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The BET bromodomain inhibitor ZEN-3365 targets the Hedgehog signaling pathway in acute myeloid leukemia

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The BET bromodomain inhibitor ZEN-3365 targets the Hedgehog signaling pathway in acute myeloid leukemia. / Wellbrock, Jasmin; Behrmann, Lena; Muschhammer, Jana; Modemann, Franziska; Khoury, Kais; Brauneck, Franziska; Bokemeyer, Carsten; Campeau, Eric; Fiedler, Walter.

in: ANN HEMATOL, Jahrgang 100, Nr. 12, 12.2021, S. 2933-2941.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Wellbrock, J, Behrmann, L, Muschhammer, J, Modemann, F, Khoury, K, Brauneck, F, Bokemeyer, C, Campeau, E & Fiedler, W 2021, 'The BET bromodomain inhibitor ZEN-3365 targets the Hedgehog signaling pathway in acute myeloid leukemia', ANN HEMATOL, Jg. 100, Nr. 12, S. 2933-2941. https://doi.org/10.1007/s00277-021-04602-z

APA

Wellbrock, J., Behrmann, L., Muschhammer, J., Modemann, F., Khoury, K., Brauneck, F., Bokemeyer, C., Campeau, E., & Fiedler, W. (2021). The BET bromodomain inhibitor ZEN-3365 targets the Hedgehog signaling pathway in acute myeloid leukemia. ANN HEMATOL, 100(12), 2933-2941. https://doi.org/10.1007/s00277-021-04602-z

Vancouver

Wellbrock J, Behrmann L, Muschhammer J, Modemann F, Khoury K, Brauneck F et al. The BET bromodomain inhibitor ZEN-3365 targets the Hedgehog signaling pathway in acute myeloid leukemia. ANN HEMATOL. 2021 Dez;100(12):2933-2941. https://doi.org/10.1007/s00277-021-04602-z

Bibtex

@article{74f7f56ec42346e28236d3c0609ff9d5,
title = "The BET bromodomain inhibitor ZEN-3365 targets the Hedgehog signaling pathway in acute myeloid leukemia",
abstract = "Modern cancer therapies increased the survival rates of acute myeloid leukemia (AML) patients tremendously. However, the complexity of the disease and the identification of new targets require the adaptation of treatment protocols to reduce side effects and increase benefit for the patients. One key regulator of leukemogenesis and chemotherapy resistance in AML is the Hedgehog (HH) signaling pathway. It is deregulated in numerous cancer entities and inhibition of its downstream transcription factors GLI translates into anti-leukemic effects. One major regulator of GLI is BRD4, a BET family member with epigenetic functions. We investigated the effect of ZEN-3365, a novel BRD4 inhibitor, on AML cells in regard to the HH pathway. We show that ZEN-3365 alone or in combination with GANT-61 reduced GLI promoter activity, cell proliferation and colony formation in AML cell lines and primary cells. Our findings strongly support the evaluation of the BRD4 inhibitor ZEN-3365 as a new therapeutic option in AML.",
author = "Jasmin Wellbrock and Lena Behrmann and Jana Muschhammer and Franziska Modemann and Kais Khoury and Franziska Brauneck and Carsten Bokemeyer and Eric Campeau and Walter Fiedler",
note = "{\textcopyright} 2021. The Author(s).",
year = "2021",
month = dec,
doi = "10.1007/s00277-021-04602-z",
language = "English",
volume = "100",
pages = "2933--2941",
journal = "ANN HEMATOL",
issn = "0939-5555",
publisher = "Springer",
number = "12",

}

RIS

TY - JOUR

T1 - The BET bromodomain inhibitor ZEN-3365 targets the Hedgehog signaling pathway in acute myeloid leukemia

AU - Wellbrock, Jasmin

AU - Behrmann, Lena

AU - Muschhammer, Jana

AU - Modemann, Franziska

AU - Khoury, Kais

AU - Brauneck, Franziska

AU - Bokemeyer, Carsten

AU - Campeau, Eric

AU - Fiedler, Walter

N1 - © 2021. The Author(s).

PY - 2021/12

Y1 - 2021/12

N2 - Modern cancer therapies increased the survival rates of acute myeloid leukemia (AML) patients tremendously. However, the complexity of the disease and the identification of new targets require the adaptation of treatment protocols to reduce side effects and increase benefit for the patients. One key regulator of leukemogenesis and chemotherapy resistance in AML is the Hedgehog (HH) signaling pathway. It is deregulated in numerous cancer entities and inhibition of its downstream transcription factors GLI translates into anti-leukemic effects. One major regulator of GLI is BRD4, a BET family member with epigenetic functions. We investigated the effect of ZEN-3365, a novel BRD4 inhibitor, on AML cells in regard to the HH pathway. We show that ZEN-3365 alone or in combination with GANT-61 reduced GLI promoter activity, cell proliferation and colony formation in AML cell lines and primary cells. Our findings strongly support the evaluation of the BRD4 inhibitor ZEN-3365 as a new therapeutic option in AML.

AB - Modern cancer therapies increased the survival rates of acute myeloid leukemia (AML) patients tremendously. However, the complexity of the disease and the identification of new targets require the adaptation of treatment protocols to reduce side effects and increase benefit for the patients. One key regulator of leukemogenesis and chemotherapy resistance in AML is the Hedgehog (HH) signaling pathway. It is deregulated in numerous cancer entities and inhibition of its downstream transcription factors GLI translates into anti-leukemic effects. One major regulator of GLI is BRD4, a BET family member with epigenetic functions. We investigated the effect of ZEN-3365, a novel BRD4 inhibitor, on AML cells in regard to the HH pathway. We show that ZEN-3365 alone or in combination with GANT-61 reduced GLI promoter activity, cell proliferation and colony formation in AML cell lines and primary cells. Our findings strongly support the evaluation of the BRD4 inhibitor ZEN-3365 as a new therapeutic option in AML.

U2 - 10.1007/s00277-021-04602-z

DO - 10.1007/s00277-021-04602-z

M3 - SCORING: Journal article

C2 - 34333666

VL - 100

SP - 2933

EP - 2941

JO - ANN HEMATOL

JF - ANN HEMATOL

SN - 0939-5555

IS - 12

ER -