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Axl inhibition: a potential road to a novel acute myeloid leukemia therapy?

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Axl inhibition: a potential road to a novel acute myeloid leukemia therapy? / Janning, Melanie; Ben-Batalla, Isabel; Loges, Sonja.

In: EXPERT REV HEMATOL, Vol. 8, No. 2, 01.04.2015, p. 135-8.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Janning, M, Ben-Batalla, I & Loges, S 2015, 'Axl inhibition: a potential road to a novel acute myeloid leukemia therapy?', EXPERT REV HEMATOL, vol. 8, no. 2, pp. 135-8. https://doi.org/10.1586/17474086.2015.997704

APA

Janning, M., Ben-Batalla, I., & Loges, S. (2015). Axl inhibition: a potential road to a novel acute myeloid leukemia therapy? EXPERT REV HEMATOL, 8(2), 135-8. https://doi.org/10.1586/17474086.2015.997704

Vancouver

Janning M, Ben-Batalla I, Loges S. Axl inhibition: a potential road to a novel acute myeloid leukemia therapy? EXPERT REV HEMATOL. 2015 Apr 1;8(2):135-8. https://doi.org/10.1586/17474086.2015.997704

Bibtex

@article{0a7193c6dd3e433bbaf91fcfd0328ab7,
title = "Axl inhibition: a potential road to a novel acute myeloid leukemia therapy?",
abstract = "Novel treatment options in acute myeloid leukemia (AML) are urgently needed; treatment has not changed significantly over the past decades and survival is still dismal, especially in elderly patients. Axl, a member of the Tyro3, Axl, Mer (TAM) receptor family, mediates proliferation and survival of AML cells and is upregulated upon cytostatic treatment. In addition, AML cells induce expression of the Axl ligand growth arrest-specific gene 6 (Gas6) in bone marrow stroma cells, which further amplifies their growth and therapy resistance. Interruption of Axl signaling by pharmacological approaches, including the small molecule Axl inhibitor BGB324, decreased disease burden and prolonged survival of AML mice. The Gas6-Axl pathway has translational relevance because Axl is expressed by approximately 50% of AML patients and Axl-targeting approaches can block growth of primary human AML cells. Thus, Axl represents a potential novel target in AML and BGB324 is now in clinical development.",
author = "Melanie Janning and Isabel Ben-Batalla and Sonja Loges",
year = "2015",
month = apr,
day = "1",
doi = "10.1586/17474086.2015.997704",
language = "English",
volume = "8",
pages = "135--8",
journal = "EXPERT REV HEMATOL",
issn = "1747-4086",
publisher = "Expert Reviews Ltd.",
number = "2",

}

RIS

TY - JOUR

T1 - Axl inhibition: a potential road to a novel acute myeloid leukemia therapy?

AU - Janning, Melanie

AU - Ben-Batalla, Isabel

AU - Loges, Sonja

PY - 2015/4/1

Y1 - 2015/4/1

N2 - Novel treatment options in acute myeloid leukemia (AML) are urgently needed; treatment has not changed significantly over the past decades and survival is still dismal, especially in elderly patients. Axl, a member of the Tyro3, Axl, Mer (TAM) receptor family, mediates proliferation and survival of AML cells and is upregulated upon cytostatic treatment. In addition, AML cells induce expression of the Axl ligand growth arrest-specific gene 6 (Gas6) in bone marrow stroma cells, which further amplifies their growth and therapy resistance. Interruption of Axl signaling by pharmacological approaches, including the small molecule Axl inhibitor BGB324, decreased disease burden and prolonged survival of AML mice. The Gas6-Axl pathway has translational relevance because Axl is expressed by approximately 50% of AML patients and Axl-targeting approaches can block growth of primary human AML cells. Thus, Axl represents a potential novel target in AML and BGB324 is now in clinical development.

AB - Novel treatment options in acute myeloid leukemia (AML) are urgently needed; treatment has not changed significantly over the past decades and survival is still dismal, especially in elderly patients. Axl, a member of the Tyro3, Axl, Mer (TAM) receptor family, mediates proliferation and survival of AML cells and is upregulated upon cytostatic treatment. In addition, AML cells induce expression of the Axl ligand growth arrest-specific gene 6 (Gas6) in bone marrow stroma cells, which further amplifies their growth and therapy resistance. Interruption of Axl signaling by pharmacological approaches, including the small molecule Axl inhibitor BGB324, decreased disease burden and prolonged survival of AML mice. The Gas6-Axl pathway has translational relevance because Axl is expressed by approximately 50% of AML patients and Axl-targeting approaches can block growth of primary human AML cells. Thus, Axl represents a potential novel target in AML and BGB324 is now in clinical development.

U2 - 10.1586/17474086.2015.997704

DO - 10.1586/17474086.2015.997704

M3 - SCORING: Journal article

C2 - 25578023

VL - 8

SP - 135

EP - 138

JO - EXPERT REV HEMATOL

JF - EXPERT REV HEMATOL

SN - 1747-4086

IS - 2

ER -