CML is thought to be an immunologically responsive disease based on the ability to cure the disease with allogeneic T cells as well as the demonstration of host immune responses to CML-associated antigens in patients who have responded to interferon-alpha. The dramatic clinical responses obtained with the selective tyrosine kinase inhibitor Imatinib Mesylate has provided a relatively non-toxic cytoreductive therapy, although complete molecular remissions remain rare. We propose to vaccinate CML patients who are in a complete hematologic remission, but have persistent cytogenetic or molecular evidence of disease, with a novel allogeneic tumor cell-based vaccine that expresses many of the antigens shown to be present in CML cells and to which T cell responses have been demonstrated. The two major objectives of this study will be to demonstrate the ability to generate and augment CML specific T cell responses in patients vaccinated while in remission on Imatinib Mesylate, and to test the hypothesis that such responses will lead to a measurable reduction in tumor burden (or its elimination) as assayed by quantitative RT-PCR of bcr/abl transcripts.
| Smith, B Douglas; Kasamon, Yvette L; Kowalski, Jeanne et al. (2010) K562/GM-CSF immunotherapy reduces tumor burden in chronic myeloid leukemia patients with residual disease on imatinib mesylate. Clin Cancer Res 16:338-47 |
