inhibition of cellular proliferation by gleevec
| PAG Title | inhibition of cellular proliferation by gleevec |
| PAG ID | WAG000009 |
| Type | P |
| Source Link |  BioCarta |
| Publication Reference | NA |
| PAG Description | 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 traditiol 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. Traditiol cytotoxic cancer agents have serious side effects such as usea, 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 occurs at the site in the genome of a protein tyrosine kise called abl, creating the abnormal bcr-abl protein, a fusion of the abl gene with another gene called bcr. The kise activity of abl in the bcr-abl fusion is activated and unregulated, driving the uncontrolled cell growth observed in CML. White blood cells containing the bcr-abl mutation become able to proliferate in the absence of growth factors they normally require. Gleevec inhibits abl kise activity, helping to reverse uncontrolled cell growth. Gleevec also inhibits the PDGF tyrosine kise and the c-kit tyrosine kise. |
| Species | Homo sapiens |
| nCoCo Score | 4,989 |
| Base PAG ID | WAG000009 |
| Human Phenotyte Annotation | |
| Curator | PAGER curation team |
| Curator Contact | PAGER-contact@googlegroups.com |
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