Inhibition of Cellular Proliferation by Gleevec Pathway

Source:http://linkedlifedata.com/resource/umls/id/C1512774

NCI: The drug Gleevec (also known as imatinib mesylate or STI-571) was approved by the FDA in 2001 for the treatment of CML, chronic myeloid leukemia. While traditional cytotoxic cancer treatments such as chemotherapy or radiation therapy kill all dividing cells, Gleevec acts on a molecular target by a mechanism that is more specific to cancer cells. Traditional cytotoxic cancer agents have serious side effects such as nausea, weight loss, hair loss and severe fatigue that result from their lack of specificity in killing cells. Gleevec was designed as an inhibitor of a specific receptor associated with CML, and so produces less severe side effects than other cancer agents. CML is associated in most cases with a specific chromosomal defect, a translocation between chromosomes 9 and 22 that creates the Philadelphia chromosome. This translocation creates the abnormal bcr-abl protein, a fusion of the Abl gene with another gene called Bcr. The kinase activity of Abl in the bcr-abl fusion is activated and unregulat

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