title: Review. TNF/VEGF cross-talk in chronic inflammation-related cancer initiation and progression: an early target in anticancer therapeutic strategy.
abstract: In the last decade a growing body of epidemiological and clinical data has emerged to support the concept that longstanding inflammation potentiates or promotes tumor development, growth and progression. Among pro-inflammatory gene products involved in such interactions are tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and vascular endothelial growth factors (VEGFs), whose expression is mainly regulated by the transcription nuclear factor (NF)-kappaB. Clinically, several reports have detected abnormally high levels of circulating cytokines in cancer patients, and inflammation is currently being investigated as a target of anticancer therapies. To date three main groups of antiangiogenic drugs approved for clinical use and experimentation can be identified: secreted VEGF inhibitors, tyrosine kinase (TK) inhibitors (mainly VEGFR inhibitors) and drugs that inhibit angiogenesis with a complex mechanism. More recently, TNF-alpha antagonists have become available. The first clinical data on anti-TNF-alpha showed that this drug can be used in cancer patients without major sideeffects. Further investigations are needed to understand if anti-TNF-alpha or NF-kappaB inhibitors may really represent a novel approach in cancer treatment, probably as adjuvant to other therapies, such as anti-angiogenic or cytotoxic agents.
authors: Department of Laboratory Medicine and Advanced Biotechnologies, IRCCS San Raffaele Pisana, Via della Pisana 235, 00163 Rome.
authors: Fiorella
authors: F
authors: Guadagni
authors: Patrizia
authors: P
authors: Ferroni
authors: Raffaele
authors: R
authors: Palmirotta
authors: Ilaria
authors: I
authors: Portarena
authors: Vincenzo
authors: V
authors: Formica
authors: Mario
authors: M
authors: Roselli
mesh_terms: D000970:Antineoplastic Agents / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D002468:Cell Physiological Phenomena; D002470:Cell Survival / Q000187:drug effects; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D008954:Models, Biological; D009369:Neoplasms / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D009389:Neovascularization, Pathologic / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*; D042461:Vascular Endothelial Growth Factor A / Q000502:physiology*
chemical_list: D000970:Antineoplastic Agents; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A