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 Blood, 2 April 2009, Vol. 113, No. 14, pp. 3139-3146.
Prepublished online as a Blood First Edition Paper on January 26, 2009; DOI 10.1182/blood-2008-12-172825.

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REVIEW ARTICLE

Regulation of macrophage function in tumors: the multifaceted role of NF-{kappa}B

Thorsten Hagemann1,*, Subhra K. Biswas2,*, Toby Lawrence1,*, Antonio Sica3,*, and Claire E. Lewis4,*

1 Centre for Cancer and Inflammation, Institute of Cancer, Barts and the London School of Medicine and Dentistry, London, United Kingdom; 2 Laboratory of Human Innate Immunity, Singapore Immunology Network, Biomedical Sciences Institutes, Agency for Science, Technology & Research, Singapore; 3 Istituto Clinico Humanitas, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Milan, and DiSCAFF, University of Piemonte Orientale A Avogadro, Novara, Italy; and 4 Academic Unit of Pathology, University of Sheffield Medical School, Sheffield, United Kingdom

The pivotal role of tumor-associated macrophages (TAMs) in tumor progression is now well established. TAMs have been shown to influence multiple steps in tumor development including the growth, survival, invasion, and metastasis of tumor cells as well as angiogenesis and lymphangiogenesis in tumors. The molecular circuits that polarize TAMs toward such a protumoral phenotype are now the focus of intense investigation. The transcription factor, nuclear factor–{kappa}B (NF-{kappa}B), is a master regulator of many cellular processes and been shown to regulate various pathways that impact on the function of TAMs. Much evidence for this has come from the use of elegant transgenic murine tumor models in which modification of single components of the NF-{kappa}B signaling pathway has been shown to regulate the pro-tumor repertoire of TAMs. Here, we outline this evidence and attempt to reconcile the various views that have emerged recently over the exact role of NF-{kappa}B in this phenomenon.


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