Caption: Glivec leukaemia drug binding to its target, the enzyme Bcr-Abl tyrosine kinase. This enzyme is produced by a genetic mutation, the swapping of parts of two chromosomes, leading to the formation of the oncogene (cancer-causing gene) Bcr-Abl, which produces a constantly-active version of normal Abl tyrosine kinase. This causes chronic myelogenous leukaemia (CML), a cancer of white blood cells. The drug Glivec (Imatinib) works by binding to the active site of the Bcr-Abl enzyme, producing a change in shape that prevents the enzyme from functioning. This causes the death of cancerous cells expressing the enzyme. Glivec, the first such tyrosine kinase inhibitor to be produced, is marketed by Novartis.

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Keywords: active site, anti-cancer, anticancer, bcr-abl, binding, biochemical, biochemistry, cancer, cancerous, chemical, chemistry, chemotherapy, chromosomal, chronic myelogenous leukaemia, cml, conformational change, designed, diagram, drug, drug design, enzyme, fusion gene, fusion protein, genetic, genetic disorder, genetics, gleevec, glivec, imatinib, inhibition, inhibitor, leukaemia, leukemia, moa, mode of action, model, molecular, molecule, mutant, mutated, novartis, oncogene, philadelphia chromosome, protein, rational, ribbon, ribbons, targeted, tki, translocation, tyrosine kinase

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Glivec leukaemia drug action

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