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Vaccine may complement conventional treatment for chronic leukaemia

A vaccine that boosts the immune response could improve the effect of conventional treatment for patients with chronic myeloid leukaemia (CML), suggest early results of a trial published in this week's issue of THE LANCET.

CML is caused by the breakage and swapping of chromosomes 9 and 22, which results in a shortened chromosome called the Philadelphia chromosome. Cells with the abnormal chromosome make a protein that encourages aberrant growth and division. Patients with CML can be treated with a drug called imatinib or interferon alfa. Treatment with imatinib can lead to complete cytogenetic remission, where no Philadelphia chromosomes are detected during cell division. However, a complete molecular response, where there is no evidence of the protein produced by the Philadelphia chromosomes, is rare.

Monica Bocchia (University of Siena, Italy) and colleagues tested whether a vaccine that targets a protein derived from the Philadelphia chromosome could help to eradicate the disease in patients. The investigators enrolled 16 individuals (10 patients on imatinib and 6 on interferon) with stable, but detectable disease into the trial. Patients were given one dose (six injections) of the protein vaccine every 2 weeks while they continued their conventional treatment. Patients were assessed before vaccination and after three and six doses for evidence of the disease.

Nine patients on imatinib showed progressive reduction of their residual disease after three and six doses of the vaccine with five patients reaching complete cytogenetic remission. Three of the five patients also obtained undetectable disease at a molecular level. Of the six patients on interferon alfa, five showed a reduction of their stable disease during vaccinations, with two reaching complete cytogenetic remission.

Dr Bocchia comments: "Our preliminary data suggest that the addition of this vaccine to patients treated with conventional treatment might favour further
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Contact: Joe Santangelo
j.santangelo@elsevier.com
1-212-633-3810
Lancet
17-Feb-2005


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