Factors relevant to finding a suitable unrelated donor and barriers to effective transplant utilization are incompletely understood. Among a consecutive series of unrelated searches (n = 531), an 8/8 HLA-A, -B, -C and -DRB1-matched unrelated donor was available for 289 (54%) patients, 7/8 for 159 (30%) and no donor for 83 (16%). Patients of Caucasian race (P < 0.0001) were more likely to find a donor. Younger age (P = 0.01), Caucasian race (P = 0.03), lower CIBMTR (Center for International Blood and Marrow Transplantation Research) risk (P = 0.005), and 8/8 HLA matching (P = 0.005) were associated with higher odds of reaching hematopoietic cell transplantation (HCT). In a univariate analysis of OS, finding a donor was associated with hazard ratio (HR) of 0.85 (95% CI 0.63–1.2), P = 0.31. Karnofsky performance status (KPS) accounted for interaction between having a donor and survival. Patients with KPS 90–100 and a donor had significantly reduced hazard for death (HR 0.59, 95% CI 0.38–0.90, P = 0.02). These data provide estimates of the probability to find an unrelated donor in the era of high-resolution HLA typing, and identify potentially modifiable barriers to reaching HCT. Further efforts are needed to enhance effective donor identification and transplant utilization, particularly in non-Caucasian ethnic groups.

HSCs and CMPs. A rise in BCR-ABL levels in GMP populations signified impending relapse. Post-SCT patients harbored more residual CML cells in CD34+ subpopulations than TKI-treated patients. Our findings suggest that in patients with persistent MRD-positivity post-SCT, the graft-versus-leukemia (GVL) effect may eliminate mature leukemic CD34+ subpopulations in vivo more readily. Primitive leukemic HSCs and CMPs, although persistent, are presumably constrained by GVL in patients who do not fulfill criteria for relapse. Conversely, TKI reduces the number of BCR-ABL-positive GMPs and CMPs more efficiently. Our data support adjuvant TKI-treatment for CML relapse post-SCT, and concurrent vaccination strategies which can target surface proteins on HSCs to eradicate CML.

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