期刊
LEUKEMIA & LYMPHOMA
卷 52, 期 7, 页码 1200-1210出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/10428194.2011.564696
关键词
NOTCH1; PI3K/PTEN/AKT/mTOR; T-cell development; T-ALL
资金
- Shandong Province Natural Science Foundation, China [ZR2009CQ011]
Activating mutations in NOTCH1 consitute the most prominent genetic abnormality in T-cell acute lymphoblastic leukemia (T-ALL). However, most T-ALL cell lines with NOTCH1 mutations are resistant to treatment with g-secretase inhibitors (GSIs). The spotlight is now shifting to the phosphatidylinositide 3-kinase (PI3K)/phosphatase and tensin homolog deleted on chromosome ten (PTEN)/AKT/mammalian target of rapamycin (mTOR) pathway as another key potential target. These two signaling routes are deregulated in many types of cancer. In this review we discuss these two pathways with respect to their signaling mechanisms, functions during T-cell development, and their mutual roles in the development of T-ALL.
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