Fig. 2
From: Structural and functional consequences of the STAT5BN642H driver mutation
STAT5BN642H promotes aggressive T-cell neoplasia and cytokine-independent cell growth. a Macroscopic images showing substantial skin lesions (upper panel; arrows) and lymphadenopathy (lower panels; arrows) observed in the STAT5BN642H transgenic mice, compared with human STAT5B and wild-type (WT) control mice. b Axillary, brachial and inguinal LN, spleen, and liver weights were measured from 7- to 9-week-old WT (n = 4–6) and STAT5BN642H (n = 5–8) transgenic mice. c Flow cytometric analysis of the percentage of CD8+, CD4+, or TCRγδ+ T-cells from the CD3+ cell population in the LNs of 7-week-old WT (n = 4) and STAT5BN642H (n = 7) mice. d Colony-forming unit (CFU) assays using bone marrow cells from 7- to 10-week-old WT (n = 4), human STAT5B (n = 4) and human STAT5BN642H (n = 5) mice, plated in duplicate in base methylcellulose in the presence (20 ng mL–1) or absence (-) of individual cytokines. Colonies were counted after 10 days. All data are graphed as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, by unpaired two-tailed Student’s t-test (b, c) or one-way ANOVA with Bonferroni’s correction (d). Source data are provided as a Source Data file
