Does interferon-a exert an anti-leukemic effect by enhancing cell mediated immunity in chronic myeloid leukemia?

mal cells having a better capacity to protect themselves.2 In CML patients developing severe BM aplasia the normal progenitor cells compartment loses the ability to adapt and the BM reservoir is severely compromised. In our case the patient received hydroxyurea for only 4 weeks and developed severe aplasia ten months later. Therefore in our case IFNplayed a pivotal role in the development of BM aplasia. Interestingly in our patient bcr/abl was still present despite no sign of BM function. Blastic crisis could never be documented and fibrosis by itself was not responsible for BM suppression. BM aplasia did not revert following discontinuation of the IFN, was unresponsive to G-CSF and finally proceded to complete BM failure and death. In CML patients lacking a normal stem cell reservoir IFNmay induce hematologic response but irreversible severe aplasia can be expected. Follow-up should be rigorous also when a stable HR is achieved since patients developing BM aplasia are at high risk of treatment-related death.