Heat-shock proteins in infection-mediated inflammation-induced tumorigenesis.
Inflammation is a necessary albeit insufficient component of tumorigenesis in some cancers. Infectious agents directly implicated in tumorigenesis have been shown to induce inflammation. This process involves both the innate and adaptive components of the immune system which contribute to tumor angiogenesis, tumor tolerance and metastatic properties of neoplasms. Recently, heat-shock proteins have been identified as mediators of this inflammatory process and thus may provide a link between infection-mediated inflammation and subsequent cancer development. In this review, the role of heat-shock proteins in infection-induced inflammation and carcinogenesis will be discussed.
Goldstein
Mark G
MG
University of Connecticut, 263 Farmington Avenue, Farmington, CT 06030, USA. mark.goldstein@comcast.net
Li
Zihai
Z
D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D006360:Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D007239:Infections / Q000150:complications* / Q000235:genetics / Q000378:metabolism; D007249:Inflammation / Q000150:complications* / Q000209:etiology / Q000235:genetics / Q000378:metabolism; D008954:Models, Biological; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000209:etiology / Q000235:genetics / Q000276:immunology / Q000473:pathology; D019139:Tumor Escape / Q000235:genetics / Q000502:physiology
D006360:Heat-Shock Proteins