fig2

Single-cell sequencing in precision management of chronic myeloid leukemia

Figure 2. Interplay between intrinsic LSC heterogeneity and extrinsic microenvironmental regulation in CML. This illustration provides a panoramic view of CML precision management, spanning cellular subpopulation dynamics, inflammatory niche remodeling, and clinically relevant marker interpretation. Left panel: the Lin-CD34 + CD38- hematopoietic stem/progenitor cell compartment is resolved into functionally distinct sub-clusters via single-cell transcriptomics, including proliferative TKI-sensitive cells, quiescent TKI-tolerant cells, and primitive quiescent clusters. Middle panel: the leukemic bone marrow microenvironment is characterized by IL-6, TNF-alpha, and TGF-beta-mediated crosstalk that facilitates immune evasion and sustains the leukemic seed bank. Right panel: clinically relevant resistance-associated markers include CD26, IL1RAP, CD93, and state-dependent CD25 expression. CD25 is shown as an early or context-specific marker rather than a stable marker for post-treatment residual LSC eradication, because residual LSCs may lose CD25 while retaining CD26. This figure was redrawn by the authors using Python-based vector drawing and Microsoft Office-compatible elements; no third-party copyrighted materials were reused. LSC: Leukemia stem cell; TKI: tyrosine kinase inhibitor; scRNA-seq: single-cell RNA sequencing; IL-6: interleukin-6; TNF-alpha: tumor necrosis factor-alpha; TGF-beta: transforming growth factor-beta; IL1RAP: interleukin-1 receptor accessory protein.

Journal of Translational Genetics and Genomics
ISSN 2578-5281 (Online)
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