Journal of Leukocyte Biology
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A more recent version of this article appeared on October 1, 2006

Published online before print July 24, 2006
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1105646

Received for publication November 10, 2005.
Revised June 22, 2006.
Accepted for publication June 26, 2006.

Article

Tumor growth or regression: powered by inflammation

Delia Nelson * and Ruth Ganss {dagger}@

*School of Biomedical Sciences, Curtin University, Western Australia; and {dagger}Centre for Medical Research, Western Australian Institute for Medical Research, University of Western Australia

@ To whom correspondence should be addressed. E-mail: ganss{at}waimr.uwa.edu.au.


  Abstract

Malignant cells thrive in a highly specialized, stromal environment, which harbors support cells, blood vessels, and diverse leukocyte populations. There is increasing evidence that "by default", intratumoral inflammation fosters angiogenic and vasculogenic processes and simultaneously creates an immunosuppressive micromilieu. This self-amplifying loop of proangiogenic inflammation represents a serious obstacle for adaptive anticancer immune responses. However, angiogenesis is a highly dynamic process, which can be reversed in the "right" inflammatory context; this in turn facilitates immune effector cell entry and tumor rejection. Thus, we propose that a shift from proangiogenic to antiangiogenic inflammation creates a tumor environment permissive for immune destruction. This is a new concept, which integrates antiangiogenic and immune therapeutic treatment modalities.

Key Words: multistep tumorigenesis • angiogenesis • stroma • chemokines • stem cells




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