BCL-2 enhances disease latency irrespective of p53-dependent signaling. (A) Functional analysis of 3 cell lines obtained from Eμ-myc/vav-bcl-2 mice. Cell lines were infected with retrovirus expressing a dnp53. The expression in turn abrogates p21 up-regulation after the addition of etoposide to the cell culture medium for 24 hours. (B) Survival analysis of mice receiving cell lines from Eμ-myc/vav-bcl-2 mice with or without a dnp53. The expression of dnp53 does not alter the survival time (n = 10 mice of each cell type, 3 different cell lines of each genotype). (C) Expression of BCL-2 in cell lines obtained from Eμ-myc/p53^+/− mice. Cell lines were infected with a retrovirus expressing BCL-2 and the empty vector (n = 4 each). The immunoblot shows the enhanced levels of BCL-2 in infected cell lines. p53 was not detected in any cell line derived from Eμ-myc/p53^+/− mice. (C) The positive control for p53 derived from HEK 293 crude cell lysate. (D) Survival analysis of mice that received a transplant with Eμ-myc/p53^+/− cell lines with or without overexpression of BCL-2. As depicted, overexpression of BCL-2 significantly increases the overall survival time (P = .0128; Eμ-myc/p53^+/−, n = 10; Eμ-myc/p53^+/− + BCL-2, n = 11).