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Bone mesenchymal stromal cells exhibit functional inhibition but no chromosomal aberrations in chronic myelogenous leukemia

Chronic myelogenous leukemia (CML) is a myeloproliferative neoplasia characterized by the presence of the Philadelphia (Ph) chromosome in hematopoietic cells (HCs). As one of the most important components of the bone marrow microenvironment (BMM), bone mesenchymal stromal cells (BMSCs) are critical...

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Detalles Bibliográficos
Autores principales: Xie, Jieqiong, Chen, Jiadi, Wang, Bin, He, Xuchun, Huang, Huifang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6312938/
https://www.ncbi.nlm.nih.gov/pubmed/30655859
http://dx.doi.org/10.3892/ol.2018.9681
Descripción
Sumario:Chronic myelogenous leukemia (CML) is a myeloproliferative neoplasia characterized by the presence of the Philadelphia (Ph) chromosome in hematopoietic cells (HCs). As one of the most important components of the bone marrow microenvironment (BMM), bone mesenchymal stromal cells (BMSCs) are critical in the development of leukemia and essential in the regulation of hematopoiesis. However, little is known regarding the alterations of BMSCs in CML. The current study performed Cell Counting Kit-8 and colony-forming unit fibroblast assays to evaluate the proliferative ability of BMSCs. The percentage of senescent BMSCs was evaluated by a senescence-associated β-galactosidase staining assay. Subsequently, a long-term culture-initiating cell assay was designed to explore the HC-supporting capacity of the BMSCs. Furthermore, cytogenetics were detected by conventional cytogenetic analysis and fluorescence in situ hybridization analysis. The current results revealed that CML-BMSCs exhibited decreased cell proliferation and impaired HC-support capacity, as well as increased susceptibility to senescence. No chromosomal aberrations, including the absence of the Ph chromosome, were noted in all CML-BMSCs. In conclusion, the current study demonstrated functional inhibition of CML-BMSCs; however, no signs of chromosomal aberrations were observed, thereby providing insight into the changes occurring in the CML-BMM.