| First Author | Hemmeryckx B | Year | 2002 |
| Journal | Oncogene | Volume | 21 |
| Issue | 20 | Pages | 3225-31 |
| PubMed ID | 12082638 | Mgi Jnum | J:76680 |
| Mgi Id | MGI:2179931 | Doi | 10.1038/sj.onc.1205452 |
| Citation | Hemmeryckx B, et al. (2002) BCR/ABL P190 transgenic mice develop leukemia in the absence of Crkl. Oncogene 21(20):3225-31 |
| abstractText | The Bcr/Abl fusion protein directly causes chronic myelogenous leukemia and Philadelphia-chromosome positive acute lymphoblastic leukemia. Multiple independent studies have implicated Crkl, a small adapter protein, in transduction of oncogenic signals of Bcr/Abl and Crkl tyrosine-phosphorylation is used as a diagnostic tool for Philadelphia-positive leukemia. To evaluate the contribution of Crkl to this type of leukemia, we generated mutant mice that lack Crkl expression. We found that the overall survival of P190 BCR/ABL crkl-/- mice was comparable to that of genetically matched P190 BCR/ABL crkl +/+ mice. Both genotypes developed lymphoid lineage leukemia/lymphoma. Western blot analysis of -/- and +/+ lymphomas showed that the related Crk protein was tyrosine phosphorylated and could be found complexed with Bcr-Abl P190. These data indicate that possible therapeutic approaches that target Crkl may be complicated by the presence of pathways that compensate for lack of Crkl function. |
