Skip to main content
. 2011 Mar 22;117(20):5453–5462. doi: 10.1182/blood-2010-09-309831

Figure 1.

Figure 1

Lmo2 collaborates with the loss of p19Arf to accelerate tumorigenesis. (A) Kaplan-Meier curves showing survival of mice transplanted with GFP, Arf+/+ (n = 5), GFP, Arf−/− (n = 8), Lmo2-GFP, Arf+/+ (n = 6), and Lmo2-GFP, Arf−/− (n = 6) bone marrow cells. The median survival for mice receiving Lmo2-GFP, Arf+/+ donor cells was 314.5 days and that for mice receiving for Lmo2-GFP, Arf−/− donor cells was 182.5 days. The differences in median survival were significant (P < .0049). (B) Kaplan-Meier curves showing survival of mice transplanted with γc-GFP, Arf−/− (n = 6) versus γc, Lmo2-GFP, Arf−/− (n = 10) donor bone marrow cells. The median survival for mice receiving γc, Lmo2-GFP, Arf−/− cells was 181.5 days. (C) Ratio of mean GFP intensity (MGI) in the Lmo2-GFP, Arf+/+, Lmo2-GFP, Arf−/− tumor populations normalized to the negative control. The MGI of each mouse was determined from the organ with the highest tumor cell population. (D) Levels of Lmo2 present in extracts of double-positive (DP) and double-negative (DN), T-cell tumors from animals transplanted in panels A and B were assessed by immunoblotting. A goat polyclonal antiserum to Lmo2 was used at a 1:500 dilution. β-actin was used as the loading control. (E) Southern blot demonstrating clonal retroviral insertions in the DNA of T-cell tumors in spleen (S) and thymus (T) of representative mice that received Lmo2-mCherry, Arf−/− donor cells. DNA was digested with EcoRI, which cuts on one side of the radiolabeled mCherry probe fragment and gives a unique band size for each integration event.