The translocation of the c-abl oncogene from chromosome 9 to the bcr gene on 
chromosome 22 in cases of Philadelphia chromosome-positive chronic myelogenous 
leukemia (CML) generates an aberrant bcr-abl fusion transcript which may be 
intimately related to the pathogenesis of CML. Because factors controlling 
normal bcr expression might also be involved in the expression of this aberrant 
bcr-abl transcript, we studied the patterns of expression of the normal bcr gene 
in different cell types. We found that the normal bcr gene was expressed in many 
different types of human cells. Moreover, the bcr gene was evolutionarily 
conserved, and homologous bcr genomic sequences and RNA transcripts were readily 
detected in chick tissue. The highest level of bcr expression in chick tissue 
was in brain tissue, the lowest level was in liver tissue, and a truncated bcr 
mRNA was noted in chick testes. Normal bcr transcripts, in addition to the 
aberrant bcr-abl hybrid transcripts, have been found in all Philadelphia 
chromosome-positive CML cells studied to date. Within a given CML sample, the 
relative amounts of normal bcr RNA and aberrant bcr-abl RNA were similar. In 
addition, the normal bcr and the aberrant bcr-abl hybrid transcripts 
demonstrated similarly prolonged half-lives compared with that of the normal 
abl-related transcripts in CML cells. These findings suggest that in CML cells, 
similar cellular mechanisms control the steady-state levels of both the normal 
bcr and the bcr-abl fusion RNAs.