Format

Send to

Choose Destination
Leuk Lymphoma. 2011 Jul;52(7):1200-10. doi: 10.3109/10428194.2011.564696. Epub 2011 Apr 4.

NOTCH and phosphatidylinositide 3-kinase/phosphatase and tensin homolog deleted on chromosome ten/AKT/mammalian target of rapamycin (mTOR) signaling in T-cell development and T-cell acute lymphoblastic leukemia.

Author information

1
Department of Hematology, The Central Hospital of Taian, Taian, Shandong, P R China. dmguo001@yahoo.com.cn

Abstract

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 γ-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.

PMID:
21463127
DOI:
10.3109/10428194.2011.564696
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Taylor & Francis
Loading ...
Support Center