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• W106695551 endingPage "3117" @default.
• W106695551 startingPage "3113" @default.
• W106695551 abstract "Abstract We assessed the chimerism of CD34+ bone marrow cells before donor leukocyte infusion (DLI) on nine occasions in seven patients with leukemic relapse after allogeneic marrow transplantation. The patients suffered from acute lymphoblastic leukemia (n = 1), acute myeloid leukemia (n = 3), and chronic myeloid leukemia (CML; n = 3). Two patients received a second DLI because of disease progression after the first one. The origin of the CD34+ cells was determined by analyzing variable number of tandem repeats with polymerase chain reaction and, in sex-mismatched cases, by fluorescence in situ hybridization. Before DLI CD34+ cells were exclusively of donor origin in four patients. In another patient 41% of CD34+ cells were derived from the donor. No aplasia occurred in these patients after DLI, whereas in the two patients with exclusively recipient hematopoiesis severe aplasia lasting for 5 and 13 weeks necessitated hematopoietic stem cell support. One patient who had only 5% CD34+ donor cells before DLI recovered without stem cell support after 10 days. Two patients in relapse of CML showed a high percentage of BCR-ABL− CD34+ cells of recipient origin before DLI. These BCR-ABL− cells of recipient type did not prevent severe aplasia which indicates that the assessment of BCR-ABL+ hematopoiesis alone is insufficient for predicting aplasia. Our data indicate that in case of sufficient donor hematopoiesis before DLI no persistent aplasia will occur. Thus, evaluation of donor hematopoiesis allows prediction of aplasia after DLI and makes early therapeutic interventions possible." @default.
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• W106695551 date "1997-05-01" @default.
• W106695551 modified "2023-10-02" @default.
• W106695551 title "Donor Leukocyte Infusion for Leukemic Relapse After Allogeneic Marrow Transplantation: Lack of Residual Donor Hematopoiesis Predicts Aplasia" @default.
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• W106695551 doi "https://doi.org/10.1182/blood.v89.9.3113" @default.
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