| First Author | Heisterkamp N | Year | 1990 |
| Journal | Nature | Volume | 344 |
| Issue | 6263 | Pages | 251-3 |
| PubMed ID | 2179728 | Mgi Jnum | J:91174 |
| Mgi Id | MGI:3046070 | Doi | 10.1038/344251a0 |
| Citation | Heisterkamp N, et al. (1990) Acute leukaemia in bcr/abl transgenic mice. Nature 344(6263):251-3 |
| abstractText | The Philadelphia chromosome, widely implicated in human leukaemia, is the result of a reciprocal translocation t(9;22) (q34;q11) in which the abl oncogene located at 9q34 is translocated to chromosome 22q11, where it is fused head-to-tail with 5' exons of the bcr gene. In acute lymphoblastic leukaemia, some patients have a breakpoint within the major breakpoint cluster region of the bcr gene, whereas others have the break within its first intron. This second type of translocation results in the transcription of a 7.0-kilobase chimaeric bcr/abl messenger RNA translated into a bcr/abl fusion protein, p190, which has an abnormal tyrosine kinase activity and is strongly autophosphorylated in vitro. We have generated mice transgenic for a bcr/abl p190 DNA construct and find that progeny are either moribund with, or die of acute leukaemia (myeloid or lymphoid) 10-58 days after birth. This finding is evidence for a causal relationship between the Philadelphia chromosome and human leukaemia. |
