JunB overexpression reduces Ab-MuLV-induced colony formation in vitro and tumor formation in vivo. (A) Clonal outgrowth of Abelson-infected fetal liver cell suspensions. Fetal livers from wild-type (n = 6) and JunB transgenic (n = 9) mice were infected with Abelson retrovirus and subsequently cloned in cytokine-free methylcellulose. The initial number of B cells was determined by FACS. Results show the average numbers ± SD of colonies obtained per 1 × 105 B cells plated (n = 13 for JunB tg and n = 8 for wild-type fetal liver cells). Mock-infected cells were used as controls and did not give rise to colonies. (B) Newborn mice were injected intraperitoneally with replication-deficient v-abl retrovirus and observed over a period of 8 months. During this time, 3 of 11 JunB transgenic mice remained free of any leukemia/lymphoma. (C) White blood cell count in wild-type (n = 6) and Ubi-junB transgenic animals (n = 7) at the time point of fully developed disease. Data represent means ± SDs. (D) Histologic sections of spleen and liver from diseased wild-type and Ubi-junB transgenic animals. Leukemic cells heavily infiltrate wild-type liver and spleen but to a lesser degree JunB transgenic organs. One representative example of each genotype is depicted (n = 3). Panels stained with H&E; original magnification, × 100.
