BIOM20001 Lecture Notes - Lecture 28: Chronic Myelogenous Leukemia, Fusion Protein, Leukemia
Document Summary
It may bind to a cofactor (atp) and phosphorylate a substrate. Can use a drug that blocks the atp binding site. In the case of an antibody we can get an antibody that binds to receptors or ligands that block the ligand from sending a disease causing signal. Disadvantage for this is that they only target ligands or receptors on the outside of cells - restricted to extracellular treatments. Small molecule inhibition therapy of chronic myeloid leukaemia. Chronic myeloid leukaemia as an example of a proto-oncogenic gene fusion translocation. Translocation fuses c-abl gene (on chr 9) with the bcr gene on 22. Bcr-abl fusion encodes a chimeric protein of 210kda with increased tyrosine kinase activity. Bcr-abl fusion encodes a chimeric protein of 210kda with increased tyrosine kinase activity and abnormal cellular localisation. Targeted therapy involves hitting a factor only present in cancer cells. When it dimerises it activates the tyrosine kinase activity. Note this protein is specific for cancer cells.
