Table 2.

Mouse models overexpressing Pim proteins.

Mouse model	Expression of transgene	Phenotype
Eμ-pim1	B- and T-cells	Enlargement of the spleen
		Monoclonal T-cell lymphoma with high expression of c-myc; 10% penetrance, 240 weeks latency (22–24)
H2K-pim1	B- and T-cells	No spontaneous tumors (23)
Pim1-Tx	Lymphoid lineage: higher expression in B lymphoid cells than in myeloid cells	Enhanced hematopoiesis, higher BrdU incorporation in long-term HSC populations, and greater ability to reconstitute lethally irradiated mice
		Acute lymphoblastic leukemia/lymphoma; 10% penetrance, 20–62 weeks latency (31)
pim1; PSA61-Cre	Prostate and bladder epithelium	100% of 10-month-old mice developed low-grade mPIN lesions
		The incidence of low-grade and high-grade mPIN lesions increases after two rounds of hormone treatment. All (100%) of the mice developed mPIN lesions at 24 weeks of age, with a 10% incidence of high-grade mPIN and in situ carcinoma (33)
		All (100%) of the mice developed high-grade bladder and urothelial hyperplasia after two rounds of hormone treatment, inducing pyelonephritis (34)
Eμ-pim2	B- and T-cells	T-cell lymphoma in 40% of the mice after 1 year (29)
alb-pim3	Hepatocytes	No tumors after 1 year (35)
Tissue recombination model coupled with lentiviral-mediated gene transfer	Prostate cells from 6-week-old C57BL/6 mice infected with lentivirus	Pim1 is weakly oncogenic in naïve adult mouse prostatic epithelium. However, it cooperates dramatically with c-myc to induce high-grade prostatic cancer with NE differentiation
		100% penetrance in 6 weeks (32)