Bcr/Abl associated leukemogenesis in bcr null mutant mice.
The BCR gene contributes to Philadelphia-positive leukemogenesis via a number of discrete mechanisms, one of which may be through interaction of its normal gene product with the Bcr/Abl oncoprotein. In the current study this hypothesis was tested in vivo by introducing a Bcr/Abl P190 transgene into mice lacking endogenous bcr protein. Our finding, that the P190 BCR/ABL oncogene is still capable of producing leukemia in these mice with indistinguishable latency and clinical pattern as in genetically matched counterparts, rules out any significant or major contribution of the bcr protein as a whole to leukemia development in these mice.
Voncken
J W
JW
Department of Pathology, Childrens Hospital of Los Angeles Research Institute, California 90027, USA.
Kaartinen
V
V
Groffen
J
J
Heisterkamp
N
N
D000818:Animals; D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000502:physiology*; D007942:Leukemia, Experimental / Q000209:etiology*; D008297:Male; D051379:Mice; D015513:Oncogene Proteins / Q000235:genetics*; D010766:Phosphorylation; D011505:Protein-Tyrosine Kinases; D011518:Proto-Oncogene Proteins; D051562:Proto-Oncogene Proteins c-bcr; D014443:Tyrosine / Q000378:metabolism
D015513:Oncogene Proteins; D011518:Proto-Oncogene Proteins; D014443:Tyrosine; D011505:Protein-Tyrosine Kinases; D016044:Fusion Proteins, bcr-abl; C496614:Bcr protein, mouse; D051562:Proto-Oncogene Proteins c-bcr