Suppression of T-cell lymphomagenesis in mice requires PTEN phosphatase activity

Ryan H Newton, Yu Lu, Antonella Papa, Greg H Whitcher, Youn-Jung Kang, Catherine Yan, Pier P Pandolfi, Laurence A Turka

Research output: Contribution to journalArticleResearchpeer-review

11 Citations (Scopus)


Mice with T-cell-specific loss of the tumor suppressor gene PTEN early in T-cell ontogeny develop thymic lymphomas that invariably harbor a reciprocal translocation involving the T-cell receptor alpha/delta locus and c-myc, t(14;15). In addition to its known function as a lipid phosphatase opposing PI3K signaling, PTEN has also been described as playing a prominent role in promoting genomic stability. As a result, it has been uncertain which one(s) of these 2 separable features were required to block the development of lymphoma. Here, using a conditional model in which T cells selectively express 1 phosphatase-dead PTEN mutant (C124S) and maintain 1 null allele, we show that PTEN phosphatase activity is required for preventing the emergence of a malignant T-cell population harboring t(14;15), thus constituting a critical function of PTEN in preventing lymphomagenesis.
Original languageEnglish
Pages (from-to)852 - 855
Number of pages4
Issue number5
Publication statusPublished - 2015

Cite this