TY  - JOUR
A1  - Jäger, Richard
A1  - Hahne, Jens
A1  - Jacob, Andrea
A1  - Egert, Angela
A1  - Schenkel, Johannes
A1  - Wernert, Nicolas
A1  - Schorle, Hubert
A1  - Wellmann, Axel
T1  - Mice transgenic for NPM-ALK develop non-Hodgkin lymphomas
T2  - Anticancer Res. (Anticancer Research)
N2  - BACKGROUND
The t(2;5)(p23;q35) translocation is associated with a high percentage of anaplastic large-cell lymphomas (ALCL) of T- or null-cell phenotype. The translocation produces an 80 kDa hyperphosphorylated chimeric protein (p80) derived from the fusion of the anaplastic lymphoma kinase (ALK) with nucleophosmin (NPM). The NPM-ALK chimeric protein is an activated tyrosine kinase that has been shown to be a potent oncogene and presumably plays a causative role in lymphomagenesis.
MATERIALS AND METHODS
A transgenic mouse line was generated, where the human NPM-ALK cDNA is driven by the lck promoter conferring transgene expression to early T-cells.
RESULTS
Mice rapidly developed large cell lymphoblastic lymphomas with a median latency of 8 weeks, primarily involving the thymus, with lymph node as well as histologically evident extranodal organ infiltration by large tumor cells.
CONCLUSION
The transgenic approach described provides direct evidence for the strong transforming potential of NPM-ALK in T-cells and furthermore represents a system for the analysis of the oncogenic events mediated by NPM-ALK in vivo, which might be instrumental in the development of tyrosine kinase inhibitor therapies of potential clinical use.
Y1  - 2005
UR  - https://pub.h-brs.de/frontdoor/index/index/docId/3748
UR  - http://ar.iiarjournals.org/content/25/5/3191
SN  - 0250-7005
VL  - 25
IS  - 5
SP  - 3191
EP  - 3196
PB  - International Institute of Anticancer Research
ER  -