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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over time the relative distribution of cancers of the proximal digestive tract has changed. Squamous cell carcinomas of the esophagus have become less common, while numbers of adenocarcinomas have greatly increased. This shift most likely reflects an increase in the incidence of gastroesophageal reflux. Moreover, there is a decline in the incidence of distal gastric cancer, which in turn may be related to Heliobacter pylori eradication. Simultaneously, there is a time trend toward a more proximal localization of gastric cancer. If the above-mentioned etiopathologic links are correct, this could indicate that the so-called cardia adenocarcinomas are not related to H pylori infection and that they may instead be related to gastroesophageal reflux and eventually may not be considered to be "gastric" cancers. The rapidly growing quantity of literature on this subject is, however, confounding. A major source of discordance would seem to be a Babylonian confusion of tongues concerning the terms cardia and cardiac carcinomas. Unfortunately, this confusion is also apparent in the classification systems available for staging of cancer, thus closing the "vicious" circle.
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PMID:Is adenocarcinoma of the esophagogastric junction or cardia different from Barrett adenocarcinoma? 1567 17

Helicobacter pylori infection causes gastritis and peptic ulcers and is associated with the development of gastric cancer. Approximately 50% of the world population is infected with H pylori , with the highest prevalence rates in developing countries. In the vast majority of individuals, infection is acquired during childhood with those of low socioeconomic means and having infected family members being at highest risk for early childhood acquisition. Definitive routes of transmission of the infection are unclear, with evidence suggesting oral-oral, gastric-oral, and fecal-oral routes. If untreated, H pylori infection is lifelong. Although clinical disease typically occurs decades after initial infection acquisition, children infected with H pylori may have gastritis, ulcers, mucosal-associated lymphoid type lymphoma, and, rarely, gastric atrophy with/without intestinal metaplasia (ie, both precursor lesions for gastric cancer). Controversy persists regarding testing for and treating H pylori , if found, in the large number of children who present with recurrent abdominal pain. Because young children (ie, younger than 5 years of age) who are treated and cured of their H pylori infection may be at risk for reinfection, the current recommendations do not recommend treatment unless an ulcer or gastric atrophy is present. However, despite the lack of clinical evidence, the trend is to more aggressively screen children for the presence of H pylori and to treat those children who are found to have the infection. H pylori infection can be eradicated by antimicrobial therapy plus a proton pump inhibitor, but no treatment regimen is 100% effective. Multiple drugs, frequent dosing, and length of treatment often contribute to poor patient compliance, and antibiotic eradication therapy is associated with increasing drug resistance.
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PMID:Helicobacter pylori infection: detection, investigation, and management. 1575 99

Worldwide gastric cancer remains one of the most common cancers, killing upwards of one million people each year. While the molecular pathogenesis remains unclear, infection with the bacterium Helicobacter pylori is considered a "necessary but not sufficient" cause, not surprisingly as gastric cancer has long been known to be associated with atrophic gastritis. Eradication of H pylori is expected to virtually eliminate gastric cancer and H pylori associated peptic ulcer within approximately 40 years and thus reduce overall mortality. In the USA, the incidence of gastric cancer in the general population is low, reflecting the change in the pattern of gastritis from atrophic to non-atrophic and in the low and decreasing prevalence of H pylori infection in the middle and upper classes. However, the plan for eradication of this important pathogen must be considered within the context of the prevalence and outcome within specific populations.
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PMID:The time to eradicate gastric cancer is now. 1588 71

Despite falling prevalence rates in the developed world, H pylori is still present in the United States and is particularly prevalent among racial minorities and recent immigrants. H pylori infection is clearly associated with an increased risk of peptic ulcer disease, gastric cancer, and MALT lymphoma, and it is associated with some cases of uninvestigated dyspepsia. Identification and eradication of H pylori improves outcomes in patients with peptic ulcer disease and causes tumor regression in patients with MALT lymphoma. It is uncertain whether H pylori eradication will improve outcomes in patients with gastric cancer. Decision analytic models suggest that a test-and-treat strategy for H pylori is rational and cost-effective for patients with uninvestigated dyspepsia.
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PMID:Helicobacter pylori: why it still matters in 2005. 1593 49

Despite its decreasing trend in Japan, gastric cancer remains an important public health problem. Although the age standardised rates of gastric cancer have been declining for decades, the absolute numbers are increasing because of the rapid aging of the population. A large proportion of Japanese gastric cancers are detected at an early stage, with a better overall survival rate. As with Western developed countries, a change in the social environment such as reduced salt use and increased fresh vegetable and fruit intake as well as improvement of food storage may play an important part in the decline. Differences in Helicobacter pylori infection rates between generations presumably have contributed to the generation related variation in the declining trends. It is expected that most gastric cancers in Japan may be preventable by lifestyle modification such as salt reduction and increased fruit and vegetable intake, together with avoidance of smoking and countermeasures against H pylori infection so that the level now evident in Western developed countries can be reached.
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PMID:Epidemiology of gastric cancer in Japan. 1599 15

Although various animal models have been developed to clarify gastric carcinogenesis, apparent mechanism of gastric cancer was not clarified in recent years. Since the recognition of the pathogenicity of Helicobacter pylori (H pylori), several animal models with H pylori infection have been developed to confirm the association between H pylori and gastric cancer. Nonhuman primate and rodent models were suitable for this study. Japanese monkey model revealed atrophic gastritis and p53 mutation after long-term infection of H pylori. Mongolian gerbil model showed the development of gastric carcinoma with H pylori infection alone, as well as with combination of chemical carcinogens, such as N-methyl-N-nitrosourea and N-methyl-N-nitro-N'-nitrosoguanidine. The histopathological changes of these animal models after H pylori inoculation are closely similar to those in human beings with H pylori infection. Eradication therapy attenuated the development of gastric cancer in H pylori-infected Mongolian gerbil. Although several features of animal models differ from those seen in human beings, these experimental models provide a starting point for further studies to clarify the mechanism of gastric carcinogenesis as a result of H pylori infection and assist the planning of eradication therapy to prevent gastric carcinoma.
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PMID:Helicobacter pylori-infected animal models are extremely suitable for the investigation of gastric carcinogenesis. 1643 49

Gastric cancer is the second most frequent cancer in the world, accounting for a large proportion of all cancer cases in Asia, Latin America, and some countries in Europe. Helicobacter pylori (H pylori) is regarded as playing a specific role in the development of atrophic gastritis, which represents the most recognized pathway in multistep intestinal-type gastric carcinogenesis. Recent studies suggest that a combination of host genetic factors, bacterial virulence factors, and environmental and lifestyle factors determine the severity of gastric damage and the eventual clinical outcome of H pylori infection. The seminal discovery of H pylori as the leading cause of gastric cancer should lead to effective eradication strategies. Prevention of gastric cancer requires better screening strategies to identify candidates for eradication.
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PMID:Causal role of Helicobacter pylori infection in gastric cancer. 1648 15

Helicobacter pylori (H pylori) has been etiologically linked to gastric cancer.H pylori infection is more frequent in less developed Asian countries like India, Bangladesh, Pakistan,and Thailand and is acquired at early age than in more developed Asian countries like Japan and China. Frequency of gastric cancer, however, is very low in India, Bangladesh, Pakistan and Thailand compared to that in Japan and China. Similar enigma has been reported from Africa as compared to the West. Seroprevalence of H pylori infection in adult populations of India, Bangladesh, Pakistan and Thailand varies from 55% to 92%. In contrast, seroprevalence of H pylori in Chinese and Japanese adults is 44% and 55%,respectively. Annual incidence rate of gastric cancer in India, Bangladesh, and Thailand is 10.6, 1.3, 7.1 per 100,000 populations, respectively; in contrast, that in China and Japan is 32-59 and 80-115 per 100,000 populations, respectively. Several studies from India failed to show higher frequency of H pylori infection in patients with gastric cancer than controls. Available evidences did not support difference in H pylori strains as an explanation for this enigma. Despite established etiological role of H pylori, situation is somewhat enigmatic in Asian countries because in countries with higher frequency of infection,there is lower rate of gastric cancer. Host's genetic make-up and dietary and environmental factors might explain this enigma. Studies are urgently needed to solve this issue.
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PMID:Causal role of Helicobacter pylori infection in gastric cancer: an Asian enigma. 1655 99

Gastric cancer is the fourth most common cancer and the second leading cause of cancer-related death in the world. Over the past 2 decades, many exciting discoveries regarding the genomics of gastric cancer have been made. There are 2 distinct histologic types of gastric adenocarcinoma, and these types differ in their epidemiology, pathogenesis, genetic profile, and clinical outcome. The development of new approaches to functional genomics has significantly improved our ability to explore molecular alterations underlying gastric carcinogenesis and progression. The pathogenesis of intestinal-type gastric cancer follows a multistep progression that usually is initiated by H pylori infection. A wide range of genetic and epigenetic abnormalities including point mutation, loss of heterozygosity, microsatellite instability, and hypermethylation are described in intestinal-type gastric cancer and its precursor lesions. In contrast to the intestinal-type, diffuse-type gastric cancer is defined by a lack of precursor lesions; mutation or epigenetic silencing of the E-cadherin gene appears to be the key carcinogenic event. An improved understanding of the genomics of gastric cancer should lead to the rapid development of novel diagnostic techniques and molecular-based treatment strategies.
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PMID:A review of the genomics of gastric cancer. 1661 44

The aetiology of dyspepsia is unknown in the majority of patients. Helicobacter pylori (H pylori) is the cause in a subset of patients. A non invasive test to assess the presence of H pylori is recommended in the management of patients under the age of 50 presenting to a family practitioner with dyspepsia. A urea breath test or a stool antigen test are the most reliable non invasive tests. Eradication of H pylori will reduce the risk to the patient with dyspepsia of developing a peptic ulcer, reduce the complication rate if prescribed non-steroid anti-inflammatory drugs and later reduce the risk of gastric cancer. The recommended treatment for non ulcer dyspepsia associated with a H pylori infection should be a 10-d course of treatment with a PPI and two antibiotics. Treatment efficacy should be assessed four weeks after completing treatment with a urea breath test or a stool antigen test.
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PMID:Role of Helicobacter pylori in functional dyspepsia. 1671 52


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