17-AAG inhibits Sin1^−/− leukemia growth preferentially in vivo. Sublethally irradiated wild-type CD45.1 congenic mice were transplanted with 1 × 10⁶Sin1^+/+ (CD45.2⁺NGFR⁺; wild-type; WT) or Sin1^−/− (CD45.2⁺GFP⁺; knockout; KO) p210 BCR-Abl–transformed mouse leukemia cells by tail vein injection. The transplanted mice were treated with 17-AAG (80 mg/kg/d in corn oil) or vehicle (corn oil) daily for 5 consecutive days beginning 24 hours after tumor-cell transplantation. Mice were killed 24 hours after the last drug treatment and the percentage and total number of Sin1^+/+ (wild-type; WT) or Sin1^−/− (knockout; KO) pre-B leukemia cells in the BM (A-B) and spleen (C-D) were analyzed by flow cytometry. The total number of mice in each treatment group are as follows: WT vehicle-treated, n = 5; WT 17-AAG–treated, n = 5; KO vehicle-treated, n = 7; and KO 17-AAG–treated, n = 7. (A) Representative FACS plots showing the percentages of transplanted WT and KO leukemia cells (numbers in the boxes) in BM. (B) Summary of total number of transplanted leukemia cells in the whole BM extracted from one long leg bone (tibia) of WT or KO mice treated with vehicle or 17-AAG. Each symbol represents the cells from one tibia of the indicated recipient mice. (C) Representative FACS plots showing the percentages of transplanted WT and KO leukemia cells (numbers in the boxes) in the spleen. (D) Summary of total number of transplanted leukemia cells in the spleen of WT or KO mice treated with vehicle or 17-AAG. Each symbol represents the cells from the spleens of the indicated recipient mice.