title: Tumor growth or regression: powered by inflammation.
abstract: Malignant cells thrive in a highly specialized, stromal environment, which harbors support cells, blood vessels, and diverse leukocyte populations. There is increasing evidence that "by default", intratumoral inflammation fosters angiogenic and vasculogenic processes and simultaneously creates an immunosuppressive micromilieu. This self-amplifying loop of proangiogenic inflammation represents a serious obstacle for adaptive anticancer immune responses. However, angiogenesis is a highly dynamic process, which can be reversed in the "right" inflammatory context; this in turn facilitates immune effector cell entry and tumor rejection. Thus, we propose that a shift from proangiogenic to antiangiogenic inflammation creates a tumor environment permissive for immune destruction. This is a new concept, which integrates antiangiogenic and immune therapeutic treatment modalities.
authors.affiliation: School of Biomedical Sciences, Curtin University, Sydney, Western Australia, Australia.
authors.forename: Delia
authors.initials: D
authors.lastname: Nelson
authors.forename: Ruth
authors.initials: R
authors.lastname: Ganss
mesh_terms: D000818:Animals; D006801:Humans; D007249:Inflammation; D008954:Models, Biological; D009369:Neoplasms / Q000276:immunology* / Q000473:pathology / Q000628:therapy; D009389:Neovascularization, Pathologic / Q000276:immunology