作者: I K Hariharan , A W Harris , M Crawford , H Abud , E Webb
DOI: 10.1128/MCB.9.7.2798
关键词: Myeloid leukemia 、 Biology 、 Long terminal repeat 、 Oncogene 、 Chromosomal translocation 、 ABL 、 Molecular biology 、 breakpoint cluster region 、 Transgene 、 Lymphoma
摘要: In chronic myeloid leukemia and some cases of acute lymphoblastic leukemia, a 9;22 chromosome translocation has fused most the c-abl oncogene to gene designated bcr. To explore in vivo biological effects chimeric gene, we introduced facsimile product, bcr-v-abl into mouse germ line under control immunoglobulin heavy-chain enhancer or retroviral long terminal repeat. Some transgenic mice bearing either construct developed clonal lymphoid tumors. T lymphomas predominated, but pre-B developed. The transgenes were expressed tumors not detectably tissues nontumorous animals, implying that transcription is activated by low-frequency somatic event. These results demonstrate tumorigenic provide new animal model for lymphomagenesis.