title: Soluble mediators of inflammation during tumor development.
abstract: Tissues maintain homeostasis by monitoring and responding to varied physical interactions between cells and their microenvironment. In situations where acute tissue damage occurs, such as wounding, pathogenic assault, or toxic exposure, regulatory circuits that monitor tissue homeostasis are rapidly engaged to initiate tissue repair by regulating cell polarity, proliferation and death, matrix metabolism, inflammation, and vascular and lymphatic function. The critical feature of regulating these acute responses is the innate ability to discriminate between homeostatic versus damaged tissue states and engage or disengage regulatory machinery as appropriate; thus, a major distinction between acute versus chronic disease is the altered ability to appropriately activate and?or inactivate reparative regulatory programs. Since cancer is a chronic disease characterized by altered cell polarity, enhanced cell survival, inflammation, increased matrix metabolism, and enhanced vascular and lymphatic function, considerable attention is now focused on understanding the cellular and molecular mechanisms regulating these responsive pathways. Since chemoattractant cytokines are important mediators of leukocyte recruitment following acute tissue stress, and demonstrate altered characteristics of expression and activation in chronically inflamed tissue, they have been implicated as key regulators of inflammation and angiogenesis during cancer development. This chapter focuses on the clinical and experimental data implicating proinflammatory cytokines and chemokines as important potentiators of carcinogenesis.
authors.affiliation: Cancer Research Institute, University of California, San Francisco, 94143, USA.
authors.forename: Stephen C
authors.initials: SC
authors.lastname: Robinson
authors.forename: Lisa M
authors.initials: LM
authors.lastname: Coussens
mesh_terms: D002450:Cell Communication / Q000502:physiology; D016207:Cytokines / Q000276:immunology*; D007249:Inflammation / Q000276:immunology*; D009369:Neoplasms / Q000276:immunology*; D009389:Neovascularization, Pathologic / Q000276:immunology; D020556:Neutrophil Infiltration / Q000276:immunology; D015398:Signal Transduction / Q000276:immunology*
chemical_list: D016207:Cytokines