Inflammation promotes the growth of BCR-ABL1⁺ B-ALL cells in vitro and in vivo. For in vitro assays, BCR-ABL1⁺ B-ALL cells were obtained from the BM of primary BCR-ABL1⁺ B-ALL mice and purified by CD19⁺ MACS, then cultured in vitro. (A-B) BCR-ABL1⁺ B-ALL cells were treated with LPS (25 µg/mL) or control PBS in a 96-well plate with FBS-deficient culture medium for 48 hours following treated with imatinib (IM) (0, 6 µM) for 24 hours. (A) Cell viability was determined b CCK-8 assays. (B) Cell apoptosis was measured by flow cytometry. The cell population of apoptosis is indicated (left); the histogram shows the percentages of apoptotic cells (right). (C) The cell cycle of LPS (25 µg/mL)-treated and PBS-treated BCR-ABL1⁺ B-ALL cells were evaluated by flow cytometry. The cell population of G0/G1, S, G2/M phase is indicated (left), the histogram shows the percentages of each period (right). (D) Schematic representation of BCR-ABL1⁺ B-ALL mouse models derived from secondary transplantation. (E) Kaplan-Meier survival curves for the recipient mice receiving either PBS-treated leukemic cells (n = 6) or LPS-treated leukemic cells (n = 6). (F) Monitoring the peripheral blood percentage of GFP⁺ cells in recipient mice transplanted with PBS- or LPS- treated leukemic cells at day 7 and day 14 after transplantation. (G) Leukemia burden was determined by measuring the percentages of GFP⁺ cells in the BM, SP, LN, liver, lung, and brain in recipient mice at day 14 after transplantation. The data are representative of at least 3 independent experiments. Error bars represent the mean ± standard error of the mean. *P < .05, **P <. 01, ***P < .001. ns indicates no significant differences.