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Published Erratum
. 2023 Aug 3;142(5):494.
doi: 10.1182/blood.2023020968.

Moujalled DM, Brown FC, Chua CC, et al. Acquired mutations in BAX confer resistance to BH3-mimetic therapy in acute myeloid leukemia. Blood. 2023;141(6):634-644

No authors listed
Published Erratum

Moujalled DM, Brown FC, Chua CC, et al. Acquired mutations in BAX confer resistance to BH3-mimetic therapy in acute myeloid leukemia. Blood. 2023;141(6):634-644

No authors listed. Blood. .
No abstract available

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Figures

Figure 4.
Figure 4.
BAX deficiency confers resistance to combined BCL-2 and MCL1 targeting in vitro. (A) BAX expression in CRISPR-Cas9–edited OCI-AML3 cells. Immunoblot demonstrating CRISPR-Cas9–induced BAX depletion in OCI-AML3 cells using guide RNAs (gRNAs) targeting BAX (gRNA-1.1 or gRNA-2.1) or a nontargeted (empty vector [EV]) control. Cells were treated with 5 μg/mL doxycycline for 72 hours to induce BAX loss. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used as a loading control. (B) Drug sensitivity of CRISPR-Cas9–edited OCI-AML3 cells. OCI-AML3 cells transduced with gRNA targeting BAX or a nontargeted control were treated with indicated drugs (0.001-10 μM for BH3-mimetics, 0.01-100 μM for cytarabine, and 0.0001 to 1 μM for idarubicin) and the LC50 determined by flow cytometry after 48-hour exposure. Error bars are SD of 2 independent experiments. ∗P < .05, ∗∗P < .01, ∗∗∗P < .001, and ∗∗∗∗P < .0001. (C) Survival of mice engrafted with BAX knockout cells in response to BH3-mimetic therapy. Irradiated NSG mice were transplanted with 105 OCI-AML3 nontargeted EV control or OCI-AML3 BAX knockout cells (gRNA 2.1). Dosing commenced on day 4 posttransplant and mice were randomly divided into cohorts of 6 mice and treated with vehicle or a combination of venetoclax (75 mg/kg, weekdays by gavage) and S63845 (25 mg/kg, IV weekly) for 4 weeks. Kaplan-Meier survival analysis (ethical end point) shows that combined treatment with venetoclax/S63845 significantly prolongs survival in OCI-AML3 EV but not OCI-AML3 BAX knockout cohorts (black bar indicates duration of treatment). (D) Survival of mice engrafted with BAK knockout cells in response to BH3-mimetic therapy. Irradiated NSG mice were transplanted with 105 OCI-AML3 nontargeted EV control or OCI-AML3 BAK knockout cells (gRNA 2.1). Dosing commenced on day 4 posttransplant and mice were randomly divided into cohorts of 6 mice and treated with vehicle or a combination of venetoclax (75 mg/kg, weekdays by gavage) and S63845 (25 mg/kg, IV weekly) for 4 weeks. Kaplan-Meier survival analysis (ethical end point) shows that combined treatment with venetoclax/S63845 significantly prolongs survival in both the OCI-AML3 EV and OCI-AML3 BAK knockout cohorts (black bar indicates duration of treatment). ns, not significant.
See this image and copyright information in PMC

Erratum for

  • Acquired mutations in BAX confer resistance to BH3-mimetic therapy in acute myeloid leukemia.
    Moujalled DM, Brown FC, Chua CC, Dengler MA, Pomilio G, Anstee NS, Litalien V, Thompson E, Morley T, MacRaild S, Tiong IS, Morris R, Dun K, Zordan A, Shah J, Banquet S, Halilovic E, Morris E, Herold MJ, Lessene G, Adams JM, Huang DCS, Roberts AW, Blombery P, Wei AH. Moujalled DM, et al. Blood. 2023 Feb 9;141(6):634-644. doi: 10.1182/blood.2022016090. Blood. 2023. PMID: 36219880 Free PMC article.

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