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Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator <t>inhibitor</t> <t>1</t> (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.
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Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator <t>inhibitor</t> <t>1</t> (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.
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Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator <t>inhibitor</t> <t>1</t> (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.
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Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator <t>inhibitor</t> <t>1</t> (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.
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Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator <t>inhibitor</t> <t>1</t> (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.
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Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator <t>inhibitor</t> <t>1</t> (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.
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Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator <t>inhibitor</t> <t>1</t> (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.
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Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator inhibitor 1 (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.

Journal: Research and Practice in Thrombosis and Haemostasis

Article Title: Comparison of changes in blood cells and hemostatic biomarkers in mouse xenograft models of acute myeloid leukemia and acute promyelocytic leukemia

doi: 10.1016/j.rpth.2025.103319

Figure Lengend Snippet: Hemostatic biomarkers in mouse models of acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL). Levels of hemostatic biomarkers in control mice and mice bearing NB4-Luc cells (APL) or HL-60-Luc2 cells (AML) for (A) cell-free DNA (cfDNA), (B) thrombin-antithrombin complexes (TAT), (C) fibrinogen, (D) plasmin-antiplasmin complexes (PAP), (E) D-dimer, and (F) plasminogen activator inhibitor 1 (PAI-1). Control ( n = 7-9), APL mice ( n = 6 at 28 [ n = 2] or 31 [ n = 4] days for cfDNA, TAT and D-dimer, n = 7 at 29 [ n = 1] or 31 [ n = 6] days for fibrinogen, PAP, and PAI-1), and AML mice ( n = 9 at 45 [ n = 2], 48 [ n = 2], or 50 [ n = 5] days for cfDNA, TAT, and D-dimer. n = 6 at 51 days for fibrinogen, PAP, and PAI-1) are shown. (B, C, E, and F) An ordinary one-way anova followed by Tukey’s test was used for TAT, fibrinogen, D-dimer, and PAI-1; (A and D) the Kruskal–Wallis test followed by Dunn’s test was used for cfDNA and PAP. ∗ P < .05; ∗∗ P < .01; ∗∗∗∗ P < .0001.

Article Snippet: Levels of different biomarkers in plasma were measured using commercial enzyme-linked immunosorbent assays: TAT (Siemens, cat number OWMG15), fibrinogen (Immunology Consultation Laboratory Inc, cat number E-90FIB), PAP (MyBioSource, cat number MBS2512896), D-dimer (Diagnostica Stago, cat number 00947), and plasminogen activator inhibitor 1 (PAI-1; Molecular Innovations, cat number IMSPAI1KTA). cfDNA was measured using the Quant-iT PicoGreen dsDNA Assay Kit (Thermo Fisher Scientific, cat number P11496).

Techniques: Control