The medicine known commercially as Gleevec serves as a powerful weapon for people fighting the blood cancer called chronic myelogenous leukemia, or CML. Although the drug appears to cure many patients, it usually provides only fleeting improvement for those who have entered the crisis stage of the lethal disease.
A new finding could help scientists patch this weakness in the drug's otherwise potent assault on CML. In an upcoming issue of Science, researchers at the University of California, Los Angeles (UCLA) reveal how this cancer rebounds.
The leukemia originates when pieces of chromosomes 9 and 22 fuse, forming a hybrid gene called Bcr-Abl (SN: 12/11/99, p. 372). This mutation encodes an enzyme, Bcr-Abl tyrosine kinase, that causes white blood cells to proliferate. Without Gleevec treatment, CML would smolder for years. Eventually, it would explode into a crisis stage in which white blood cells multiply rapidly and crowd out healthy cells in the bon