Molecular biology of chronic myelogenous leukemia.
In this review we have described molecular consequences of the t(9;22) translocation typical of CML and some cases of ALL. This data indicates an important role for abl and bcr and suggest some common mechanisms of activation of c-abl related tyrosine kinase activity. This data also provides insight into the relationship between Ph1 positive, Ph1 negative CML and Ph1 positive ALL. Although this data answers some questions, they raise others; eg, what is the molecular basis of the t(9;22) translocation? How does increased abl related kinase activity eventuate in CML? Finally, this data reviewed suggests that factors other than abl and bcr must play a role in CML. Definition of these factors will be important in the future.
Dreazen
O
O
Department of Medicine, UCLA School of Medicine 90024.
Canaani
E
E
Gale
R P
RP
D006801:Humans; D007951:Leukemia, Myeloid / Q000235:genetics*; D010677:Philadelphia Chromosome; D014176:Protein Biosynthesis; D011505:Protein-Tyrosine Kinases; D011518:Proto-Oncogene Proteins / Q000235:genetics; D016315:Proto-Oncogene Proteins c-abl; D051562:Proto-Oncogene Proteins c-bcr; D011519:Proto-Oncogenes; D013601:T-Lymphocytes / Q000473:pathology; D014178:Translocation, Genetic
D011518:Proto-Oncogene Proteins; D011505:Protein-Tyrosine Kinases; D016315:Proto-Oncogene Proteins c-abl; C496613:BCR protein, human; D051562:Proto-Oncogene Proteins c-bcr