Human Bone Marrow Mononuclear Cells-CML+
Cat.No.: CSC-C8143L
Species: Human
Source: Bone Marrow
Cell Type: Mononuclear Cell
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Desease: chronic myeloid leukemia, Philadelphia positive (CML(+))
Application: These cells can be used to investigate stem cell properties in tissue engineering, regenerative medicine, and developmental studies.
Human Bone Marrow Mononuclear Cells-CML+ are primary mononuclear cells isolated from the bone marrow of patients with chronic myeloid leukaemia (CML) known to carry the Philadelphia chromosome and the characteristic BCR-ABL1 fusion gene. These heterogeneous cell populations include leukemic stem cells (LSCs), progenitor cells, lymphocytes, monocytes and other bone marrow-derived immune cells. These cells are a highly relevant ex vivo model for the study of CML pathogenesis and bone marrow microenvironment interactions. CML+ bone marrow mononuclear cells are commonly used for studies of leukemic stem cell biology, tyrosine kinase inhibitor (TKI) resistance, disease progression and molecular signaling pathways related to BCR-ABL activity. These primary cells retain patient specific genetic and phenotypic characteristics and provide a useful platform for the study of mechanisms of drug resistance, regulation of apoptosis, autophagy and cytokine mediated survival signaling.
Human Bone Marrow Mononuclear Cells-CML+ are also commonly utilized in studies on leukemia-stromal interactions, immune dysregulation and bone marrow niche remodeling. They are also used in translational research to evaluate novel targeted therapies, combination treatment strategies and personalized medicine approaches. The CML-derived bone marrow mononuclear cells are of clinical relevance and biological complexity, which makes them an important model for both basic leukaemia research and therapeutic development in haematological malignancies.
OIP5-AS1 was Highly Expressed in LSCs From CML Patients with Poor Response to TKI and K562/G01 Cells
Despite tyrosine kinase inhibitors (TKIs) transforming CML treatment, resistance-often linked to cytoprotective autophagy-remains a major challenge. While lncRNAs contribute to drug resistance, their role in modulating autophagy in CML is unclear. This study investigates how the lncRNA OIP5-AS1 influences autophagy and TKI resistance.
Analyzing single-cell sequencing data (GSE76312), they found that OIP5-AS1 expression was significantly higher in leukemic stem cells (LSCs) from TKI poor-responders (defined by failure to achieve MMR) compared to good-responders (Fig. 1A). This was validated by RT-qPCR, which showed elevated OIP5-AS1 levels in the imatinib-resistant K562/G01 cell line versus parental K562 cells (Fig. 1B). Furthermore, OIP5-AS1 expression was upregulated in bone marrow mononuclear cells (BMMNCs) from CML patients relative to normal controls (Fig. 1C). These data suggest a correlation between OIP5-AS1 and TKI resistance in CML.
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