Normal development is an integral part of tumorigenesis in T cell-specific PTEN-deficient mice.

ABSTRACT: PTEN is a tumor suppressor gene but whether cancer can develop in all PTEN-deficient cells is not known. In T cell-specific PTEN-deficient (tPTEN-/-) mice, which suffer from mature T cell lymphomas, we found that premalignancy, as defined by elevated AKT and senescence pathways, starts in immature T cell precursors and surprisingly not in mature T cells. Premalignancy only starts in 6-week-old mice and becomes much stronger in 9-week-old mice although PTEN is lost since birth. tPTEN-/- immature T cells do not become tumors, and senescence has no role in this model because these cells exist in a novel cell cycle state, expressing proliferating proteins but not proliferating to any significant degree. Instead, the levels of p27(kip1), which is lower in tPTEN-/- immature T cells and almost no

SUBMITTER: Xue L 

PROVIDER: S-EPMC2538875 | biostudies-literature | 2008 Feb

REPOSITORIES: biostudies-literature