Macrophage–tumor crosstalk: role of TAMR tyrosine kinase receptors and of their ligands View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2012-05

AUTHORS

Thomas Schmidt, Isabel Ben-Batalla, Alexander Schultze, Sonja Loges

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. More... »

PAGES

1391-1414

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s00018-011-0863-7

    DOI

    http://dx.doi.org/10.1007/s00018-011-0863-7

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1021124349

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/22076650


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