Journal
CANCER CELL
Volume 1, Issue 2, Pages 157-168Publisher
CELL PRESS
DOI: 10.1016/S1535-6108(02)00029-6
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Funding
- NCI NIH HHS [1 R01 CA 46283, 5 U01 CA84314] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA046283, U01CA084314] Funding Source: NIH RePORTER
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We have inactivated pRb, p107, and p130 in astrocytes by transgenic expression of T-121 (a truncated SV40 T antigen) under the GFAP promoter. Founder mice died perinatally with extensive expansion of neural precursor and anaplastic astrocyte populations. In astrocytes, aberrant proliferation and extensive apoptosis were induced. Using a conditional allele of T-121, early lethality was circumvented, and adult mice developed high-grade astrocytoma, in which regions of decreased apoptosis expressed activated Akt. Indeed, astrocytoma development was accelerated in a PTEN+/-, but not p53(+/-), background. These studies establish a highly penetrant preclinical model for astrocytoma based on events observed in the human disease and further provide insight into the role of PTEN mutation in astrocytoma progression.
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