Macrophage-tumor crosstalk: role of TAMR tyrosine kinase receptors and of their ligands.

Standard

Macrophage-tumor crosstalk: role of TAMR tyrosine kinase receptors and of their ligands. / Schmidt, Thomas; Ben-Batalla, Isabella; Schultze, Alexander; Loges, Sonja.

in: CELL MOL LIFE SCI, Jahrgang 69, Nr. 9, 9, 2012, S. 1391-1414.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

APA

Vancouver

Bibtex

@article{600a00bd07494e59978a59b730acae5e,
title = "Macrophage-tumor crosstalk: role of TAMR tyrosine kinase receptors and of their ligands.",
abstract = "Ample clinical and preclinical evidence indicates that macrophages interact with tumor cells as well as with virtually all populations of host cells present in the tumor microenvironment. This crosstalk can strongly promote malignancy, but also has in principle the potential to inhibit tumor growth. Thus, it is of the utmost importance to improve our understanding of the mechanisms driving the pro- and antimalignant behavior of tumor-associated macrophages (TAMs) in order to develop better anticancer therapies. In this review, we discuss the biological consequences of reciprocal interactions between TAMs, cancer cells, endothelial cells, fibroblasts and other leukocyte subfractions within tumors. It was recently elucidated that tumors specifically educate macrophages to secrete growth arrest-specific gene 6 (Gas6), the common ligand of the Tyro3, Axl, Mer receptor (TAMR) family. In turn, Gas6 fosters tumor growth by promoting cancer cell proliferation. Therefore, the Gas6-TAMR axis might represent a novel target for disrupting tumor-macrophage crosstalk. We summarize here what is known about TAMR and their ligands in (human) cancer biology. In order to shed more light on the role of macrophages in human cancer, we additionally provide an overview of what is currently known about the prognostic impact of TAMs in human cancer.",
author = "Thomas Schmidt and Isabella Ben-Batalla and Alexander Schultze and Sonja Loges",
year = "2012",
language = "English",
volume = "69",
pages = "1391--1414",
journal = "CELL MOL LIFE SCI",
issn = "1420-682X",
publisher = "Birkhauser Verlag Basel",
number = "9",

}

RIS

TY - JOUR

T1 - Macrophage-tumor crosstalk: role of TAMR tyrosine kinase receptors and of their ligands.

AU - Schmidt, Thomas

AU - Ben-Batalla, Isabella

AU - Schultze, Alexander

AU - Loges, Sonja

PY - 2012

Y1 - 2012

N2 - Ample clinical and preclinical evidence indicates that macrophages interact with tumor cells as well as with virtually all populations of host cells present in the tumor microenvironment. This crosstalk can strongly promote malignancy, but also has in principle the potential to inhibit tumor growth. Thus, it is of the utmost importance to improve our understanding of the mechanisms driving the pro- and antimalignant behavior of tumor-associated macrophages (TAMs) in order to develop better anticancer therapies. In this review, we discuss the biological consequences of reciprocal interactions between TAMs, cancer cells, endothelial cells, fibroblasts and other leukocyte subfractions within tumors. It was recently elucidated that tumors specifically educate macrophages to secrete growth arrest-specific gene 6 (Gas6), the common ligand of the Tyro3, Axl, Mer receptor (TAMR) family. In turn, Gas6 fosters tumor growth by promoting cancer cell proliferation. Therefore, the Gas6-TAMR axis might represent a novel target for disrupting tumor-macrophage crosstalk. We summarize here what is known about TAMR and their ligands in (human) cancer biology. In order to shed more light on the role of macrophages in human cancer, we additionally provide an overview of what is currently known about the prognostic impact of TAMs in human cancer.

AB - Ample clinical and preclinical evidence indicates that macrophages interact with tumor cells as well as with virtually all populations of host cells present in the tumor microenvironment. This crosstalk can strongly promote malignancy, but also has in principle the potential to inhibit tumor growth. Thus, it is of the utmost importance to improve our understanding of the mechanisms driving the pro- and antimalignant behavior of tumor-associated macrophages (TAMs) in order to develop better anticancer therapies. In this review, we discuss the biological consequences of reciprocal interactions between TAMs, cancer cells, endothelial cells, fibroblasts and other leukocyte subfractions within tumors. It was recently elucidated that tumors specifically educate macrophages to secrete growth arrest-specific gene 6 (Gas6), the common ligand of the Tyro3, Axl, Mer receptor (TAMR) family. In turn, Gas6 fosters tumor growth by promoting cancer cell proliferation. Therefore, the Gas6-TAMR axis might represent a novel target for disrupting tumor-macrophage crosstalk. We summarize here what is known about TAMR and their ligands in (human) cancer biology. In order to shed more light on the role of macrophages in human cancer, we additionally provide an overview of what is currently known about the prognostic impact of TAMs in human cancer.

M3 - SCORING: Journal article

VL - 69

SP - 1391

EP - 1414

JO - CELL MOL LIFE SCI

JF - CELL MOL LIFE SCI

SN - 1420-682X

IS - 9

M1 - 9

ER -