Figure 1.

Phf6 loss decreases the leukemogenic potential of cells in vivo and triggers a change in disease presentation. (A) PHF6 is a lineage-specific regulator of tumor growth in B-ALL and T-cell acute lymphoblastic leukemia (T-ALL). (B). Kaplan-Meier survival analysis of mice injected with either 10³ (dotted) or 10⁶ (solid) Phf6^WT (blue) and Phf6^KO (red) B-ALL cells. The number (n) of mice per genotype analyzed is shown. Statistical analysis (log-rank test, Mantel-Cox) was performed for the different groups in comparison with mice injected with Phf6^WT cells. P-values are shown for the comparisons. (C) Representative hematoxylin and eosin (H&E) (top) and immunohistochemistry (bottom) staining of serial sections from lymph nodes (LNs) and lymphoma (mass) of recipient mice injected with Phf6^WT, shPhf6, and Phf6^KO cells. mCherry immunochemistry demarcates tumor cells. Bars, 600 µm. (D, top) Size comparison of representative LNs from Phf6^WT (left) and Phf6^KO (right) recipient mice. (Bottom) Quantification of combined LN weight of Phf6^WT (blue; n = 5) and Phf6^KO (red; n = 5) recipients. (E) Tumor burden in the blood of Phf6^WT (blue; n = 7) and Phf6^KO (red; n = 8) recipient mice. mCherry demarcates tumor cells. (F) Bar graphs showing the percentage of the CD4⁺ fraction among mCherry⁺ cells isolated from Phf6^WT (blue; n = 9) and Phf6^KO (red; n = 5) tumors in bone marrow (left) and LNs (right). Data represent the mean ± standard deviation (SD) in D–F. Statistics were calculated with two-sided Student's t-test. (***) P < 0.001; (****) P < 0.0001.