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Prepublished online as a Blood First Edition Paper on November 21, 2002; DOI 10.1182/blood-2002-08-2675.
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Blood, 15 April 2003, Vol. 101, No. 8, pp. 3236-3239
NEOPLASIA
Brief report
Cotreatment with the histone deacetylase inhibitor
suberoylanilide hydroxamic acid (SAHA) enhances imatinib-induced
apoptosis of Bcr-Abl-positive human acute leukemia cells
Ramadevi Nimmanapalli,
Lianne Fuino,
Corinne Stobaugh,
Victoria Richon, and
Kapil Bhalla
From the Department of Interdisciplinary Oncology,
Moffitt Cancer Center and Research Institute University of South
Florida, Tampa; and Aton Pharma, Tarrytown, NY.
Here we demonstrate that treatment with SAHA (suberoylanilide
hydroxamic acid), a known inhibitor of histone deacetylases (HDACs),
alone induced p21 and/or p27 expressions but decreased the mRNA and
protein levels of Bcr-Abl, which was associated with apoptosis of
Bcr-Abl-expressing K562 and LAMA-84 cells. Cotreatment with SAHA and
imatinib (Gleevec) caused more down-regulation of the levels and
auto-tyrosine phosphorylation of Bcr-Abl and apoptosis of these cell
types, as compared with treatment with either agent alone
(P < .05). This finding was also associated with a
greater decline in the levels of phospho-AKT and Bcl-xL.
Significantly, treatment with SAHA also down-regulated Bcr-Abl levels
and induced apoptosis of CD34+ leukemia blast progenitor
cells derived from patients who had developed progressive blast crisis
(BC) of chronic myelocytic leukemia (CML) while receiving therapy with
imatinib. Taken together, these findings indicate that cotreatment with
SAHA enhances the cytotoxic effects of imatinib and may have activity
against imatinib-refractory CML-BC.
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