Open AccessA bcr-v-abl oncogene induces lymphomas in transgenic mice.
Author(s) -
Iswar K. Hariharan,
Alan W. Harris,
M Crawford,
Helen E. Abud,
Elizabeth Webb,
Suzanne Cory,
Jerry M. Adams
Publication year - 1989
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.9.7.2798
Subject(s) - biology , oncogene , cancer research , abl , transgene , breakpoint cluster region , chromosomal translocation , enhancer , microbiology and biotechnology , immunoglobulin heavy chain , myeloid , gene , gene expression , genetics , signal transduction , cell cycle , tyrosine kinase
In chronic myeloid leukemia and some cases of acute lymphoblastic leukemia, a 9;22 chromosome translocation has fused most of the c-abl oncogene to a gene designated bcr. To explore in vivo the biological effects of the chimeric gene, we introduced a facsimile of the translocation product, a bcr-v-abl gene, into the mouse germ line under the control of the immunoglobulin heavy-chain enhancer or a retroviral long terminal repeat. Some transgenic mice bearing either construct developed clonal lymphoid tumors. T lymphomas predominated, but some pre-B lymphomas developed. The transgenes were expressed in the tumors but not detectably in the lymphoid tissues of nontumorous transgenic animals, implying that transcription is activated by a low-frequency somatic event. These results demonstrate that bcr-v-abl is tumorigenic in vivo and provide a new animal model for lymphomagenesis.