1,721,138 research outputs found
Diet, H pylori infection and gastric cancer: evidence and controversies.
No full textDespite decreasing incidence and mortality rates, gastric cancer (GC) still remains the fourth most common cancer and the second most common cause of cancer-related deaths worldwide. Due to the limited treatment options, at present, prevention is likely to be the only effective means of controlling this disease. The success of a prevention strategy depends upon the understanding of etiological and pathogenic mechanisms underlying gastric carcinogenesis. The etiology of GC is multi-factorial, however, in the recent years, mounting evidence suggests that environmental factors play a key role. The most important environmental factors implicated in the pathogenesis of GC are diet and H pylori infection. Thus, modifications in lifestyle and dietary habit associated with eradication of H pylori infection could hypothetically represent the most promising potential targets for GC prevention. In this review we will address the evidence and the controversies on the role of these agents in non-cardia GC by focusing on retrospective and prospective observational studies and interventional trials
CHEMOPREVENTION OF GASTRIC CANCER: ROLE OF COX-2 INHIBITORS AND OTHER AGENTS
No full textDespite the decrease in incidence, gastric cancer remains the second leading cause of cancer-related death worldwide. Prevention is likely to be the most effective means of not only reducing the incidence but also mortality from this disease. The term 'chemoprevention' has been referred to the prevention of cancer using specific agents to suppress or reverse the carcinogenic process. In recent years, attention has been focused on the anticancer properties of non-steroidal anti-inflammatory drugs (NSAIDs), Helicobacter pylori eradication therapy and diet life-style. In vitro and in vivo studies show that widespread and long-term use of NSAIDs may be adopted in the healthy population for gastric chemoprevention. Albeit, enthusiasm has been thwarted by the potential toxic effects, i.e., risk of peptic ulcer disease. The new NSAIDs, selective cyclooxygenase-2 inhibitors, causing less injury to the mucosa of the upper gastrointestinal tract may be a valid alternative. However, fundamental questions such as safety, efficacy, mechanisms of actions, and optimal treatment regimens need to be defined. H. pylori triggers gastric carcinogenesis, however, cost-effect analyses suggest that only a subgroup of H. pylori-infected subjects present beneficial changes following eradication therapy. Diet plays an important role in the pathogenesis of gastric cancer either increasing the risks of or protecting against, cancer development. Thus, a reasonable suggestion for the general population is a natural chemoprevention based on life-style 'eat to live, not live to eat'
Probiotics: a potential target for the prevention and treatment of steatohepatitis.
No full textThe accumulation of fat in hepatocytes with a necroinflammatory component-steatohepatitis-that may or may not have associated fibrosis is becoming a frequent lesion. Although steatohepatitis is currently recognized to be a leading cause of cryptogenic cirrhosis, the pathogenesis has not been fully elucidated. Among the various factors implicated, intestinal bacterial overgrowth may play a role. Indeed, various rat models of intestinal bacterial overgrowth have been associated with liver lesions similar to NASH, and bacterial overgrowth has been observed significantly more often in patients with NASH compared with control subjects. The authors discuss the relationship among intestinal bacterial overgrowth, steatohepatitis development, and probiotic treatment
Is it the Time for Prevention and Chemoprevention of Gastric Cancer? The Role of Dietary Intervention, Helicobacter Pylori Eradication and COX-2 Inhibitors
No full textPrevention and Chemoprevention of Gastric Cancer: Dietary Habits, Helicobacter pylori and COX-2 Inhibitors
No full textCancer stem cell hypothesis and gastric carcinogenesis: Experimental evidence and unsolved questions
No full textTraditionally, the clonal evolution model has been used to explain gastric cancer (GC) growth dynamics. According to this model, GC cells result from multiple mutations over time resulting in a population of continually diversifying cells. This heterogeneity enables the survival of different clones under particular conditions allowing growth at metastatic locations or resistance to chemotherapeutics. Cancer stem cell (CSC) theory completely overturns this traditional understanding of cancer suggesting that only CSCs can self-renew and promote tumor growth. CSCs are relatively refractory to conventional therapies, thus explaining why anti-cancer therapies are far from curative and why relapses of cancer are frequent. The identification of the CSC component of a tumor might, thus, open new therapeutic perspective based on the selective targeting of this small population of cells. In this review we examine the current scientific evidence supporting the existence of CSC in gastric tumors and analyze the main unsolved questions of this difficult field of cancer research
Molecular alteration of gastric carcinoma.
No full textGastric cancer is constituted by two histomorphological entities ''intestinal'' and ''diffuse'' that differ in epidemiology, pathogenesis, clinical outcome and genetic profile. Two distinct molecular pathways of genomic destabilization have been identified in gastric carcinogenesis: the microsatellite mutator phenotype (MMP) and a phenotype associated with chromosomal and intrachromosomal instability (CIN). The microsatellite mutator phenotype is caused by mismatch repair (MMR) deficiency and is associated with mutational inactivation; this condition is identified as microsatellite instability (MIN). CIN is characterized by chromosomal rearrangements and losses or gains of chromosomes, which in turn can induce oncogene activation and/or tumour-suppressor-gene inactivation. Mounting evidence suggests that MMP alterations, DNA aneuploidy and expression of the products of cancer-related genes are early markers of cell transformation, and may serve to identify the genetic pathway of gastric carcinoma. However, the lack of a clear genetic basis lends weight to the notion that gastric cancer may be affected by exposure to environmental factors. Helicobacter pylori is one of the most frequent infections worldwide and is the most important environmental risk factor associated with sporadic gastric cancer. Exposure of gastric epithelial cells to H. pylori results in the generation of reactive oxygen species and an increased level of inducible nitric oxide synthase that in turn may cause genetic alterations leading to cancer in a subset of subjects. In conclusion gastric cancer is the result of an interplay between genetic and environmental factors. The new technologies for the molecular analysis will be a useful tool to understand the individual's risk and settle novel biological therapeutic strategies
Reply to: "Prediction of liver fibrosis progression by non-invasive tests in chronic hepatitis C: the impact of validation".
No full textDoes Helicobacter Pylori play a role in inflammatory bowel disease?
No full textThe cause of inflammatory bowel disease is still unknown although several bacterial and viral agents have been implicated in their aetiologies. Helicobacter pylori infection, the main cause of gastroduodenal diseases, could, theoretically, be involved in the pathogenesis of inflammatory bowel disease. In fact, it induces permeability alterations and immunological derangements in the stomach similar to those detected in the colon of inflammatory bowel disease patients. However, epidemiological data do not support this hypothesis and recent evidence even points to a low prevalence of Helicobacter pylori in inflammatory bowel disease. These data are discussed in the light of possible confounding factors
Angiodysplasia as a possible cause of gastrointestinal bleeding in cirrhosis and octreotide treatment.
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