Biochemia Medica, Vol. 21 No. 3, 2011.
Other
Molecular pathways in cancer-related inflammation
Annalisa Dep Prete
orcid.org/0000-0002-3738-412X
; Istituto Clinico Humanitas IRCCS, Via Manzoni 56, 20089 Rozzano, Milan, Italy; Department of Basic Medical Sciences, University of Bari, Bari, Italy
Paola Allavena
; Istituto Clinico Humanitas IRCCS, Via Manzoni 56, 20089 Rozzano, Milan, Italy
Giuseppe Santoro
; Department of Biomedical Sciences and Human Oncology, University of Bari, Bari, Italy
Ruggiero Fumarulo
; Department of Biomedical Sciences and Human Oncology, University of Bari, Bari, Italy
Massimiliano M. Corsi
; Department of Human Morphology and Biomedical Sciences “Città Studi”, University of Milan, and Soc. Clinical Pathology and IRCCS Policlinico San Donato, Milan, Italy
Alberto Mantovani
; Istituto Clinico Humanitas IRCCS, Via Manzoni 56, 20089 Rozzano, Milan, Italy; Department of Translational Medicine, University of Milan, Milan, Italy
Abstract
Accumulating evidence shows that chronic inflammation is associated to increased risk of cancer. An inflammatory component is present also in the microenvironment of tumours epidemiologically unre-lated to inflammation. Extensive investigations over the past decade have uncovered many of the important mechanistic pathways underlying cancer-related inflammation. Pathways linking inflamma-tion and cancer have been identified: an intrinsic one (driven by genetic events that cause neoplasia) and an extrinsic one (driven by inflammatory conditions which predispose to cancer). Smouldering inflammation is a component of the tumour microenvironment and is a recognized hallmark of cancer. Key orchestrators at the intersection of the intrinsic and extrinsic pathways include transcription fac-tors (e.g. Nuclear Factor kappa-B, NFκB) that modulate the inflammatory response through soluble mediators (cytokines, chemokines) and cellular components (e.g. tumor-associated macrophages), promoting tumorigenesis. NFκB aids in the proliferation and survival of malignant cells, promotes an-giogenesis and metastasis, subverts adaptive immunity, and alters responses to hormones and che-motherapeutic agents. Emerging evidence also suggests that persistent inflammation promotes ge-netic instability. Thus, cancer-related inflammation represents a target for innovative diagnostic and therapeutic strategies.
Keywords
cancer-related inflammation; cytokines; chemokines; macrophages
Hrčak ID:
72947
URI
Publication date:
15.10.2011.
Visits: 3.217 *