Inflammation and cancer.
Journal: 2003/January - Nature
ISSN: 0028-0836
Abstract:
Recent data have expanded the concept that inflammation is a critical component of tumour progression. Many cancers arise from sites of infection, chronic irritation and inflammation. It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration. In addition, tumour cells have co-opted some of the signalling molecules of the innate immune system, such as selectins, chemokines and their receptors for invasion, migration and metastasis. These insights are fostering new anti-inflammatory therapeutic approaches to cancer development.
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Nature 420(6917): 860-867

Inflammation and cancer

Cancer Research Institute, University of California, San Francisco, California 94143 USA
Department of Pathology, University of California, San Francisco, California 94143 USA
Department of Anatomy, University of California, San Francisco, California 94143 USA
UCSF Comprehensive Cancer Center, University of California, San Francisco, California 94143 USA
Lisa M. Coussens: ude.fscu.cc@snessuoc; Zena Werb: ude.fscu.asti@anez
Lisa M. Coussens: ude.fscu.cc@snessuoc; Zena Werb: ude.fscu.asti@anez

Abstract

Recent data have expanded the concept that inflammation is a critical component of tumour progression. Many cancers arise from sites of infection, chronic irritation and inflammation. It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration. In addition, tumour cells have co-opted some of the signalling molecules of the innate immune system, such as selectins, chemokines and their receptors for invasion, migration and metastasis. These insights are fostering new anti-inflammatory therapeutic approaches to cancer development.

Abstract

The functional relationship between inflammation and cancer is not new. In 1863, Virchow hypothesized that the origin of cancer was at sites of chronic inflammation, in part based on his hypothesis that some classes of irritants, together with the tissue injury and ensuing inflammation they cause, enhance cell proliferation1. Although it is now clear that proliferation of cells alone does not cause cancer, sustained cell proliferation in an environment rich in inflammatory cells, growth factors, activated stroma, and DNA-damage-promoting agents, certainly potentiates and/or promotes neoplastic risk. During tissue injury associated with wounding, cell proliferation is enhanced while the tissue regenerates; proliferation and inflammation subside after the assaulting agent is removed or the repair completed. In contrast, proliferating cells that sustain DNA damage and/or mutagenic assault (for example, initiated cells) continue to proliferate in microenvironments rich in inflammatory cells and growth/survival factors that support their growth. In a sense, tumours act as wounds that fail to heal2.

Today, the causal relationship between inflammation, innate immunity and cancer is more widely accepted; however, many of the molecular and cellular mechanisms mediating this relationship remain unresolved — these are the focus of this review. Furthermore, tumour cells may usurp key mechanisms by which inflammation interfaces with cancers, to further their colonization of the host. Although the acquired immune response to cancer is intimately related to the inflammatory response, this topic is beyond the scope of this article, but readers are referred to several excellent reviews34.

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