Apaf-1 and caspase-9 do not act as tumor suppressors in myc-induced lymphomagenesis or mouse embryo fibroblast transformation
- Scott, CL; Schuler, M; Marsden, VS; Egle, A; Pellegrini, M; Nesic, D; Gerondakis, S; Nutt, SL; Green, DR; Strasser, A;
Publication Year 2004-01-05, Volume 164, Issue #1, Page 89-96
- Journal Title
- JOURNAL OF CELL BIOLOGY
- Publication Type
- Journal Article
- Based on experiments with cultured fibroblasts, the apoptosis regulators caspase-9 and Apaf-l are hypothesized to function as tumor suppressors. To investigate their in vivo role in lymphomagenesis, an IgH enhancer-driven c-myc transgene was crossed onto Apaf-1(-/-) and caspase-9(-/-) mice. Due to perinatal lethality, Emu-myc transgenic Apaf-1(-/-) or caspase-9(-/-) fetal liver cells were used to reconstitute lethally irradiated recipient mice. Surprisingly, no differences were seen in rate, incidence, or severity of lymphoma with loss of Apaf-l or caspase-9, and Apaf-l was not a critical determinant of anticancer drug sensitivity of c-myc-induced lymphomas. Moreover, loss of Apaf-l did not promote oncogene-induced transformation of mouse embryo fibroblasts. Thus, Apaf-l and caspase-9 do not suppress c-myc-induced lymphomagenesis and embryo fibroblast transformation.
- ROCKEFELLER UNIV PRESS
- C-MYC; TRANSGENIC MICE; CELL-DEATH; B-CELLS; P53-DEPENDENT APOPTOSIS; IN-VIVO; BCL-2; DEFICIENCY; ACTIVATION; P53
- Publisher's Version
- Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2004-01-05 12:00:00Last Modified: 0001-01-01 12:00:00