Scientists have identified an alternative to reduce the risk of drug resistance in chronic myeloid leukemia patients
Chronic Myeloid Leukemia (CML) is characterized by an uncontrolled proliferation of white blood cells and their precursors. Chronic Myeloid Leukemia develops because of a balanced genetic translocation, which involves a fusion of the Abelson oncogene (ABL) from chromosome 9q34 with the breakpoint cluster region (BCR) gene on chromosome 22q11.2. This reshuffling is called the Philadelphia chromosome. The BCR-ABL fusion oncogene, which is a consequence of this molecular translocation, translates a protein known as Bcr-Abl oncoprotein. This protein, also known as a tyrosine kinase, leads to an uncontrolled proliferation of white blood cells and their precursors.