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. Author manuscript; available in PMC: 2024 Jun 15.
Published in final edited form as: Br J Haematol. 2024 Mar 20;204(6):2487–2491. doi: 10.1111/bjh.19421

Figure 2. Clonal evolution of STAT5B mutated myeloid neoplasm and its role in leukemogenesis.

Figure 2.

(A) Flow cytometry sorting strategy highlighting different cell populations labeled by various colors. (B) Summary of mutations detected in each cell population using an in-house myeloid and lymphoid NGS panel. (C) Hypothesized clonal evolution steps based on NGS mutational testing results from (B). (D) Schematic representation of the investigation into the role of STAT5B overexpression in leukemogenesis in a mouse model. Mouse hematopoietic stem/progenitor cells (HSPCs) were isolated from the bone marrows of control or TET2 knockout mice, then transduced with MSCV-IRES-GFP based retroviruses carrying an empty vector (Con), wild type (WT) or STAT5B N642H, and subsequently injected into lethally irradiated recipient mice. (E) Representative flow cytometry profile illustrating the development of myeloid leukemia induced by both WT and N642H STAT5B overexpression. (F) Survival curve of mice receiving STAT5B WT or mutant transduced HSPCs, showing accelerated myeloid leukemia development in the STAT5B mutant group compared to the STAT5B wild-type group (p<0.05), with further expedited leukemia development upon TET2 deletion (p<0.01).