Suppression of T-cell lymphomagenesis in mice requires PTEN phosphatase activity.
Blood
; 125(5): 852-5, 2015 Jan 29.
Article
in En
| MEDLINE
| ID: mdl-25477498
ABSTRACT
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 α/δ 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.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Thymus Neoplasms
/
T-Lymphocytes
/
Gene Expression Regulation, Neoplastic
/
Lymphoma, T-Cell
/
PTEN Phosphohydrolase
Limits:
Animals
Language:
En
Journal:
Blood
Year:
2015
Type:
Article