Philadelphia-negative acute lymphoblastic leukemia in a chronic myeloid leukemia patient receiving dasatinib
Background aims Dasatinib is a second-generation tyrosine kinase inhibitor (TKI) for use in patients who have developed resistance or clinical progression with imatinib. There are few cases described in the literature regarding the development of Philadelphia (Ph)-negative lymphoid blast crisis in p...
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Published in | Cytotherapy (Oxford, England) Vol. 12; no. 1; pp. 113 - 115 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Elsevier Inc
2010
Informa UK Ltd. (Informa Healthcare, Taylor & Francis AS) |
Subjects | |
Online Access | Get full text |
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Summary: | Background aims Dasatinib is a second-generation tyrosine kinase inhibitor (TKI) for use in patients who have developed resistance or clinical progression with imatinib. There are few cases described in the literature regarding the development of Philadelphia (Ph)-negative lymphoid blast crisis in patients with a complete cytogenetic response to TKI. Methods and Results We report on the case of a chronic myeloid leukemia (CML) patient who developed a Ph-negative acute lymphoblastic leukemia (ALL) while in complete cytogenetic remission (CCyR) with dasatinib. With the diagnosis of Ph-negative ALL, the patient was started on prednisone and proceeded to autologous hematopoietic stem cell transplantation (ASCT) using cells collected during cytogenetic remission with imatinib. In the third month post-transplantation, the patient was started on nilotinib and the patient now has an excellent performance status, maintaining CCyR and major molecular response 1 year after the procedure. Conclusions There are seven reports of patients with CML who have developed Ph-negative ALL, two of them while being treated with imatinib. In five of these, the karyotype was diploid, as in our patient. Our patient was successfully treated with prednisone and ASCT, and has been using nilotinib since then, maintaining a cytogenetic and molecular response. |
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ISSN: | 1465-3249 1477-2566 |
DOI: | 10.3109/14653240903300666 |