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aml cell line sig m5  (DSMZ)


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    DSMZ aml cell line sig m5
    A CD8 T-cell clones showed specific binding to PE- or APC-conjugated pMHC-tetramers containing neopeptides from the long ARF created by RUNX1 frameshift mutations by flow cytometry. No binding was observed to control pMHC-tetramers containing an irrelevant peptide in the same HLA molecule. Clones 5.2A12, 4.2C6, 5.3A11, 31.2D9, 31.2D12 and 40.2E5 were isolated from donors positive for the HLA-I binding molecules of the neopeptides, whereas clones 32.5G10, 26.1C6 and 31.3G3 were isolated from donors negative for the HLA-I binding alleles. B Reactivity of T-cell clones against EBV-B cells exogenously pulsed with RUNX1 neopeptides. EBV-B cells were positive for the relevant HLA-I restriction alleles. IFNγ release was measured after overnight coincubation by ELISA (R&D) in single or duplicate wells. C Reactivity of T-cell clones against K562 transduced with the relevant HLA-I restriction allele and the full-length RUNX1c.883dup gene (ENST00000675419.1) encoding p.Ser295PhefsTer305 with 304 amino acids in the long ARF (K562 + HLA +fs-mRUNX1). K562 cells transduced with the relevant HLA and full-length wildtype RUNX1 gene (K562 + HLA +wtRUNX1) and K562 transduced with the relevant HLA and exogenously pulsed with RUNX1 neopeptides were included as controls. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons (unpaired t tests) were performed for each clone between K562 + HLA +wtRUNX1 and K562 + HLA +fs-mRUNX1 (clone 5.2A12: p = 0.002; 32.5G10: p = 0.006; 4.2C6: p = 0.02; 5.3A11: p = 0.0003; 31.2D9: p > 0.99; 26.1C6: p = 0.03; 31.2D12: p = 0.00003; 31.3G3: p = 0.004; 40.2E5: p = 0.002). D Reactivity of T-cell clones against <t>AML</t> <t>cell</t> <t>line</t> <t>SIG-M5</t> C9 carrying a RUNX1 c.906_907insG mutation introduced by CRISPR/Cas9, encoding p.Ser303ValfsTer297 with 296 amino acids in the long ARF. The parental SIG-M5 cell line, unloaded or exogenously pulsed with RUNX1 neopeptides, was included as a control. SIG-M5 and SIG-M5 C9 are HLA-B*07:02 positive and were retrovirally transduced with other relevant HLA alleles. Transduced cell lines were >90% positive for marker gene murine CD19. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons (unpaired t tests) were performed for each clone between SIG-M5 ( + HLA) and SIG-M5 C9 ( + HLA) (clone 5.2A12: p = 0.42; 32.5G10: p = 0.04; 4.2C6: p = 0.03; 5.3A11: p = 0.002; 31.2D9: p > 0.99; 26.1C6: p = 0.91; 31.2D12: p = 0.06; 31.3G3: p = 0.42; 40.2E5: p > 0.99). E Reactivity of T-cell clones against EBV-B cells pulsed with titrated concentrations of the indicated RUNX1 neopeptides. EBV-B cells were positive for the relevant HLA-I restriction alleles. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. T-cell clone 32.5G10 recognized APGGGRVEALL with an EC50 of 263.8 nM, and T-cell clones 4.2C6 and 5.3A11 recognized GPRAPDQGDL with EC50 values of 25.8 and 102.1 nM, respectively. Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.
    Aml Cell Line Sig M5, supplied by DSMZ, used in various techniques. Bioz Stars score: 93/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/aml+cell+line+sig+m5/SIG-M5/pmc12875866-90-0-4
    Average 93 stars, based on 24 article reviews
    aml cell line sig m5 - by Bioz Stars, 2026-09
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    1) Product Images from "A T-cell receptor targeting RUNX1 frameshift mutations in acute myeloid leukemia"

    Article Title: A T-cell receptor targeting RUNX1 frameshift mutations in acute myeloid leukemia

    Journal: Leukemia

    doi: 10.1038/s41375-025-02817-x

    A CD8 T-cell clones showed specific binding to PE- or APC-conjugated pMHC-tetramers containing neopeptides from the long ARF created by RUNX1 frameshift mutations by flow cytometry. No binding was observed to control pMHC-tetramers containing an irrelevant peptide in the same HLA molecule. Clones 5.2A12, 4.2C6, 5.3A11, 31.2D9, 31.2D12 and 40.2E5 were isolated from donors positive for the HLA-I binding molecules of the neopeptides, whereas clones 32.5G10, 26.1C6 and 31.3G3 were isolated from donors negative for the HLA-I binding alleles. B Reactivity of T-cell clones against EBV-B cells exogenously pulsed with RUNX1 neopeptides. EBV-B cells were positive for the relevant HLA-I restriction alleles. IFNγ release was measured after overnight coincubation by ELISA (R&D) in single or duplicate wells. C Reactivity of T-cell clones against K562 transduced with the relevant HLA-I restriction allele and the full-length RUNX1c.883dup gene (ENST00000675419.1) encoding p.Ser295PhefsTer305 with 304 amino acids in the long ARF (K562 + HLA +fs-mRUNX1). K562 cells transduced with the relevant HLA and full-length wildtype RUNX1 gene (K562 + HLA +wtRUNX1) and K562 transduced with the relevant HLA and exogenously pulsed with RUNX1 neopeptides were included as controls. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons (unpaired t tests) were performed for each clone between K562 + HLA +wtRUNX1 and K562 + HLA +fs-mRUNX1 (clone 5.2A12: p = 0.002; 32.5G10: p = 0.006; 4.2C6: p = 0.02; 5.3A11: p = 0.0003; 31.2D9: p > 0.99; 26.1C6: p = 0.03; 31.2D12: p = 0.00003; 31.3G3: p = 0.004; 40.2E5: p = 0.002). D Reactivity of T-cell clones against AML cell line SIG-M5 C9 carrying a RUNX1 c.906_907insG mutation introduced by CRISPR/Cas9, encoding p.Ser303ValfsTer297 with 296 amino acids in the long ARF. The parental SIG-M5 cell line, unloaded or exogenously pulsed with RUNX1 neopeptides, was included as a control. SIG-M5 and SIG-M5 C9 are HLA-B*07:02 positive and were retrovirally transduced with other relevant HLA alleles. Transduced cell lines were >90% positive for marker gene murine CD19. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons (unpaired t tests) were performed for each clone between SIG-M5 ( + HLA) and SIG-M5 C9 ( + HLA) (clone 5.2A12: p = 0.42; 32.5G10: p = 0.04; 4.2C6: p = 0.03; 5.3A11: p = 0.002; 31.2D9: p > 0.99; 26.1C6: p = 0.91; 31.2D12: p = 0.06; 31.3G3: p = 0.42; 40.2E5: p > 0.99). E Reactivity of T-cell clones against EBV-B cells pulsed with titrated concentrations of the indicated RUNX1 neopeptides. EBV-B cells were positive for the relevant HLA-I restriction alleles. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. T-cell clone 32.5G10 recognized APGGGRVEALL with an EC50 of 263.8 nM, and T-cell clones 4.2C6 and 5.3A11 recognized GPRAPDQGDL with EC50 values of 25.8 and 102.1 nM, respectively. Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.
    Figure Legend Snippet: A CD8 T-cell clones showed specific binding to PE- or APC-conjugated pMHC-tetramers containing neopeptides from the long ARF created by RUNX1 frameshift mutations by flow cytometry. No binding was observed to control pMHC-tetramers containing an irrelevant peptide in the same HLA molecule. Clones 5.2A12, 4.2C6, 5.3A11, 31.2D9, 31.2D12 and 40.2E5 were isolated from donors positive for the HLA-I binding molecules of the neopeptides, whereas clones 32.5G10, 26.1C6 and 31.3G3 were isolated from donors negative for the HLA-I binding alleles. B Reactivity of T-cell clones against EBV-B cells exogenously pulsed with RUNX1 neopeptides. EBV-B cells were positive for the relevant HLA-I restriction alleles. IFNγ release was measured after overnight coincubation by ELISA (R&D) in single or duplicate wells. C Reactivity of T-cell clones against K562 transduced with the relevant HLA-I restriction allele and the full-length RUNX1c.883dup gene (ENST00000675419.1) encoding p.Ser295PhefsTer305 with 304 amino acids in the long ARF (K562 + HLA +fs-mRUNX1). K562 cells transduced with the relevant HLA and full-length wildtype RUNX1 gene (K562 + HLA +wtRUNX1) and K562 transduced with the relevant HLA and exogenously pulsed with RUNX1 neopeptides were included as controls. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons (unpaired t tests) were performed for each clone between K562 + HLA +wtRUNX1 and K562 + HLA +fs-mRUNX1 (clone 5.2A12: p = 0.002; 32.5G10: p = 0.006; 4.2C6: p = 0.02; 5.3A11: p = 0.0003; 31.2D9: p > 0.99; 26.1C6: p = 0.03; 31.2D12: p = 0.00003; 31.3G3: p = 0.004; 40.2E5: p = 0.002). D Reactivity of T-cell clones against AML cell line SIG-M5 C9 carrying a RUNX1 c.906_907insG mutation introduced by CRISPR/Cas9, encoding p.Ser303ValfsTer297 with 296 amino acids in the long ARF. The parental SIG-M5 cell line, unloaded or exogenously pulsed with RUNX1 neopeptides, was included as a control. SIG-M5 and SIG-M5 C9 are HLA-B*07:02 positive and were retrovirally transduced with other relevant HLA alleles. Transduced cell lines were >90% positive for marker gene murine CD19. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons (unpaired t tests) were performed for each clone between SIG-M5 ( + HLA) and SIG-M5 C9 ( + HLA) (clone 5.2A12: p = 0.42; 32.5G10: p = 0.04; 4.2C6: p = 0.03; 5.3A11: p = 0.002; 31.2D9: p > 0.99; 26.1C6: p = 0.91; 31.2D12: p = 0.06; 31.3G3: p = 0.42; 40.2E5: p > 0.99). E Reactivity of T-cell clones against EBV-B cells pulsed with titrated concentrations of the indicated RUNX1 neopeptides. EBV-B cells were positive for the relevant HLA-I restriction alleles. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. T-cell clone 32.5G10 recognized APGGGRVEALL with an EC50 of 263.8 nM, and T-cell clones 4.2C6 and 5.3A11 recognized GPRAPDQGDL with EC50 values of 25.8 and 102.1 nM, respectively. Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Techniques Used: Clone Assay, Binding Assay, Flow Cytometry, Control, Isolation, Enzyme-linked Immunosorbent Assay, Transduction, Mutagenesis, CRISPR, Marker

    A CD8 T cells from HLA-B*07:02 positive healthy donor 1 were transduced with HLA-B*07:02-restricted RUNX1 neoantigen-specific TCRs derived from T-cell clones 32.5G10, 4.2C6, or 5.3A11. CD8 T cells were also transduced with an HLA-B*07:02-restricted control TCR for CMV peptide TPRVTGGGAM (CMV-B7 TCR). pMHC-tetramer staining confirms surface expression of the introduced TCRs on transduced CD8 T cells. 32.5G10 TCR-T cells showed specific binding to the pMHC-tetramer with RUNX1 neopeptide APGGGRVEALL in HLA-B*07:02, and 4.2C6 and 5.3A11 TCR-T cells to the pMHC-tetramer containing RUNX1 neopeptide GPRAPDGQDL in HLA-B*07:02. B TCR-T cell reactivity (donor 1) against HLA-B*07:02 positive AML cell lines SIG-M5 (wildtype RUNX1 ) and SIG-M5 C9 (mutated RUNX1 ), unloaded or exogenously pulsed with RUNX1 neopeptides GPRAPDGQDL and APGGGRVEALL and CMV peptide TPRVTGGGAM (SIG-M5 C9 +pep). IFNγ release was measured after overnight coincubation by ELISA (Medix Biochemica) in duplicate wells. SIG-M5 C9 was most strongly recognized by CD8 T cells transduced with the RUNX1-GPR specific 4.2C6 TCR. Statistical comparisons using unpaired t tests were performed for each TCR-T cell line between SIG-M5 and SIG-M5 C9 (32.5G10 TCR: p = 0.91; 4.2C6 TCR: p = 0.04; 5.3A11 TCR: p = 0.49; CMV-B7 TCR: p = 0.91). C Reactivity of 4.2C6 TCR-T cells (donor 1) against five malignant myeloid cell lines with RUNX1 frameshift mutations introduced by CRISPR/Cas9 (SIG-M5 C9, MUTZ-3 2D9 + B7, K562 E4 + B7, K562 E9D12 + B7, and MonoMac6 3A10), and their parental cell lines. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons using unpaired t tests were performed between RUNX1 -mutated and parental cell lines (SIG-M5 C9: p = 0.0004; MUTZ-3 2D9: p = 0.05; K562 E4: p = 0.0002; K562 E9D12: p = 0.06; MonoMac6 3A10: p = 0.99). D CD8 T cells from HLA-B*07:02 positive healthy donors 1 and 2 were transduced with the RUNX1-GPR specific 4.2C6 TCR or control CMV-B7 TCR, and tested for specific lysis of the HLA-B*07:02 positive AML cell lines SIG-M5 C9 and MonoMac6 3A10 carrying RUNX1 frameshift mutations. After 48 h of coincubation, numbers of viable AML cells were measured in triplicate wells in a quantitative flow cytometry-based cytolysis assay. 4.2C6 TCR-T cells from both donors specifically killed SIG-M5 C9 ( p < 0.0001) and MonoMac6 3A10 ( p = 0.0024–0.04) with RUNX1 frameshift mutations, but not parental SIG-M5 and MonoMac6 ( p = 0.17–0.98). E Potential cross-reactivity of the 4.2C6 RUNX1 neoantigen-specific TCR-T cells (donor 1) against a panel of EBV-B cells expressing a large variety of common HLA-I and -II alleles. No reactivity was observed against the panel. An HLA-B*07:02 positive EBV-B cell line exogenously pulsed with RUNX1 neopeptide GPRAPDGQDL was included as a positive control (EBV 5098 +pep). IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.
    Figure Legend Snippet: A CD8 T cells from HLA-B*07:02 positive healthy donor 1 were transduced with HLA-B*07:02-restricted RUNX1 neoantigen-specific TCRs derived from T-cell clones 32.5G10, 4.2C6, or 5.3A11. CD8 T cells were also transduced with an HLA-B*07:02-restricted control TCR for CMV peptide TPRVTGGGAM (CMV-B7 TCR). pMHC-tetramer staining confirms surface expression of the introduced TCRs on transduced CD8 T cells. 32.5G10 TCR-T cells showed specific binding to the pMHC-tetramer with RUNX1 neopeptide APGGGRVEALL in HLA-B*07:02, and 4.2C6 and 5.3A11 TCR-T cells to the pMHC-tetramer containing RUNX1 neopeptide GPRAPDGQDL in HLA-B*07:02. B TCR-T cell reactivity (donor 1) against HLA-B*07:02 positive AML cell lines SIG-M5 (wildtype RUNX1 ) and SIG-M5 C9 (mutated RUNX1 ), unloaded or exogenously pulsed with RUNX1 neopeptides GPRAPDGQDL and APGGGRVEALL and CMV peptide TPRVTGGGAM (SIG-M5 C9 +pep). IFNγ release was measured after overnight coincubation by ELISA (Medix Biochemica) in duplicate wells. SIG-M5 C9 was most strongly recognized by CD8 T cells transduced with the RUNX1-GPR specific 4.2C6 TCR. Statistical comparisons using unpaired t tests were performed for each TCR-T cell line between SIG-M5 and SIG-M5 C9 (32.5G10 TCR: p = 0.91; 4.2C6 TCR: p = 0.04; 5.3A11 TCR: p = 0.49; CMV-B7 TCR: p = 0.91). C Reactivity of 4.2C6 TCR-T cells (donor 1) against five malignant myeloid cell lines with RUNX1 frameshift mutations introduced by CRISPR/Cas9 (SIG-M5 C9, MUTZ-3 2D9 + B7, K562 E4 + B7, K562 E9D12 + B7, and MonoMac6 3A10), and their parental cell lines. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons using unpaired t tests were performed between RUNX1 -mutated and parental cell lines (SIG-M5 C9: p = 0.0004; MUTZ-3 2D9: p = 0.05; K562 E4: p = 0.0002; K562 E9D12: p = 0.06; MonoMac6 3A10: p = 0.99). D CD8 T cells from HLA-B*07:02 positive healthy donors 1 and 2 were transduced with the RUNX1-GPR specific 4.2C6 TCR or control CMV-B7 TCR, and tested for specific lysis of the HLA-B*07:02 positive AML cell lines SIG-M5 C9 and MonoMac6 3A10 carrying RUNX1 frameshift mutations. After 48 h of coincubation, numbers of viable AML cells were measured in triplicate wells in a quantitative flow cytometry-based cytolysis assay. 4.2C6 TCR-T cells from both donors specifically killed SIG-M5 C9 ( p < 0.0001) and MonoMac6 3A10 ( p = 0.0024–0.04) with RUNX1 frameshift mutations, but not parental SIG-M5 and MonoMac6 ( p = 0.17–0.98). E Potential cross-reactivity of the 4.2C6 RUNX1 neoantigen-specific TCR-T cells (donor 1) against a panel of EBV-B cells expressing a large variety of common HLA-I and -II alleles. No reactivity was observed against the panel. An HLA-B*07:02 positive EBV-B cell line exogenously pulsed with RUNX1 neopeptide GPRAPDGQDL was included as a positive control (EBV 5098 +pep). IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Techniques Used: Transduction, Derivative Assay, Clone Assay, Control, Staining, Expressing, Binding Assay, Enzyme-linked Immunosorbent Assay, CRISPR, Lysis, Flow Cytometry, Positive Control

    Immunodeficient hIL-7xhIL-15 KI NSG mice were injected with 3×10 6 cells of the HLA-B*07:02 positive and RUNX1- mutated AML cell line SIG-M5 C9 transduced with luciferase to follow in vivo tumor growth (SIG-M5 C9 +Luc). Two weeks after injection (day 14), mice were injected with 6 × 10 6 4.2C6 TCR-T cells (donor 1) specific for RUNX1 neopeptide GPRAPDGQDL, or CMV-B7 control TCR-T cells. TCR-T cells were injected 10 days after in vitro restimulation. A On the day of injection, 4.2C6 TCR-T cells were tested for reactivity against SIG-M5 C9, SIG-M5 C9 +Luc, and SIG-M5 C9 exogenously pulsed with GPRAPDGQDL (SIG-M5 C9 +pep) in vitro. 4.2C6 TCR-T cells were less reactive against SIG-M5 C9 +Luc than against SIG-M5 C9. IFNγ release was measured after overnight coincubation by ELISA (Medix Biochemica) in duplicate wells. Statistical comparisons using unpaired t tests were performed for each cell line between the 4.2C6 TCR and the CMV-B7 control TCR (SIG-M5 C9: p = 0.0004; SIG-M5 C9 +Luc: p = 0.049). Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. B 4.2C6 TCR-T cells were tested for reactivity against SIG-M5 C9 +Luc in vivo. Tumor growth is shown for individual mice treated with RUNX1-specific 4.2C6 or CMV-B7 TCR-T cells. C Mean and standard deviations of tumor loads (average radiance) on different days before and after T-cell injection are shown for treatment groups (left panel) and individual mice (right panel). Average tumor outgrowth was significantly reduced in mice treated with RUNX1-GPR specific 4.2C6 TCR-T cells as compared to CMV-B7 TCR-T cells on days 3 and 10 after T-cell injection.
    Figure Legend Snippet: Immunodeficient hIL-7xhIL-15 KI NSG mice were injected with 3×10 6 cells of the HLA-B*07:02 positive and RUNX1- mutated AML cell line SIG-M5 C9 transduced with luciferase to follow in vivo tumor growth (SIG-M5 C9 +Luc). Two weeks after injection (day 14), mice were injected with 6 × 10 6 4.2C6 TCR-T cells (donor 1) specific for RUNX1 neopeptide GPRAPDGQDL, or CMV-B7 control TCR-T cells. TCR-T cells were injected 10 days after in vitro restimulation. A On the day of injection, 4.2C6 TCR-T cells were tested for reactivity against SIG-M5 C9, SIG-M5 C9 +Luc, and SIG-M5 C9 exogenously pulsed with GPRAPDGQDL (SIG-M5 C9 +pep) in vitro. 4.2C6 TCR-T cells were less reactive against SIG-M5 C9 +Luc than against SIG-M5 C9. IFNγ release was measured after overnight coincubation by ELISA (Medix Biochemica) in duplicate wells. Statistical comparisons using unpaired t tests were performed for each cell line between the 4.2C6 TCR and the CMV-B7 control TCR (SIG-M5 C9: p = 0.0004; SIG-M5 C9 +Luc: p = 0.049). Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. B 4.2C6 TCR-T cells were tested for reactivity against SIG-M5 C9 +Luc in vivo. Tumor growth is shown for individual mice treated with RUNX1-specific 4.2C6 or CMV-B7 TCR-T cells. C Mean and standard deviations of tumor loads (average radiance) on different days before and after T-cell injection are shown for treatment groups (left panel) and individual mice (right panel). Average tumor outgrowth was significantly reduced in mice treated with RUNX1-GPR specific 4.2C6 TCR-T cells as compared to CMV-B7 TCR-T cells on days 3 and 10 after T-cell injection.

    Techniques Used: Injection, Transduction, Luciferase, In Vivo, Control, In Vitro, Enzyme-linked Immunosorbent Assay

    Related Articles

    Cell Culture:

    Article Title: A T-cell receptor targeting RUNX1 frameshift mutations in acute myeloid leukemia.
    Article Snippet: .. AML cell line SIG-M5 (DSMZ, Braunschweig, Germany) was cultured in IMDM with 20% FBS, MonoMac6 (DSMZ) in RPMI 1640 with 10% FBS, 1% non-essential amino acids (Lonza, Basel, Switzerland), 1% sodium pyruvate (Thermo Fisher, Waltham, Massachusetts, USA) and 10 μg/ml human insulin (Thermo Fisher), and MUTZ-3 as previously described [30, 31]. ..

    Article Title: A T-cell receptor targeting RUNX1 frameshift mutations in acute myeloid leukemia
    Article Snippet: .. AML cell line SIG-M5 (DSMZ, Braunschweig, Germany) was cultured in IMDM with 20% FBS, MonoMac6 (DSMZ) in RPMI 1640 with 10% FBS, 1% non-essential amino acids (Lonza, Basel, Switzerland), 1% sodium pyruvate (Thermo Fisher, Waltham, Massachusetts, USA) and 10 μg/ml human insulin (Thermo Fisher), and MUTZ-3 as previously described [ , ]. ..



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    A CD8 T-cell clones showed specific binding to PE- or APC-conjugated pMHC-tetramers containing neopeptides from the long ARF created by RUNX1 frameshift mutations by flow cytometry. No binding was observed to control pMHC-tetramers containing an irrelevant peptide in the same HLA molecule. Clones 5.2A12, 4.2C6, 5.3A11, 31.2D9, 31.2D12 and 40.2E5 were isolated from donors positive for the HLA-I binding molecules of the neopeptides, whereas clones 32.5G10, 26.1C6 and 31.3G3 were isolated from donors negative for the HLA-I binding alleles. B Reactivity of T-cell clones against EBV-B cells exogenously pulsed with RUNX1 neopeptides. EBV-B cells were positive for the relevant HLA-I restriction alleles. IFNγ release was measured after overnight coincubation by ELISA (R&D) in single or duplicate wells. C Reactivity of T-cell clones against K562 transduced with the relevant HLA-I restriction allele and the full-length RUNX1c.883dup gene (ENST00000675419.1) encoding p.Ser295PhefsTer305 with 304 amino acids in the long ARF (K562 + HLA +fs-mRUNX1). K562 cells transduced with the relevant HLA and full-length wildtype RUNX1 gene (K562 + HLA +wtRUNX1) and K562 transduced with the relevant HLA and exogenously pulsed with RUNX1 neopeptides were included as controls. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons (unpaired t tests) were performed for each clone between K562 + HLA +wtRUNX1 and K562 + HLA +fs-mRUNX1 (clone 5.2A12: p = 0.002; 32.5G10: p = 0.006; 4.2C6: p = 0.02; 5.3A11: p = 0.0003; 31.2D9: p > 0.99; 26.1C6: p = 0.03; 31.2D12: p = 0.00003; 31.3G3: p = 0.004; 40.2E5: p = 0.002). D Reactivity of T-cell clones against <t>AML</t> <t>cell</t> <t>line</t> <t>SIG-M5</t> C9 carrying a RUNX1 c.906_907insG mutation introduced by CRISPR/Cas9, encoding p.Ser303ValfsTer297 with 296 amino acids in the long ARF. The parental SIG-M5 cell line, unloaded or exogenously pulsed with RUNX1 neopeptides, was included as a control. SIG-M5 and SIG-M5 C9 are HLA-B*07:02 positive and were retrovirally transduced with other relevant HLA alleles. Transduced cell lines were >90% positive for marker gene murine CD19. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons (unpaired t tests) were performed for each clone between SIG-M5 ( + HLA) and SIG-M5 C9 ( + HLA) (clone 5.2A12: p = 0.42; 32.5G10: p = 0.04; 4.2C6: p = 0.03; 5.3A11: p = 0.002; 31.2D9: p > 0.99; 26.1C6: p = 0.91; 31.2D12: p = 0.06; 31.3G3: p = 0.42; 40.2E5: p > 0.99). E Reactivity of T-cell clones against EBV-B cells pulsed with titrated concentrations of the indicated RUNX1 neopeptides. EBV-B cells were positive for the relevant HLA-I restriction alleles. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. T-cell clone 32.5G10 recognized APGGGRVEALL with an EC50 of 263.8 nM, and T-cell clones 4.2C6 and 5.3A11 recognized GPRAPDQGDL with EC50 values of 25.8 and 102.1 nM, respectively. Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.
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    A CD8 T-cell clones showed specific binding to PE- or APC-conjugated pMHC-tetramers containing neopeptides from the long ARF created by RUNX1 frameshift mutations by flow cytometry. No binding was observed to control pMHC-tetramers containing an irrelevant peptide in the same HLA molecule. Clones 5.2A12, 4.2C6, 5.3A11, 31.2D9, 31.2D12 and 40.2E5 were isolated from donors positive for the HLA-I binding molecules of the neopeptides, whereas clones 32.5G10, 26.1C6 and 31.3G3 were isolated from donors negative for the HLA-I binding alleles. B Reactivity of T-cell clones against EBV-B cells exogenously pulsed with RUNX1 neopeptides. EBV-B cells were positive for the relevant HLA-I restriction alleles. IFNγ release was measured after overnight coincubation by ELISA (R&D) in single or duplicate wells. C Reactivity of T-cell clones against K562 transduced with the relevant HLA-I restriction allele and the full-length RUNX1c.883dup gene (ENST00000675419.1) encoding p.Ser295PhefsTer305 with 304 amino acids in the long ARF (K562 + HLA +fs-mRUNX1). K562 cells transduced with the relevant HLA and full-length wildtype RUNX1 gene (K562 + HLA +wtRUNX1) and K562 transduced with the relevant HLA and exogenously pulsed with RUNX1 neopeptides were included as controls. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons (unpaired t tests) were performed for each clone between K562 + HLA +wtRUNX1 and K562 + HLA +fs-mRUNX1 (clone 5.2A12: p = 0.002; 32.5G10: p = 0.006; 4.2C6: p = 0.02; 5.3A11: p = 0.0003; 31.2D9: p > 0.99; 26.1C6: p = 0.03; 31.2D12: p = 0.00003; 31.3G3: p = 0.004; 40.2E5: p = 0.002). D Reactivity of T-cell clones against AML cell line SIG-M5 C9 carrying a RUNX1 c.906_907insG mutation introduced by CRISPR/Cas9, encoding p.Ser303ValfsTer297 with 296 amino acids in the long ARF. The parental SIG-M5 cell line, unloaded or exogenously pulsed with RUNX1 neopeptides, was included as a control. SIG-M5 and SIG-M5 C9 are HLA-B*07:02 positive and were retrovirally transduced with other relevant HLA alleles. Transduced cell lines were >90% positive for marker gene murine CD19. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons (unpaired t tests) were performed for each clone between SIG-M5 ( + HLA) and SIG-M5 C9 ( + HLA) (clone 5.2A12: p = 0.42; 32.5G10: p = 0.04; 4.2C6: p = 0.03; 5.3A11: p = 0.002; 31.2D9: p > 0.99; 26.1C6: p = 0.91; 31.2D12: p = 0.06; 31.3G3: p = 0.42; 40.2E5: p > 0.99). E Reactivity of T-cell clones against EBV-B cells pulsed with titrated concentrations of the indicated RUNX1 neopeptides. EBV-B cells were positive for the relevant HLA-I restriction alleles. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. T-cell clone 32.5G10 recognized APGGGRVEALL with an EC50 of 263.8 nM, and T-cell clones 4.2C6 and 5.3A11 recognized GPRAPDQGDL with EC50 values of 25.8 and 102.1 nM, respectively. Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Journal: Leukemia

    Article Title: A T-cell receptor targeting RUNX1 frameshift mutations in acute myeloid leukemia

    doi: 10.1038/s41375-025-02817-x

    Figure Lengend Snippet: A CD8 T-cell clones showed specific binding to PE- or APC-conjugated pMHC-tetramers containing neopeptides from the long ARF created by RUNX1 frameshift mutations by flow cytometry. No binding was observed to control pMHC-tetramers containing an irrelevant peptide in the same HLA molecule. Clones 5.2A12, 4.2C6, 5.3A11, 31.2D9, 31.2D12 and 40.2E5 were isolated from donors positive for the HLA-I binding molecules of the neopeptides, whereas clones 32.5G10, 26.1C6 and 31.3G3 were isolated from donors negative for the HLA-I binding alleles. B Reactivity of T-cell clones against EBV-B cells exogenously pulsed with RUNX1 neopeptides. EBV-B cells were positive for the relevant HLA-I restriction alleles. IFNγ release was measured after overnight coincubation by ELISA (R&D) in single or duplicate wells. C Reactivity of T-cell clones against K562 transduced with the relevant HLA-I restriction allele and the full-length RUNX1c.883dup gene (ENST00000675419.1) encoding p.Ser295PhefsTer305 with 304 amino acids in the long ARF (K562 + HLA +fs-mRUNX1). K562 cells transduced with the relevant HLA and full-length wildtype RUNX1 gene (K562 + HLA +wtRUNX1) and K562 transduced with the relevant HLA and exogenously pulsed with RUNX1 neopeptides were included as controls. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons (unpaired t tests) were performed for each clone between K562 + HLA +wtRUNX1 and K562 + HLA +fs-mRUNX1 (clone 5.2A12: p = 0.002; 32.5G10: p = 0.006; 4.2C6: p = 0.02; 5.3A11: p = 0.0003; 31.2D9: p > 0.99; 26.1C6: p = 0.03; 31.2D12: p = 0.00003; 31.3G3: p = 0.004; 40.2E5: p = 0.002). D Reactivity of T-cell clones against AML cell line SIG-M5 C9 carrying a RUNX1 c.906_907insG mutation introduced by CRISPR/Cas9, encoding p.Ser303ValfsTer297 with 296 amino acids in the long ARF. The parental SIG-M5 cell line, unloaded or exogenously pulsed with RUNX1 neopeptides, was included as a control. SIG-M5 and SIG-M5 C9 are HLA-B*07:02 positive and were retrovirally transduced with other relevant HLA alleles. Transduced cell lines were >90% positive for marker gene murine CD19. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons (unpaired t tests) were performed for each clone between SIG-M5 ( + HLA) and SIG-M5 C9 ( + HLA) (clone 5.2A12: p = 0.42; 32.5G10: p = 0.04; 4.2C6: p = 0.03; 5.3A11: p = 0.002; 31.2D9: p > 0.99; 26.1C6: p = 0.91; 31.2D12: p = 0.06; 31.3G3: p = 0.42; 40.2E5: p > 0.99). E Reactivity of T-cell clones against EBV-B cells pulsed with titrated concentrations of the indicated RUNX1 neopeptides. EBV-B cells were positive for the relevant HLA-I restriction alleles. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. T-cell clone 32.5G10 recognized APGGGRVEALL with an EC50 of 263.8 nM, and T-cell clones 4.2C6 and 5.3A11 recognized GPRAPDQGDL with EC50 values of 25.8 and 102.1 nM, respectively. Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Article Snippet: AML cell line SIG-M5 (DSMZ, Braunschweig, Germany) was cultured in IMDM with 20% FBS, MonoMac6 (DSMZ) in RPMI 1640 with 10% FBS, 1% non-essential amino acids (Lonza, Basel, Switzerland), 1% sodium pyruvate (Thermo Fisher, Waltham, Massachusetts, USA) and 10 μg/ml human insulin (Thermo Fisher), and MUTZ-3 as previously described [ , ].

    Techniques: Clone Assay, Binding Assay, Flow Cytometry, Control, Isolation, Enzyme-linked Immunosorbent Assay, Transduction, Mutagenesis, CRISPR, Marker

    A CD8 T cells from HLA-B*07:02 positive healthy donor 1 were transduced with HLA-B*07:02-restricted RUNX1 neoantigen-specific TCRs derived from T-cell clones 32.5G10, 4.2C6, or 5.3A11. CD8 T cells were also transduced with an HLA-B*07:02-restricted control TCR for CMV peptide TPRVTGGGAM (CMV-B7 TCR). pMHC-tetramer staining confirms surface expression of the introduced TCRs on transduced CD8 T cells. 32.5G10 TCR-T cells showed specific binding to the pMHC-tetramer with RUNX1 neopeptide APGGGRVEALL in HLA-B*07:02, and 4.2C6 and 5.3A11 TCR-T cells to the pMHC-tetramer containing RUNX1 neopeptide GPRAPDGQDL in HLA-B*07:02. B TCR-T cell reactivity (donor 1) against HLA-B*07:02 positive AML cell lines SIG-M5 (wildtype RUNX1 ) and SIG-M5 C9 (mutated RUNX1 ), unloaded or exogenously pulsed with RUNX1 neopeptides GPRAPDGQDL and APGGGRVEALL and CMV peptide TPRVTGGGAM (SIG-M5 C9 +pep). IFNγ release was measured after overnight coincubation by ELISA (Medix Biochemica) in duplicate wells. SIG-M5 C9 was most strongly recognized by CD8 T cells transduced with the RUNX1-GPR specific 4.2C6 TCR. Statistical comparisons using unpaired t tests were performed for each TCR-T cell line between SIG-M5 and SIG-M5 C9 (32.5G10 TCR: p = 0.91; 4.2C6 TCR: p = 0.04; 5.3A11 TCR: p = 0.49; CMV-B7 TCR: p = 0.91). C Reactivity of 4.2C6 TCR-T cells (donor 1) against five malignant myeloid cell lines with RUNX1 frameshift mutations introduced by CRISPR/Cas9 (SIG-M5 C9, MUTZ-3 2D9 + B7, K562 E4 + B7, K562 E9D12 + B7, and MonoMac6 3A10), and their parental cell lines. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons using unpaired t tests were performed between RUNX1 -mutated and parental cell lines (SIG-M5 C9: p = 0.0004; MUTZ-3 2D9: p = 0.05; K562 E4: p = 0.0002; K562 E9D12: p = 0.06; MonoMac6 3A10: p = 0.99). D CD8 T cells from HLA-B*07:02 positive healthy donors 1 and 2 were transduced with the RUNX1-GPR specific 4.2C6 TCR or control CMV-B7 TCR, and tested for specific lysis of the HLA-B*07:02 positive AML cell lines SIG-M5 C9 and MonoMac6 3A10 carrying RUNX1 frameshift mutations. After 48 h of coincubation, numbers of viable AML cells were measured in triplicate wells in a quantitative flow cytometry-based cytolysis assay. 4.2C6 TCR-T cells from both donors specifically killed SIG-M5 C9 ( p < 0.0001) and MonoMac6 3A10 ( p = 0.0024–0.04) with RUNX1 frameshift mutations, but not parental SIG-M5 and MonoMac6 ( p = 0.17–0.98). E Potential cross-reactivity of the 4.2C6 RUNX1 neoantigen-specific TCR-T cells (donor 1) against a panel of EBV-B cells expressing a large variety of common HLA-I and -II alleles. No reactivity was observed against the panel. An HLA-B*07:02 positive EBV-B cell line exogenously pulsed with RUNX1 neopeptide GPRAPDGQDL was included as a positive control (EBV 5098 +pep). IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Journal: Leukemia

    Article Title: A T-cell receptor targeting RUNX1 frameshift mutations in acute myeloid leukemia

    doi: 10.1038/s41375-025-02817-x

    Figure Lengend Snippet: A CD8 T cells from HLA-B*07:02 positive healthy donor 1 were transduced with HLA-B*07:02-restricted RUNX1 neoantigen-specific TCRs derived from T-cell clones 32.5G10, 4.2C6, or 5.3A11. CD8 T cells were also transduced with an HLA-B*07:02-restricted control TCR for CMV peptide TPRVTGGGAM (CMV-B7 TCR). pMHC-tetramer staining confirms surface expression of the introduced TCRs on transduced CD8 T cells. 32.5G10 TCR-T cells showed specific binding to the pMHC-tetramer with RUNX1 neopeptide APGGGRVEALL in HLA-B*07:02, and 4.2C6 and 5.3A11 TCR-T cells to the pMHC-tetramer containing RUNX1 neopeptide GPRAPDGQDL in HLA-B*07:02. B TCR-T cell reactivity (donor 1) against HLA-B*07:02 positive AML cell lines SIG-M5 (wildtype RUNX1 ) and SIG-M5 C9 (mutated RUNX1 ), unloaded or exogenously pulsed with RUNX1 neopeptides GPRAPDGQDL and APGGGRVEALL and CMV peptide TPRVTGGGAM (SIG-M5 C9 +pep). IFNγ release was measured after overnight coincubation by ELISA (Medix Biochemica) in duplicate wells. SIG-M5 C9 was most strongly recognized by CD8 T cells transduced with the RUNX1-GPR specific 4.2C6 TCR. Statistical comparisons using unpaired t tests were performed for each TCR-T cell line between SIG-M5 and SIG-M5 C9 (32.5G10 TCR: p = 0.91; 4.2C6 TCR: p = 0.04; 5.3A11 TCR: p = 0.49; CMV-B7 TCR: p = 0.91). C Reactivity of 4.2C6 TCR-T cells (donor 1) against five malignant myeloid cell lines with RUNX1 frameshift mutations introduced by CRISPR/Cas9 (SIG-M5 C9, MUTZ-3 2D9 + B7, K562 E4 + B7, K562 E9D12 + B7, and MonoMac6 3A10), and their parental cell lines. IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Statistical comparisons using unpaired t tests were performed between RUNX1 -mutated and parental cell lines (SIG-M5 C9: p = 0.0004; MUTZ-3 2D9: p = 0.05; K562 E4: p = 0.0002; K562 E9D12: p = 0.06; MonoMac6 3A10: p = 0.99). D CD8 T cells from HLA-B*07:02 positive healthy donors 1 and 2 were transduced with the RUNX1-GPR specific 4.2C6 TCR or control CMV-B7 TCR, and tested for specific lysis of the HLA-B*07:02 positive AML cell lines SIG-M5 C9 and MonoMac6 3A10 carrying RUNX1 frameshift mutations. After 48 h of coincubation, numbers of viable AML cells were measured in triplicate wells in a quantitative flow cytometry-based cytolysis assay. 4.2C6 TCR-T cells from both donors specifically killed SIG-M5 C9 ( p < 0.0001) and MonoMac6 3A10 ( p = 0.0024–0.04) with RUNX1 frameshift mutations, but not parental SIG-M5 and MonoMac6 ( p = 0.17–0.98). E Potential cross-reactivity of the 4.2C6 RUNX1 neoantigen-specific TCR-T cells (donor 1) against a panel of EBV-B cells expressing a large variety of common HLA-I and -II alleles. No reactivity was observed against the panel. An HLA-B*07:02 positive EBV-B cell line exogenously pulsed with RUNX1 neopeptide GPRAPDGQDL was included as a positive control (EBV 5098 +pep). IFNγ release was measured after overnight coincubation by ELISA (R&D) in duplicate wells. Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

    Article Snippet: AML cell line SIG-M5 (DSMZ, Braunschweig, Germany) was cultured in IMDM with 20% FBS, MonoMac6 (DSMZ) in RPMI 1640 with 10% FBS, 1% non-essential amino acids (Lonza, Basel, Switzerland), 1% sodium pyruvate (Thermo Fisher, Waltham, Massachusetts, USA) and 10 μg/ml human insulin (Thermo Fisher), and MUTZ-3 as previously described [ , ].

    Techniques: Transduction, Derivative Assay, Clone Assay, Control, Staining, Expressing, Binding Assay, Enzyme-linked Immunosorbent Assay, CRISPR, Lysis, Flow Cytometry, Positive Control

    Immunodeficient hIL-7xhIL-15 KI NSG mice were injected with 3×10 6 cells of the HLA-B*07:02 positive and RUNX1- mutated AML cell line SIG-M5 C9 transduced with luciferase to follow in vivo tumor growth (SIG-M5 C9 +Luc). Two weeks after injection (day 14), mice were injected with 6 × 10 6 4.2C6 TCR-T cells (donor 1) specific for RUNX1 neopeptide GPRAPDGQDL, or CMV-B7 control TCR-T cells. TCR-T cells were injected 10 days after in vitro restimulation. A On the day of injection, 4.2C6 TCR-T cells were tested for reactivity against SIG-M5 C9, SIG-M5 C9 +Luc, and SIG-M5 C9 exogenously pulsed with GPRAPDGQDL (SIG-M5 C9 +pep) in vitro. 4.2C6 TCR-T cells were less reactive against SIG-M5 C9 +Luc than against SIG-M5 C9. IFNγ release was measured after overnight coincubation by ELISA (Medix Biochemica) in duplicate wells. Statistical comparisons using unpaired t tests were performed for each cell line between the 4.2C6 TCR and the CMV-B7 control TCR (SIG-M5 C9: p = 0.0004; SIG-M5 C9 +Luc: p = 0.049). Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. B 4.2C6 TCR-T cells were tested for reactivity against SIG-M5 C9 +Luc in vivo. Tumor growth is shown for individual mice treated with RUNX1-specific 4.2C6 or CMV-B7 TCR-T cells. C Mean and standard deviations of tumor loads (average radiance) on different days before and after T-cell injection are shown for treatment groups (left panel) and individual mice (right panel). Average tumor outgrowth was significantly reduced in mice treated with RUNX1-GPR specific 4.2C6 TCR-T cells as compared to CMV-B7 TCR-T cells on days 3 and 10 after T-cell injection.

    Journal: Leukemia

    Article Title: A T-cell receptor targeting RUNX1 frameshift mutations in acute myeloid leukemia

    doi: 10.1038/s41375-025-02817-x

    Figure Lengend Snippet: Immunodeficient hIL-7xhIL-15 KI NSG mice were injected with 3×10 6 cells of the HLA-B*07:02 positive and RUNX1- mutated AML cell line SIG-M5 C9 transduced with luciferase to follow in vivo tumor growth (SIG-M5 C9 +Luc). Two weeks after injection (day 14), mice were injected with 6 × 10 6 4.2C6 TCR-T cells (donor 1) specific for RUNX1 neopeptide GPRAPDGQDL, or CMV-B7 control TCR-T cells. TCR-T cells were injected 10 days after in vitro restimulation. A On the day of injection, 4.2C6 TCR-T cells were tested for reactivity against SIG-M5 C9, SIG-M5 C9 +Luc, and SIG-M5 C9 exogenously pulsed with GPRAPDGQDL (SIG-M5 C9 +pep) in vitro. 4.2C6 TCR-T cells were less reactive against SIG-M5 C9 +Luc than against SIG-M5 C9. IFNγ release was measured after overnight coincubation by ELISA (Medix Biochemica) in duplicate wells. Statistical comparisons using unpaired t tests were performed for each cell line between the 4.2C6 TCR and the CMV-B7 control TCR (SIG-M5 C9: p = 0.0004; SIG-M5 C9 +Luc: p = 0.049). Significance is indicated as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. B 4.2C6 TCR-T cells were tested for reactivity against SIG-M5 C9 +Luc in vivo. Tumor growth is shown for individual mice treated with RUNX1-specific 4.2C6 or CMV-B7 TCR-T cells. C Mean and standard deviations of tumor loads (average radiance) on different days before and after T-cell injection are shown for treatment groups (left panel) and individual mice (right panel). Average tumor outgrowth was significantly reduced in mice treated with RUNX1-GPR specific 4.2C6 TCR-T cells as compared to CMV-B7 TCR-T cells on days 3 and 10 after T-cell injection.

    Article Snippet: AML cell line SIG-M5 (DSMZ, Braunschweig, Germany) was cultured in IMDM with 20% FBS, MonoMac6 (DSMZ) in RPMI 1640 with 10% FBS, 1% non-essential amino acids (Lonza, Basel, Switzerland), 1% sodium pyruvate (Thermo Fisher, Waltham, Massachusetts, USA) and 10 μg/ml human insulin (Thermo Fisher), and MUTZ-3 as previously described [ , ].

    Techniques: Injection, Transduction, Luciferase, In Vivo, Control, In Vitro, Enzyme-linked Immunosorbent Assay

    Journal: bioRxiv

    Article Title: TP53 mutations and drug sensitivity in acute myeloid leukaemia cells with acquired MDM2 inhibitor resistance

    doi: 10.1101/404475

    Figure Lengend Snippet:

    Article Snippet: The AML cell lines MV4-11, OCI-AML-2, OCI-AML-3, and SIG-M5 were obtained from DSMZ (Braunschweig, Germany).

    Techniques: Mutagenesis

    Drug sensitivity profiles of the AML cell line MV4-11 and its sub-lines adapted to nutlin-3 (20µM). Concentrations that inhibit cell viability by 50% (IC50) as determined by MTT assay after 120h incubation and relative sensitivity expressed as fold change (IC50 nutlin-3-resistant MV4-11 sub-line/ IC50 MV4-11). Numerical data are presented in Suppl. .

    Journal: bioRxiv

    Article Title: TP53 mutations and drug sensitivity in acute myeloid leukaemia cells with acquired MDM2 inhibitor resistance

    doi: 10.1101/404475

    Figure Lengend Snippet: Drug sensitivity profiles of the AML cell line MV4-11 and its sub-lines adapted to nutlin-3 (20µM). Concentrations that inhibit cell viability by 50% (IC50) as determined by MTT assay after 120h incubation and relative sensitivity expressed as fold change (IC50 nutlin-3-resistant MV4-11 sub-line/ IC50 MV4-11). Numerical data are presented in Suppl. .

    Article Snippet: The AML cell lines MV4-11, OCI-AML-2, OCI-AML-3, and SIG-M5 were obtained from DSMZ (Braunschweig, Germany).

    Techniques: MTT Assay, Incubation

    Drug sensitivity profiles of the AML cell line OCI-AML-2 and its sub-lines adapted to nutlin-3 (20µM). Concentrations that inhibit cell viability by 50% (IC50) as determined by MTT assay after 120h incubation and relative sensitivity expressed as fold change (IC50 nutlin-3-resistant OCI-AML-2 sub-line/ IC50 OCI-AML-2). Numerical data are presented in Suppl. .

    Journal: bioRxiv

    Article Title: TP53 mutations and drug sensitivity in acute myeloid leukaemia cells with acquired MDM2 inhibitor resistance

    doi: 10.1101/404475

    Figure Lengend Snippet: Drug sensitivity profiles of the AML cell line OCI-AML-2 and its sub-lines adapted to nutlin-3 (20µM). Concentrations that inhibit cell viability by 50% (IC50) as determined by MTT assay after 120h incubation and relative sensitivity expressed as fold change (IC50 nutlin-3-resistant OCI-AML-2 sub-line/ IC50 OCI-AML-2). Numerical data are presented in Suppl. .

    Article Snippet: The AML cell lines MV4-11, OCI-AML-2, OCI-AML-3, and SIG-M5 were obtained from DSMZ (Braunschweig, Germany).

    Techniques: MTT Assay, Incubation

    Drug sensitivity profiles of the AML cell line OCI-AML-3 and its sub-lines adapted to nutlin-3 (20µM). Concentrations that inhibit cell viability by 50% (IC50) as determined by MTT assay after 120h incubation and relative sensitivity expressed as fold change (IC50 nutlin-3-resistant OCI-AML-3 sub-line/ IC50 OCI-AML-3). Numerical data are presented in Suppl. .

    Journal: bioRxiv

    Article Title: TP53 mutations and drug sensitivity in acute myeloid leukaemia cells with acquired MDM2 inhibitor resistance

    doi: 10.1101/404475

    Figure Lengend Snippet: Drug sensitivity profiles of the AML cell line OCI-AML-3 and its sub-lines adapted to nutlin-3 (20µM). Concentrations that inhibit cell viability by 50% (IC50) as determined by MTT assay after 120h incubation and relative sensitivity expressed as fold change (IC50 nutlin-3-resistant OCI-AML-3 sub-line/ IC50 OCI-AML-3). Numerical data are presented in Suppl. .

    Article Snippet: The AML cell lines MV4-11, OCI-AML-2, OCI-AML-3, and SIG-M5 were obtained from DSMZ (Braunschweig, Germany).

    Techniques: MTT Assay, Incubation

    Drug sensitivity profiles of the AML cell line SIG-M5 and its sub-lines adapted to nutlin-3 (20µM). Concentrations that inhibit cell viability by 50% (IC50) as determined by MTT assay after 120h incubation and relative sensitivity expressed as fold change (IC50 nutlin-3-resistant SIG-M5 sub-line/ IC50 SIG-M5). Numerical data are presented in Suppl. .

    Journal: bioRxiv

    Article Title: TP53 mutations and drug sensitivity in acute myeloid leukaemia cells with acquired MDM2 inhibitor resistance

    doi: 10.1101/404475

    Figure Lengend Snippet: Drug sensitivity profiles of the AML cell line SIG-M5 and its sub-lines adapted to nutlin-3 (20µM). Concentrations that inhibit cell viability by 50% (IC50) as determined by MTT assay after 120h incubation and relative sensitivity expressed as fold change (IC50 nutlin-3-resistant SIG-M5 sub-line/ IC50 SIG-M5). Numerical data are presented in Suppl. .

    Article Snippet: The AML cell lines MV4-11, OCI-AML-2, OCI-AML-3, and SIG-M5 were obtained from DSMZ (Braunschweig, Germany).

    Techniques: MTT Assay, Incubation