11. Inflammation as a Niche for Tumor Progression

  1. Yusuke Hiraku1,
  2. Shosuke Kawanishi2 and
  3. Hiroshi Ohshima3
  1. Futoshi Okada

Published Online: 4 APR 2014

DOI: 10.1002/9781118826621.ch11

Cancer and Inflammation Mechanisms: Chemical, Biological, and Clinical Aspects

Cancer and Inflammation Mechanisms: Chemical, Biological, and Clinical Aspects

How to Cite

Okada, F. (2014) Inflammation as a Niche for Tumor Progression, in Cancer and Inflammation Mechanisms: Chemical, Biological, and Clinical Aspects (eds Y. Hiraku, S. Kawanishi and H. Ohshima), John Wiley & Sons, Inc., Hoboken, NJ, USA. doi: 10.1002/9781118826621.ch11

Editor Information

  1. 1

    Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, Tsu, Mie, Japan

  2. 2

    Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, Suzuka, Mie, Japan

  3. 3

    Department of Nutritional and Environmental Sciences, Graduate School of Integrated Pharmaceutical and Nutritional Sciences, University of Shizuoka, Shizuoka, Japan

Publication History

  1. Published Online: 4 APR 2014
  2. Published Print: 4 APR 2014

ISBN Information

Print ISBN: 9781118160305

Online ISBN: 9781118826621



  • animal model;
  • chronic inflammation;
  • inflammation-based tumor progression;
  • inflammation-related carcinogenesis;
  • inflammatory cell–derived factors


Inflammation acts as a key regulator of tumor progression by aberrant mechanisms such as increased mutagenicity, accelerated DNA replication and cell proliferation, disruption of cell death machinery, enhanced angiogenesis, suppression of antitumor immunity, acquired resistance to chemo- or radiation therapy, and invasive and metastatic abilities. Fibroblasts, myofibroblasts, endothelial cells, pericytes, and inflammatory cells create an environment in which inflammatory cells accumulate, soluble factors are secreted, and tissues called sustentacula are provided; all of them support tumor progression. Fibroblasts present in tumor tissues are designated as cancer-associated fibroblasts (CAFs). In an inflammatory environment, inflammatory cytokines, growth factors, chemokines, ROS, NO, reactive aldehydes, arachidonic acid metabolites, proteases, adhesion molecules, and so on, are induced; they accelerate the entire carcinogenic process. The authors, in this chapter, describe a unique animal model they developed in which progression of benign mouse regressive tumor cells can be observed consistently under concomitant inflammation.