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From chronic liver disorders to hepatocellular carcinoma: Molecular and genetic pathways

World Journal of Gastrointestinal Oncology 2010年第6期2卷 259-264页

作者： Enzo Ierardi Rosa Rosania mariangela zotti Floriana Giorgio Simonetta Prencipe Nicola Della Valle Vincenzo De Francesco Carmine Panella Section of Gastroenterology Department of Medical Sciences University of Foggia

Hepatocarcinogenesis is a process attributed to progressive genomic changes that alter the hepatocellular phenotype producing cellular intermediates that evolve into hepatocellular carcinoma (HCC). During the preneoplastic phase, the liver is often the site of chronic hepatitis and/or cirrhosis, and these conditions induce liver regeneration with accelerated hepatocyte cycling in an organ that is otherwise proliferatively at rest. Hepatocyte regeneration is accelerated by upregulation of mitogenic pathways involving molecular and genetic mechanisms. Hepatic growth factors, inhibitors and triggers may also play a role. This process leads to the production of monoclonal populations of aberrant and dysplastic hepatocytes that have telomerase reexpression, microsatellite instability, and occasionally structural aberrations in genes and chromosomes. Development of dysplastic hepatocytes in foci and nodules and the emergence of HCC are associated with the accumulation of irreversible structural alterations in genes and chromosomes even if the genomic basis of the malignant phenotype is largely heterogeneous. Therefore, a malignant hepatocyte phenotype may be produced by changes in genes acting through different regulatory pathways, thus producing several molecular variants of HCC. On these bases, a key point for future research will be to determine whether the deletions are specific, due to particular loci in the minimally deleted regions of affected chromosome arms, or whether they are nonspecific with loss of large portions of chromosomes or entire chromosome arms leading to passive deletion of loci. The final aim is the possibility of identifying a step where carcinogenetic processes could be terminated.

关键词： Hepatocarcinoma Chronic liver disorders Genetic pathways Molecular pathways Hepatic growth factors Augmenter liver regeneration

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Metabolic syndrome and gastro-esophageal reflux:A link towards a growing interest in developed countries

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World Journal of Gastrointestinal Pathophysiology 2010年第3期1卷 91-96页

作者： Enzo Ierardi Rosa Rosania mariangela zotti Simonetta Principe Giulio Laonigro Floriana Giorgio Vincenzo de Francesco Carmine Panella Gastroenterology Section Department of Medical SciencesUniversity of Foggia

The aim of this Editorial is to describe the growing possibility of a link between gastro-esophageal reflux disease (GERD) and metabolic syndrome on the light of recent epidemiological and pathophysiological evidence. The state of the art of GERD is described,based on recent definitions,pathophysiological evidence,epidemiology in developed countries,clinical subtypes together with a diagnostic approach specifically focussed on the appropriateness of endoscopy. Metabolic syndrome is accurately defined and the pivotal role of insulin resistance is emphasized. The strong relationship between GERD and metabolic syndrome has been pathophysiologically analyzed,taking into account the role of obesity,mechanical factors and metabolic changes. Data collected by our group regarding eating habits and GERD are briefly summarized at the end of a pathophysiological analysis. The literature on the subject strongly supports the possibility that lifestyle and eating habits may be involved in both GERD and metabolic syndrome in developed countries.

关键词： Gastroesophageal reflux disease Metabolic syndrome Obesity Insulin resistance

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