Mice transgenic for NPM-ALK develop non-Hodgkin lymphomas.
Anticancer Res
; 25(5): 3191-6, 2005.
Article
em En
| MEDLINE
| ID: mdl-16101126
ABSTRACT
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 ANDMETHODS:
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.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas Tirosina Quinases
/
Linfoma de Células T
Limite:
Animals
/
Female
/
Humans
/
Pregnancy
Idioma:
En
Revista:
Anticancer Res
Ano de publicação:
2005
Tipo de documento:
Article
País de afiliação:
Alemanha