Chemokine-Based Pathogenetic Mechanisms in Cancer

  1. Derek J. Chadwick Organizer,
  2. Jamie A. Goode
  1. Ilaria Conti1,2,
  2. Christine Dube1,2,
  3. Barrett J. Rollins1,2,*

Published Online: 7 OCT 2008

DOI: 10.1002/0470856734.ch3

Cancer and Inflammation: Novartis Foundation Symposium 256

Cancer and Inflammation: Novartis Foundation Symposium 256

How to Cite

Conti, I., Dube, C. and Rollins, B. J. (2008) Chemokine-Based Pathogenetic Mechanisms in Cancer, in Cancer and Inflammation: Novartis Foundation Symposium 256 (eds D. J. Chadwick and J. A. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/0470856734.ch3

Author Information

  1. 1

    Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA

  2. 2

    Department of Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, MA, USA

*Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA

Publication History

  1. Published Online: 7 OCT 2008
  2. Published Print: 23 JAN 2004

Book Series:

  1. Novartis Foundation Symposia

Book Series Editors:

  1. Novartis Foundation

ISBN Information

Print ISBN: 9780470855102

Online ISBN: 9780470856734

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Summary

The chemokine system has evolved primarily to control the trafficking of leukocytes during immune or inflammatory responses. However, through their expression of chemokine ligands and receptors, cancers have commandeered various aspects of this host defence system in order to enhance their growth. Although engineered over-expression of some tumour-derived chemokines can stimulate host antitumour responses, this is unlikely to be the reason that tumour cells express them. Rather, a growing body of clinical and laboratory evidence indicates that cancer cells may secrete chemokines in order to attract host cells that supply the tumours with growth and angiogenic factors. In addition, chemokine receptor expression by tumour cells may permit them to use the host's pre-existing leukocyte trafficking system to invade target tissues during metastatic spread. Together, these observations suggest that therapies directed against chemokine ligands or receptors may be beneficial in cancer.