IP administration of Δ¹²-PGJ₃ eradicates LSCs and prolongs survival in a murine CML model. (A) Analysis of the effect of Δ¹²-PGJ₃ treatment on the development of splenomegaly in mice transplanted with BCR-ABL-GFP⁺ LSCs. Representative photographs of spleens from control and BCR-ABL–transplanted mice treated with Δ¹²-PGJ₃ (0.025 mg/kg) or vehicle control with corresponding spleen weights. n = 10 per treatment group. *P < .05. (B) Analysis of WBC counts of BCR-ABL⁺ LSC- or MSCV-HSC–transplanted mice treated with Δ¹²-PGJ₃ or vehicle control. *P < .0001. (C) Flow cytometric analysis of Sca-1⁺Kit⁺GFP⁺ cells in the spleens of mice transplanted with BCR-ABL⁺ LSCs or MSCV⁺ HSCs treated with Δ¹²-PGJ₃ or vehicle control. n = 5 per group. *P < .001. (D) Analysis of LSCs (Kit⁺Sca-1⁺Lin⁻GFP⁺) in the BM of BCR-ABL⁺ LSC-transplanted and Δ¹²-PGJ₃–treated mice after 5 weeks of last dose of Δ¹²-PGJ₃ (0.025 mg/kg). As a control, BCR-ABL⁺ LSC–transplanted mice treated with vehicle for 1 week were used for comparison. (E) Survival curves of mice transplanted with BCR-ABL⁺ LSCs or MSCV-GFP⁺ HSCs on treatment with Δ¹²-PGJ₃ (0.025 mg/kg) or vehicle. n = 8 per treatment group. (F). HSCs were isolated from the BM of C57BL/6 mice and plated in methylcellulose (1 × 10⁶ cells/mL/well; erythropoietin, SCF, IL-3, and BMP4) with PBS or Δ¹²-PGJ₃ (25nM) and cultured for 1 week and then hematopoietic CFCs were scored. Data shown are representative of triplicate experiments.