BM-expressing TEL2 causes a myeloid proliferative disease in mice. (A) Schematic representation of the MSCV-IRES-GFP and MSCV-TEL2-IRES-GFP retroviral vectors used for the transduction of the Lin^- BM cells. The TEL2 cDNA was cloned in the single EcoRI site and is followed by an IRES-GFP marker gene. LTR, long terminal repeat. (B) Myeloid clonogenic activity of BM cells transduced with TEL2 retrovirus (TEL2-BM) compared with BM cells transduced with vector (MSCV-BM) or untransduced BM cells (Un-BM). Bars indicate the number of colonies counted at each round of serial replating in MC1 to MC5. CFU (1000 cells per dish plated) counts show no difference among the 3 samples with regard to their successive colony-forming capacity. This graph depicts the result of 1 of 4 experiments that gave almost identical results. (C) Successive MC assays of TEL2-BM, MSCV-BM, and Un-BM cells after 4 weeks of LTC-IC culture on an M2-10B4 stromal layer showing an increased colony-forming capacity of the TEL2-BM cells during the first 2 rounds of MC culture. This graph depicts the result of 1 of 4 experiments that gave almost identical results. (D) Average monthly peripheral blood leukocyte counts of all mice receiving transplants with TEL2-BM, showing an increase of the WBCs starting at 6 months after transplantation. Error bars show the standard deviation of each data point. (E) Monthly percentage of GFP-positive cells in the peripheral blood of mice receiving transplants with MSCV-BM or TEL2-BM, showing a steady increase in GFP-positive cells in mice receiving transplants with TEL2-BM starting at 5 months after transplantation. Error bars show the standard deviation of each data point. (F) Comparison of the average leukocyte count—in peripheral blood of mice receiving transplants with UN-BM, MSCV-BM and TEL2-BM—at the moment of death of the TEL2-BM mice. (G) Combined Kaplan-Meier survival plot of 14 (2 × 7) lethally irradiated mice receiving transplants with MSCV-BM or TEL2-BM (n = 2).