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Inflammatory colonic carcinogenesis: A review on pathogenesis and immunosurveillance mechanisms in ulcerative colitis

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World Journal of Gastroenterology 2014年第22期20卷 6774-6785页

作者： Marco Scarpa Ignazio Castagliuolo Carlo Castoro Anna Pozza Melania Scarpa andromachi kotsafti Imerio Angriman Surgical Oncology Unit Veneto Institute of Oncology (IOV-IRCCS)35128 PadovaItaly Department of Molecular Medicine University of Padova35128 PadovaItaly Department of Surgery Gastroenterology and OncologyUniversity of Padova35128 PadovaItaly

Ulcerative colitis(UC)is characterized by repeated flare-ups of inflammation that can lead to oncogenic insults to the colonic ***-associated carcinogenesis presents a different sequence of tumorigenic events compared to those that contribute to the development of sporadic colorectal *** fact,in UC,the early events are represented by oxidative DNA damage and DNA methylation that can produce an inhibition of oncosuppressor genes,mutation of p53,aneuploidy,and microsatellite *** of tumor suppressor and DNA mismatch repair gene promoter regions is an epigenetic mechanism of gene silencing that contribute to tumorigenesis and may represent the first step in inflammatory ***,p53 is frequently mutated in the early stages of UC-associated *** is an independentrisk factor for forthcoming carcinogenesis in *** cell-T-cell cross-talk mediated by CD80 is a key factor in controlling the progression from low to high grade dysplasia in UC-associated carcinogenesis.

关键词： Colorectal cancer Ulcerative colitis Carcinogenesis Immune surveillance

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Oxidative damage in the progression of chronic liver disease to hepatocellular carcinoma:An intricate pathway

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World Journal of Gastroenterology 2014年第12期20卷 3078-3086页

作者： Romilda Cardin Marika Piciocchi Marina Bortolami andromachi kotsafti Luisa Barzon Enrico Lavezzo Alessandro Sinigaglia Kryssia Isabel Rodriguez-Castro Massimo Rugge Fabio Farinati Department of Surgery Oncology and GastroenterologyUniversity of Padova Department of Molecular Medicine University of Padova Department of Medicine University of Padova

The histo-pathologic and molecular mechanisms leading to initiation and progression of hepatocellular carcinoma (HCC) are still ill-defined; however, there is increasing evidence that the gradual accumulation of mutations, genetic and epigenetic changes which occur in preneoplastic hepatocytes results in the development of dysplastic foci, nodules, and finally, overt HCC. As well as many other neoplasias, liver cancer is considered an “inflammatory cancer”, arising from a context of inflammation, and characterized by inflammation-related mechanisms that favor tumor cell survival, proliferation, and invasion. Molecular mechanisms that link inflammation and neoplasia have been widely investigated, and it has been well established that inflammatory cells recruited at these sites with ongoing inflammatory activity release chemokines that enhance the production of reactive oxygen species. The latter, in turn, probably have a major pathogenic role in the continuum starting from hepatitis followed by chronic inflammation, and ultimately leading to cancer. The relationship amongst chronic liver injury, free radical production, and development of HCC is explored in the present review, particularly in the light of the complex network that involves oxidative DNA damage, cytokine synthesis, telomere dysfunction, and microRNA regulation.

关键词： Reactive oxygen species Viral hepatitis Hepatocellular carcinoma Telomere dysfunction Cytokines mitochondria Antioxidant mechanisms MicroRNA and circulating free DNA

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