Detection of Aur-A207-215–specific CTL precursors in patients with leukemia. (A) Representative data of the tetramer assay for Aur-A207-215–specific CTL precursors. PBMCs isolated from HLA-A*0201–positive and HLA-A*2402–positive patients with CML in chronic phase were stimulated with Aur-A207-215 peptide and then stained with HLA-A*0201/Aur-A207-215 tetramer and HLA-A*2402/Aur-A207-215 tetramer, respectively. HLA-A*0201/HIV-1 p17 Gag77-85 (SLYNTVATL) tetramer and HLA-A*2402/HIV-1 Env584-592 (RYLRDQQLL) tetramer were used as negative controls. (B) Summary of tetramer assays for Aur-A207-215–specific CTL precursors. PBMCs isolated from 3 HLA-A*0201–positive patients with leukemia (a patient with AML in complete remission after allogeneic stem cell transplantation, a patient with ALL in complete remission after chemotherapy, and a patient with untreated CML in chronic phase; ■), 2 HLA-A*2402–positive patients with leukemia (2 patients with CML in chronic phase after therapy with interferon or imatinib; ▴), 8 HLA-A*0201–positive healthy individuals (□), and 2 HLA-A*2402–positive healthy individuals (▵) were stained with HLA-A*0201/Aur-A207-215 or HLA-A*2402/Aur-A207-215 tetramer. The frequency of Aur-A207-215–specific CTL precursors in the patients with leukemia was significantly higher than that in healthy individuals (Student t test; P < .001).