Published in Proteomics Weekly, August 7th, 2006
According to a study from the United States, "GIST are characterized by activating mutations in the c-KIT gene which confers ligand-independent activation of the KIT receptor. Imatinib mesylate has been shown to effectively block constitutively active KIT and delay tumor growth. However, resistance to imatinib mesylate is emerging as a major clinical problem and novel therapies are needed."
"We report that treatment of GIST cells with the transcriptional inhibitor flavopiridol, initially down-regulates the...
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Source: Proteomics Weekly (2006-08-07)
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