Title : Valproate enhances imatinib-induced growth arrest and apoptosis in chronic myeloid leukemia cells.

Pub. Date : 2006 Mar 1

PMID : 16444746






3 Functional Relationships(s)
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1 BACKGROUND: The objective of this study was to evaluate the ability of the clinically available histone deacetylase (HDAC) inhibitor valproate to enhance the cytotoxicity of the Bcr-Abl inhibitor imatinib in imatinib-resistant cell lines. Valproic Acid ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens
2 Coexposure of cells to valproate and imatinib was associated with repression of several genes involved in Bcr-Abl transformation. Valproic Acid ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens
3 In particular, the combination valproate-imatinib downregulated the expression of Bcr-Abl and the antiapoptotic protein Bcl-2, which is particularly overexpressed in imatinib-resistant clones. Valproic Acid ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens