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[摘要]:Regulation of the Pten tumor suppressor is complex and mediated by varied mechanisms. In this issue of Blood, Wey and colleagues show in a biallelic conditional knockout mouse model of GRP78 and PTEN that heterozygous loss of Grp78 suppresses leukemogenesis mediated by Pten.(1) These findings suggest a novel manner of down-regulation of PI 3 kinase signaling that may have potential therapeutic benefit. |
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