Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10909428 | Leukemia Research | 2011 | 11 Pages |
Abstract
Chronic myeloid leukaemia has a specific therapy: BCR/ABL inhibitor imatinib. Resistance due to BCR/ABL dependent and independent mechanisms is partially reversible by histone deacetylase inhibitors. We analysed by 2D-electrophoresis and anti-pan-acetylated and anti-phosphotyrosine immunoblots, followed by spot-matching and MALDI-TOF mass spectrometry, which proteome modifications would parallel restoration of sensitivity to imatinib by valproic acid (VPA). VPA plus imatinib significantly increased acetylation of HSP90 and hnRNP L and decreased phosphorylation of HSPs and hnRNPs in imatinib resistant cells. VPA was able to modify profoundly acetylome and phosphoproteome of CML cells, while reverting resistance to imatinib.
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Authors
Francesca Buchi, Roberta Pastorelli, Germano Ferrari, Elena Spinelli, Antonella Gozzini, Francesca Sassolini, Alberto Bosi, Donatella Tombaccini, Valeria Santini,