 gene gives rise to BCR-ABL protein with a constitutive tyrosine kinase activity and transforms HSCs and/or hematopoietic progenitor cells (HPCs) into disease-propagating leukemia stem cells (LSCs) in chronic myeloid leukemia (CML). LSCs can self-renew, proliferate, and differentiate under the influence of the signals delivered by bone marrow microenvironments including niche, as HSCs can. Thus, the interaction with bone marrow microenvironments is indispensable for the initiation, maintenance, and progression of CML. Moreover, the crosstalk between LSCs and bone marrow microenvironments can contribute to some instances of therapeutic resistance. Furthermore, evidence is accumulating to indicate the important roles of bone marrow microenvironment-derived chemokines. Hence, we will herein discuss the roles of chemokines in CML with a focus on bone marrow microenvironments.
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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.