The Role of BCR-ABL Gene on Chronic Myeloid Leukemia: An Overview

Abstract

The Breakpoint Cluster Region is a protein encoded by the BCR gene with its partially discovered function to generate instructions for producing a protein and also to encode serine/threonine kinase protein. There are three Breakpoint cluster regions; major (M-bcr) which is high in CML patients, minor (m-bcr) with a 1-2% contribution in the CML, and micro (μ-bcr) which is very rare in the case of CML. The ABL1 encodes for the ABL1 protein which can function as a tyrosine kinase. The translocation of the ABL gene on chromosome 9 at the band 34 to the BCR gene on chromosome 22 at band 11 leads to the fusion of the BCR-ABL gene which is responsible for Chronic Myeloid Leukemia (CML), Acute Myeloid Leukemia (AML), and Acute Lymphoblastic Leukemia (ALL). Chromosome 22 with this hybrid gene called a Philadelphia chromosome codes for a BCR-ABL protein that enhances the activity of tyrosine kinase thereby activating numerous signaling pathways. If there is a translocation of BCR to chromosome 9, which will cause the emergence of the ABL-BCR gene (9q+). [1][4][5][6] The role of the BCR-ABL gene in CML is to increase the growth and proliferation of myeloid cells, avoid apoptosis, increase c-independent growth, induce aberrations in the cytoskeletons, etc.