Figure 3.
Leukemic blasts from pDC-AML and AML with RUNX1 mutations have greater differentiation propensity to pDCs in vitro. (A-C) The sorted leukemic blasts were cultured in vitro for 2 weeks and subjected to immunophenotyping by flow cytometry. (D) pDC proportions in the culture after 2 weeks were compared. Data are mean ± SD. (E) Time course experiments showed that a high pDC proportion persisted from the leukemic blasts of pDC-AML. Data are mean ± SEM. (F) Wright-Giemsa staining of sorted pDCs (were CD303+ and had bright CD123 and HLA-DR expression and were negative for CD11b, CD14, CD19, CD3, and CD56) from the in vitro culture. AML RUNX1, AML with RUNX1 mutations but no pDC expansion; AML no RUNX1, AML without RUNX1 mutations or pDC expansion. *P < .05, ***P < .001. Original magnification, ×1000 (F).

Leukemic blasts from pDC-AML and AML with RUNX1 mutations have greater differentiation propensity to pDCs in vitro. (A-C) The sorted leukemic blasts were cultured in vitro for 2 weeks and subjected to immunophenotyping by flow cytometry. (D) pDC proportions in the culture after 2 weeks were compared. Data are mean ± SD. (E) Time course experiments showed that a high pDC proportion persisted from the leukemic blasts of pDC-AML. Data are mean ± SEM. (F) Wright-Giemsa staining of sorted pDCs (were CD303+ and had bright CD123 and HLA-DR expression and were negative for CD11b, CD14, CD19, CD3, and CD56) from the in vitro culture. AML RUNX1, AML with RUNX1 mutations but no pDC expansion; AML no RUNX1, AML without RUNX1 mutations or pDC expansion. *P < .05, ***P < .001. Original magnification, ×1000 (F).

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