As with the study of any oncogene, the field now turned from structure to function: what did Bcr-abl do to cause leukemia? When Baltimore’s lab and Owen Witte’s lab investigated the function of the aberrant Bcr-abl oncogene, they found that, like src, it was yet another kinase—a protein that tagged other proteins with a phosphate group and thus unleashed a cascade of signals in a cell. In normal cells, the Bcr and abl genes existed separately; both were tightly regulated during cell division. In CML cells, the translocation created a new chimera—Bcr-abl, a hyperactive, overexuberant kinase
...more
