LETTER TO THE EDITOR Kinetics of peripheral blood chimerism for surveillance of patients with leukemia and chronic myeloid malignancies after reduced-intensity conditioning allogeneic hematopoietic SCT Bone Marrow Transplantation (2015) 50, 743–745; doi:10.1038/ bmt.2015.3; published online 2 March 2015 Chimerism is universally used to monitor engraftment after hematopoietic SCT (HSCT); it is valuable for predicting graft failure, rejection as well as relapses in malignant diseases. Chimerism kinetics are clinically significant and are influenced by the type of conditioning regimens and transplanted diseases. After reduced-intensity conditioning (RIC), dynamics to reach full donor chimerism seem to be slower compared with myeloablative conditioning; however, most patients obtain full chimerism within the first 6 months. 1 Underlying diseases might influence significantly the kinetics of chimerism. In aplastic anemia, stable mixed chimerism provided similar survival advantage to complete donor chimerism compared with progressive mixed chimerism; 2 however, in AML conditioned with myeloablative or RIC, full donor chimerism is related with a lower risk of relapse and mortality. 3 Knowledge of the clinical significance of chimerism kinetics over 41 year after RIC–HSCT is scarce; hence, we aimed to evaluate in a population transplanted due myeloid neoplasms, the impact on outcome of chimerism kinetics. All patients with acute leukemia or chronic myeloid neoplasm transplanted with RIC between 1998 and 2013 at the Hematology Division of the University of Basel (Basel, Switzerland) were included in this retrospective study. After allogeneic HSCT, all recipients were regularly followed up at 1, 3, 6 and 12 months, and thereafter at yearly intervals or more often when indicated. These consultations included assessment of past history, clinical examination, standard laboratory tests and chimerism of periph- eral blood. Leukocyte subpopulation chimerism of CD+ (T lymphocytes) and CD66+ (granulocytes) cells was performed in patients without full donor chimerism or under persistent immunosuppression. Patients provided written informed consent to have their data reported in an anonymous way to the register. Clinical surveillance of HSCT recipients was approved by the local Institutional Review Board. Patient characteristics, HSCT condition- ing regimens and clinical outcome data were collected prospec- tively and stored in the local institution database registry. Chimerism was analyzed by PCR-based DNA amplification of nine different STR loci. Separation of CD3+ and myeloid cells was performed with RoboSep (STEMCELL Technologies, Inc., Vancou- ver, BC, Canada). The results of subpopulation chimerism were provided only if the selection resulted in a purity of 460%. Full donor chimerism was considered when the donor contribution was ⩾ 95%. For this study, patients were classified according to chimerism kinetics. Chimerism A: patients with either full donor chimerism or mixed chimerism converting to full chimerism. Chimerism B: patients with either stable mixed, full chimerism converting to mixed, loss or absence of donor chimerism. We compared the impact of chimerism on survival, acute and chronic GVHD, relapse and TRM. Outcomes were assessed using the Kaplan–Meier estimator and compared among the chimerism groups using the log-rank test. To identify independent prognostic risk factors, a multivariate linear regression analysis using a stepwise backward elimination of significant variables was performed. Differences between the results of comparative tests were considered significant if the two- sided P-value was o0.05. Statistical analysis was performed by using SPSS statistical software (SPSS for Windows, Release 17, SPSS, Chicago, lL, USA). Seventy-seven patients with 81 transplants were included (Table 1). Median age was 61 years (range 10–70), 52 patients (68%) were males, 35 patients (45%) had acute leukemia and 42 (55%) had chronic myeloid malignancy, 46 patients (60%) had advanced disease stage before HSCT, 59 (77%) were conditioned with fludarabine and 2 Gy TBI, 71 (92%) received PBSC as the stem cell source, 38 patients (49%) were transplanted from a sibling donor and 39 (51%) from an alternative donor (37 with an unrelated donor and 2 with a mismatched related donor). At 3 years, TRM was 26 ± 14%, grade II–IV acute GVHD 32 ± 11% and chronic GVHD of any grade 75 ± 14%. Full blood chimerism was Table 1. Patient characteristics N (%) Number of patients 77 Male patients 52 (67.5) Median age (years) (range ) 61 (10–70) Number of transplantations 81 Diagnosis Acute leukemia 35 (45%) ALL 5 (6.5%) AML 30 (39%) Chronic myeloid malignancies 42 (55%) CML 10 (13%) MDS 23 (29.9%) MPN 5 (6.5%) MDS/MPN 4 (5.2%) Advanced disease stage before HSCT 46 (59.7%) Conditioning Fludarabine and TBI 59 (76.6%) Others (fludarabine–melphalan = 12, endoxan–ATG = 6) 18 (23.4%) Stem cell source PBSC 71 (92.2%) BM 5 (6.5%) Cord blood 1 (1.3%) Donor Matched sibling donor 38 (49.4%) Alternative donor 39 (50.6%) Unrelated donor 37 (48.1%) Mismatched related donor 2 (2.6%) Abbreviations: ATG = antithymocyte globulin; MDS = myelodysplastic syn- drome; MPN = myeloproliferative neoplasm. Bone Marrow Transplantation (2015) 50, 743 – 745 © 2015 Macmillan Publishers Limited All rights reserved 0268-3369/15 www.nature.com/bmt