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Originally published online as doi:10.1189/jlb.1105646 on July 24, 2006

Published online before print July 24, 2006
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(Journal of Leukocyte Biology. 2006;80:685-690.)
© 2006 by Society for Leukocyte Biology

Tumor growth or regression: powered by inflammation

Delia Nelson* and Ruth Ganss{dagger},1

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

1 Correspondence: Western Australian Institute for Medical Research (WAIMR), Rear, 50 Murray Street, Perth WA 6000, Australia. 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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