K562/GM-CSF immunotherapy reduces tumor burden in chronic myeloid leukemia patients with residual disease on imatinib mesylate.
K562/GM-CSF immunotherapy reduces tumor burden in chronic myeloid leukemia patients with residual disease on imatinib mesylate.
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DOI：
10.1158/1078-0432.ccr-09-2046
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发表时间：
2010-01-01
期刊：
影响因子：
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通讯作者：
Levitsky HI
中科院分区：
文献类型：
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作者：
Smith BD;Kasamon YL;Kowalski J;Gocke C;Murphy K;Miller CB;Garrett-Mayer E;Tsai HL;Qin L;Chia C;Biedrzycki B;Harding TC;Tu GH;Jones R;Hege K;Levitsky HI
CML can be responsive to T cell mediated immunity. K562/GM-CSF is a GM-CSF producing vaccine derived from a CML cell line that expresses several CML associated antigens. A pilot study was developed to determine if K562/GM-CSF immunotherapy could improve clinical responses to imatinib mesylate (IM) in patients with chronic myeloid leukemia. Patients with chronic phase CML who achieved at least a major cytogeneic response but remained with persistent, measurable disease despite one or more years on IM were eligible. Each was given a series of four vaccines administered in three week intervals, with or without topical imiquimod, while remaining on a stable dose of IM. CML disease burden was measured serially before and after vaccination. Nineteen patients were vaccinated, with a median duration of previous IM therapy of 37 (13–53) months. Mean PCR measurements of BCR-ABL for the group declined significantly following the vaccines (p=0.03). Thirteen patients had a progressive decline in disease burden, 8 of whom had increasing disease burden prior to vaccination. Twelve patients achieved their lowest tumor burden measurements to date following vaccine, including seven subjects who became PCR-undetectable. K562/GM-CSF vaccine appears to improve molecular responses in patients on IM, including achieving complete molecular remissions, despite long durations of previous IM therapy.
