Student or educator? Sign up with your school email and get 6 months of Pro free.
CoChat
Sign Up
Cited by 18

The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.

miR-451a abrogates treatment resistance in FLT3-ITD-positive acute myeloid leukemia.

Krakowsky, Rosanna H. E., Wurm, Alexander A., Gerloff, Dennis, Katzerke, Christiane, Bräuer-Hartmann, Daniela, Hartmann, Jens-Uwe, Wilke, Franziska, Thiede, Christian, Müller-Tidow, Carsten, Niederwieser, Dietger, Behre, Gerhard·2018·Blood Cancer Journal
DOI 10.1038/s41408-018-0070-yPMC PMC5862828
Open this paper in CoChat — free account

Abstract

Acute myeloid leukemia (AML) is a fatal disease with up to 95% of patients remaining incurable. While supportive care has been increased in quantity and quality; substantial progress of AML therapy itself is still lacking. Primarily two predicaments challenge current therapy: first, the heterogeneity of the disease; second, the phenomenon of treatment resistance. Although many AML patients initially respond to therapy, the majority of patients relapse caused by chemoresistant clones, ultimately leading to the incurability of the disease 1 , 2 , 3 .

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/s41408-018-0070-y

Cites

15 of 15 references verified0 citation errors · 0 not checkable

Statistics

Figures

Fig. 1 FLT3-ITD downregulates miR-451a. a NGS of bone marrow mononuclear cells from healthy donors and normal karyotype AML patients with FLT3-WT, FLT3-ITD or FLT3-TKD. Heatmap of the top 50 miRs differentially expressed in AML samples compared to healthy donors ranked by p-value. miR-451a exhibited the lowest p-value. b Median expression levels of miR-451a are lowest in FLT3-ITD+ AML samples. Significance was determined by Wilcoxon test (two-tailed **p < 0.01). c MiR-451a expression among FLT3-WT and FLT3-ITD AML patients of the TCGA cohort. Patients depicted were of normal karyotype. Significance was determined by Wilcoxon test (two-tailed *p < 0.05). d,e Transduction of U937 and 32D cells with FLT3-ITD led to significant decrease of miR-451a levels, measured by qPCR. (two-tailed t-test *p < 0.05; **p < 0.01). f MiR-451a levels of MV4;11 cells after 48 h treatment with FLT3 inhibitors quizartinib (black bars) and gilteritinib (gray bars). Both FLT3 inhibitors raised significantly miR-451a levels measured by qPCR. (two-tailed t-test *p < 0.05; **p < 0.01). g MiR-451a expression in umbilical cord blood (UCB) cells does not change upon 48 h treatment with quizartinib and gilteritinib. (two-tailed t-test; n.s. p > 0.05). All experiments were performed at least three times
Fig. 1 FLT3-ITD downregulates miR-451a. a NGS of bone marrow mononuclear cells from healthy donors and normal karyotype AML patients with FLT3-WT, FLT3-ITD or FLT3-TKD. Heatmap of the top 50 miRs differentially expressed in AML samples compared to healthy donors ranked by p-value. miR-451a exhibited the lowest p-value. b Median expression levels of miR-451a are lowest in FLT3-ITD+ AML samples. Significance was determined by Wilcoxon test (two-tailed **p < 0.01). c MiR-451a expression among FLT3-WT and FLT3-ITD AML patients of the TCGA cohort. Patients depicted were of normal karyotype. Significance was determined by Wilcoxon test (two-tailed *p < 0.05). d,e Transduction of U937 and 32D cells with FLT3-ITD led to significant decrease of miR-451a levels, measured by qPCR. (two-tailed t-test *p < 0.05; **p < 0.01). f MiR-451a levels of MV4;11 cells after 48 h treatment with FLT3 inhibitors quizartinib (black bars) and gilteritinib (gray bars). Both FLT3 inhibitors raised significantly miR-451a levels measured by qPCR. (two-tailed t-test *p < 0.05; **p < 0.01). g MiR-451a expression in umbilical cord blood (UCB) cells does not change upon 48 h treatment with quizartinib and gilteritinib. (two-tailed t-test; n.s. p > 0.05). All experiments were performed at least three timesCC BY · PubMed Central
Fig. 2 MiR-451a sensitizes FLT3-ITD+ cells to chemotherapy. a Stable transduction of U937 cells with FLT3-ITD and GFP. In comparison to the GFP control, transduced FLT3-ITD led to increased MDR1 levels in U937 cells (two-tailed t-test ***p < 0.001). b Western blot analysis revealed increased MDR1 protein levels in FLT3-ITD transduced U937 cells in comparison to GFP control (c) MV4;11 cells treated for 48 h with quizartinib and gilteritinib. Flow cytometric analysis exhibited decreased MDR1 protein levels (two-tailed t-test *p < 0.05; **p < 0.01). d Transient transfection of miR-451a resulted in enhanced sensitivity of MV4;11 cells toward cytarabine. Cell viability was measured by MTS-assay (two-tailed t-test *p < 0.05). e Annexin V levels of stable miR-451a-transduced MV4;11 parental cells after 48 h treatment. Flow cytometry revealed a significant increment of Annexin V+ cells in miR-451a transduced cells compared to the non-silencing control (NSC) (two-tailed t-test *p < 0.05). f MiR-451a abrogates treatment resistance of MV4;11-R cells. Resistant MV4;11 cells were stably transduced with miR-451a and treated for 48 h with quizartinib or gilteritinib. NSC non-silencing control (two-tailed t-test *p < 0.05; **p < 0.01). g MV4;11-R cells transduced with miR-451a showed decreased MDR1 levels compared to the NSC. All experiments were performed at least three times (two-tailed t-test *p < 0.05). h Western blot analysis revealed reduced MDR1 protein levels in miR-451a transduced MV4;11-R cells in comparison to NSC control. i Proposed scheme of the FLT3-ITD-MDR1-miR-451a axis
Fig. 2 MiR-451a sensitizes FLT3-ITD+ cells to chemotherapy. a Stable transduction of U937 cells with FLT3-ITD and GFP. In comparison to the GFP control, transduced FLT3-ITD led to increased MDR1 levels in U937 cells (two-tailed t-test ***p < 0.001). b Western blot analysis revealed increased MDR1 protein levels in FLT3-ITD transduced U937 cells in comparison to GFP control (c) MV4;11 cells treated for 48 h with quizartinib and gilteritinib. Flow cytometric analysis exhibited decreased MDR1 protein levels (two-tailed t-test *p < 0.05; **p < 0.01). d Transient transfection of miR-451a resulted in enhanced sensitivity of MV4;11 cells toward cytarabine. Cell viability was measured by MTS-assay (two-tailed t-test *p < 0.05). e Annexin V levels of stable miR-451a-transduced MV4;11 parental cells after 48 h treatment. Flow cytometry revealed a significant increment of Annexin V+ cells in miR-451a transduced cells compared to the non-silencing control (NSC) (two-tailed t-test *p < 0.05). f MiR-451a abrogates treatment resistance of MV4;11-R cells. Resistant MV4;11 cells were stably transduced with miR-451a and treated for 48 h with quizartinib or gilteritinib. NSC non-silencing control (two-tailed t-test *p < 0.05; **p < 0.01). g MV4;11-R cells transduced with miR-451a showed decreased MDR1 levels compared to the NSC. All experiments were performed at least three times (two-tailed t-test *p < 0.05). h Western blot analysis revealed reduced MDR1 protein levels in miR-451a transduced MV4;11-R cells in comparison to NSC control. i Proposed scheme of the FLT3-ITD-MDR1-miR-451a axisCC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 15 references

Cited by

See all 18

Metadata

Authors
Krakowsky, R. H. E., Wurm, A. A., Gerloff, D., Katzerke, C., Bräuer-Hartmann, D., Hartmann, J.-U., Wilke, F., Thiede, C., Müller-Tidow, C., Niederwieser, D., & Behre, G.
Venue
Blood Cancer Journal
Publisher
Springer Science and Business Media LLC
Published
2018-03-21
Volume
8
Issue
3
ISSN
2044-5385
DOI
10.1038/s41408-018-0070-y
PMC
PMC5862828
Cited by
18
References
15
Language
en
Licence

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: miR-451a abrogates treatment resistance in FLT3-ITD-positive acute myeloid leukemia. https://app.cochat.ai/papers/10.1038/s41408-018-0070-y
The paper
Krakowsky, R. H. E., Wurm, A. A., Gerloff, D., Katzerke, C., Bräuer-Hartmann, D., Hartmann, J.-U., Wilke, F., Thiede, C., Müller-Tidow, C., Niederwieser, D., & Behre, G. (2018). miR-451a abrogates treatment resistance in FLT3-ITD-positive acute myeloid leukemia. Blood Cancer Journal. https://doi.org/10.1038/s41408-018-0070-y

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.