Fig. 2

Mechanisms that Drive Leukemia Propagating Cell Frequency and Latency Can Evolve Independently

(A) Fish were transplanted with 25 LPCs from various clones and assessed for time to leukemia onset (n = 8–10 animals transplanted per individual clone). Denotes significant differences in latency between clones that have low (upper left panel) or high (lower left panel) LPC frequencies (<0.001). Representative fluorescent images of animals following 28 days of engraftment are shown.

(B) Correlation between LPC frequency and T-ALL latency across all clones.

(C) EDU analysis of selected clones and correlation with LPC frequency and latency. Each datum point represents a single clone. NS, not significant. Denotes a significant difference in the percent of cells that are EDU-positive (p = 0.0004).

(D) Animals were transplanted with 25 LPCs from clone 11.2 (dsRED-positive, 1:78 LPC frequency, 88 days latency) and 25 LPCs from clone 4.3 (GFP-positive, 1:246 LPC frequency, 28 days latency). Representative images of whole fish and confocal images of T-ALL cells harvested at 15 days and 45 days posttransplantation. The percentages of dsRED-positive and GFP-positive cells at 15 days and 45 days were analyzed by FACS. Data are represented as ± SE (n = 4–7 transplant recipients per time point).

(E) Twenty-five LPCs from clone 1.3 (zsYellow-positive, 1:13 LPC frequency, 58 days latency) were competed with 25 LPCs from clone 5.1 (amCyan-positive, 1:184 LPC frequency, 30 days latency), and analyzed as in (D). Scale bars represent 5 mm in images of whole fish and 40 µm in confocal images.

See also Figure S2.