T cell tumorigenesis in Lmo2 transgenic mice is independent of V-D-J recombinase activity.
Oncogene
; 20(32): 4412-5, 2001 Jul 19.
Article
in En
| MEDLINE
| ID: mdl-11466623
ABSTRACT
The LMO2 gene is involved in T-cell acute leukaemia (T-ALL) in children with chromosomal translocations t(11;14)(p13;q11) or (7;11)(q35;p13). Transgenic expression of Lmo2 in T cells results in clonal tumours with long latency indicating that mutations in other genes are required for the development of overt tumours. RAG V-D-J recombinase can mediate genetic transposition and thus might create the secondary mutations necessary for T-ALL. Tumour development was compared in Lmo2 transgenic mice in the presence or absence of the Rag1 gene. No difference was observed in the rate of tumour formation nor in tumour histology in Lmo2-transgenic mice with or without Rag1. We conclude that, in this model, RAG recombinase is not a major mediator of mutations needed for T cell tumorigenesis and that antigen binding to alpha-beta or to gamma-delta T cell receptor does not play a role in tumorigenesis. The driving force behind the mutational process involved in this transgenic model remains obscure.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Leukemia-Lymphoma, Adult T-Cell
/
Homeodomain Proteins
/
DNA-Binding Proteins
/
Metalloproteins
Type of study:
Etiology_studies
Limits:
Animals
Language:
En
Journal:
Oncogene
Journal subject:
BIOLOGIA MOLECULAR
/
NEOPLASIAS
Year:
2001
Document type:
Article
Affiliation country:
United kingdom