Apaf-1 and caspase-9 do not act as tumor suppressors in myc-induced lymphomagenesis or mouse embryo fibroblast transformation
Details
Publication Year 2004-01-05, Volume 164, Issue #1, Page 89-96
Journal Title
JOURNAL OF CELL BIOLOGY
Publication Type
Journal Article
Abstract
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.
Publisher
ROCKEFELLER UNIV PRESS
Keywords
C-MYC; TRANSGENIC MICE; CELL-DEATH; B-CELLS; P53-DEPENDENT APOPTOSIS; IN-VIVO; BCL-2; DEFICIENCY; ACTIVATION; P53
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Creation Date: 2004-01-05 12:00:00
Last Modified: 0001-01-01 12:00:00
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