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

Helicobacter pylori (H. pylori) infection leads to profound changes in gastric physiology. Several clinical and animal studies have been performed to clarify the influence of H. pylori on gastric acid secretion. Published data, however, are not consistent throughout. Infection of the gastric antrum, which can be observed mainly in duodenal ulcer patients, increases gastrin release and consecutively acid output. The net effect of corpus and antrum gastritis, such as in patients with gastric cancer, is to decrease acid secretion. Chronic H. pylori infection may finally promote gastric atrophy with irreversibly diminished acid secretion but in earlier stages of this infection eradication of H. pylori normalizes gastric secretory activity.
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PMID:[Helicobacter pylori and gastric acid secretion]. 1019 Feb 51

Cancer of the distal stomach, both of the intestinal and diffuse type, is strongly associated with Helicobacter pylori colonization. This bacterium causes chronic active inflammation of the gastric mucosa in the majority of colonized subjects. In a considerable number of them, this will eventually lead to a loss of gastric glands, and thus the establishment of atrophic gastritis, which is associated with the development of intestinal metaplasia and dysplasia. Development of atrophy and metaplasia of the gastric mucosa are thus strongly associated with H. pylori infection, instead of a direct and inevitable consequence of ageing. Approximately 40-50% of infected subjects develop these conditions, but they are rare in non-infected subjects. The presence of these consecutive disorders leads to a 5-90-fold increased risk for cancer of the distal stomach, in particular of the intestinal type. This sequence explains the increased risk for gastric cancer in H. pylori-infected subjects, as has been shown in various cross-sectional and longitudinal studies. In a combined analysis of three longitudinal studies, a significant trend was observed towards an increased odds ratio with longer intervals between (retrospective) serological diagnosis of H. pylori infection and observation of gastric cancer, this risk being more than eight-fold increased if the interval had been at least 15 years. This is thought to reflect development of atrophic gastritis and intestinal metaplasia with loss of H. pylori colonization in the years prior to development of cancer. Atrophic gastritis and gastric cancer thus appear closely associated with the presence of H. pylori, yet not all infected subjects will eventually develop atrophy and only a small minority develop gastric cancer. Factors that influence the risks for atrophy and cancer in the presence of infection may be related to the time that infection occurred and to characteristics of the bacterial strain and the host. Evidence for the role of these factors is now increasing. Recognition of the causal role of H. pylori in the induction of gastric cancer theoretically presents tools for cancer prevention. The efficacy of screening and bacterial eradication for prevention of distal gastric cancer is being studied in a number of large-scale intervention studies in different populations. It is hoped that these studies will also provide answers to the potential preventive role of H. pylori colonization in the development of gastro-oesophageal reflux disease and associated conditions, in particular development of cancer of the proximal stomach. Infection with H. pylori plays an important role in the aetiology of atrophic gastritis and gastric cancer. Studies suggest an eight-fold increased risk for both conditions in the presence of infection. Factors that influence the risk for both conditions in the presence of infection are the age at which infection occurred and the presence of cagA as a marker for more pathogenetic H. pylori strains. The efficacy and side-effects of intervention for the prevention of distal gastric cancer has yet to be established.
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PMID:Review article: exploring the link between Helicobacter pylori and gastric cancer. 1020 81

Infection with Helicobacter pylori is now recognized as the primary cause of peptic ulcers and their recurrence. Compelling evidence has also been found linking H. pylori infection to gastric cancer, the second most common cancer in the world. Given the high rate of patient morbidity and mortality associated with gastric cancer, any method by which one can reduce the occurrence of the disease or increase its early detection is desirable. The strong correlation with H. pylori infection and the current availability of easily administered tests for the detection of the pathogen argue for screening at least those individuals with a family history of gastric cancer or other risk factors. This article reviews the association between H. pylori and gastric cancer and the pathologic changes that the infection produces in the gastric mucosa, as well as the cost-effectiveness of universal testing and eradication of the infection in H. pylori-positive individuals to reduce gastric cancer.
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PMID:Helicobacter pylori and gastric cancer. 1062 41

Infection with the bacterium Helicobacter pylori is associated epidemiologically with development of gastric cancer. To better understand the role of H. pylori in carcinogenesis, we examined the effects of H. pylori on cell cycle-related events in the AGS gastric cancer cell line. During coculture, wild-type, toxigenic, cagA-positive H. pylori induced both apoptosis and inhibition of cell cycle progression at G1-S in AGS cells. These effects were most apparent in AGS cells synchronized by serum-deprivation and then stimulated to progress through the cell cycle by refeeding. An isogenic cagA-negative mutant H. pylori, produced similar effects. In contrast to changes induced by 5-fluorouracil, the inhibition of cell cycle progression from G1 to S caused by H. pylori was not accompanied by sustained changes in p53 or p21cip1, but was associated with reduced expression of p27kip1 and inhibition of transcriptional activation of the serum-response element of c-fos. Our results indicate that H. pylori inhibits cell cycle progression at G1-S and induces apoptosis, associated with reduced expression of p27kip1 in AGS gastric cancer cells. In vivo, similar effects as a result of H. pylori infection may lead to potentially deleterious compensatory hyperproliferation by nonneoplastic gastric epithelial cells.
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PMID:Helicobacter pylori inhibits the G1 to S transition in AGS gastric epithelial cells. 1034 28

Infection with Helicobacter pylori has been associated with an increased risk of gastric cancer in low-risk populations. However, our previous results (P. M. Webb et al., Int. J. Cancer, 67: 603-607, 1996) from an ongoing prospective study in Shanghai, China, a relatively high-risk population, failed to show an association between H. pylori infection and the subsequent risk of gastric cancer. That previous study had a relatively short time period of follow-up and the enzyme-linked immunosorbent assay (ELISA) used was based on strains found in Southern England and without validation among the Chinese. Either one of these two factors could have had an impact on the validity of those earlier observations. An ELISA developed and validated among Shanghai residents was used in the present study to reexamine specific antibodies to H. pylori in 188 gastric cancer patients and 548 control subjects. All of the cases of gastric cancer were identified during the first 12 years of follow-up of a cohort of 18,244 men, ages 45-64 years in Shanghai, from whom blood samples were collected at enrollment during 1986-1989. For each cancer case, three cancer-free control subjects were randomly selected from the cohort and matched to the index cases by age (within 2 years), month and year of sample collection, and neighborhood of residence. The Shanghai-based ELISA detected a higher prevalence of serum antibodies to H. pylori than the English-based assay in both gastric cancer cases (86 versus 53%) and control subjects (85 versus 56%). Virtually all of the subjects (98%) who were H. pylori-seropositive by the English-based assay tested positive by the Shanghai-based assay. On the other hand, 73% of gastric cancer cases and 68% of control subjects who were seronegative according to the English-based assay tested positive by the Shanghai-based assay. Using this alternative assay, combined with increased follow-up, our latest data contradict our earlier findings and show a statistically significant association between H. pylori seropositivity and gastric cancer risk (odds ratio, 1.84; 95% confidence interval, 1.08-3.11). We noted an increasing rate of seropositivity among cases as the time interval between cohort enrollment and cancer diagnosis increased. Among subjects followed for 5 or more years after enrollment, the odds ratio for gastric cancer related to H. pylori seropositivity was 3.74 (95% confidence interval, 1.51-9.30).
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PMID:Helicobacter pylori infection and risk of gastric cancer in Shanghai, China: updated results based upon a locally developed and validated assay and further follow-up of the cohort. 1042

With an aim of promoting primary prevention of cancer, major avoidable risk factors as well as protective factors of cancer are reviewed based on previous epidemiological studies. Among various risk factors of cancer, tobacco is the most important avoidable risk factor for cancers of the oral cavity, larynx, lung, pharynx, esophagus, stomach, liver, pancreas, kidney (pelvis), ureter, bladder, and cervix. Tobacco accounts for some 20-30% of all sites of cancer. Betel quid and tobacco chewing is an important risk factor for cancer of the oro-pharynx in some parts of South-East Asia. Diet also plays an important role in the etiology of cancer, but its relation to cancer is complicated. An excess or insufficient intake of some food components elevates risk of cancer of several sites. Eating habits, available foods, methods of food processing may vary from country to country. Infection of oncogenic viruses (especially, HBV, HVC, HPVs) is an important avoidable risk factor of cancer where liver cancer and cervical cancer are common. Infection of Helicobacter pylori could also be an important risk factor of stomach cancer. Attributable risks of other avoidable risk factors, such as occupation, environmental pollution, sun light, radiation, food additives, pesticides, drugs, etc. are relatively small compared to those of tobacco, diet and infection. Exercise and stress are also manageable risk factor of cancer.
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PMID:Major avoidable risk factors of cancer. 1054 92

Infection with Helicobacter pylori has been linked to numerous severe gastroduodenal diseases including peptic ulcer and gastric cancer. Several techniques have been used to measure the genetic heterogeneity of H. pylori at several different levels and to determine whether there is any correlation with severity of disease. The availability of two completed genome sequences from unrelated strains (J99 and 26,695) has allowed an analysis of the level of diversity from a large-scale yet detailed perspective. Although the two chromosomes are organized differently in a limited number of discrete regions, the genome size and gene order of these two "high-virulence" (cagA+ and vacA+) H. pylori isolates was found to be highly similar. The regions of organizational difference are associated with insertion sequences, DNA restriction/modification genes, repeat sequences, or a combination of the above. A significant level of variation at the nucleotide level is seen across the genome, providing an explanation for why the nucleotide-based typing techniques have such high discriminatory power among independent H. pylori isolates. This nucleotide variation together with the organizational rearrangements appears to have provided an over-estimation of the gene order diversity of H. pylori as assessed by pulse-field gel electrophoresis. Functional assignments are assigned to approximately only 60% of the gene products in each strain, with one-half of the remaining gene products of unknown function having homologues in other bacteria, while the remainder appear to be H. pylori-specific. Between 6% and 7% of the coding capacity of each strain are genes that are absent from the other strain, with almost one-half of these strain-specific genes located in a single hypervariable region called the plasticity zone. The majority of the strain-specific genes in each strain are also H. pylori-specific, with no homologues being identified in the public databases. Significantly, over one-half of the functionally assigned strain-specific genes in both H. pylori J99 and 26695 encode DNA restriction/modification enzymes. Analysis of the level of conservation between orthologues from the two strains indicates that the H. pylori specific genes have a lower level of conservation than those orthologues to which a putative function can be assigned. The plasticity zone represents one of several regions across each genome that is comprised of lower (G+C)% content DNA, some of which has been detected in self-replicating plasmids, suggesting that both horizontal transfer from other species and plasmid integration are responsible for the strain-specific diversity at this locus. These analyses have yielded results with important implications for understanding the genetic diversity of H. pylori and its associated diseases, and imply a need to reassess the respective roles of bacterial and host factors in H. pylori associated diseases.
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PMID:Analysis of the genetic diversity of Helicobacter pylori: the tale of two genomes. 1068 19

Prevalence determinations have been performed around the world, and regardless of how exotic a location, H. pylori is found in a substantial proportion of the population. H. pylori remains among the most universal of infections. Understanding of some features of infection has changed. Infection can be gained and lost at rates higher than previously realized. Oral-oral and oral-fecal transmission account for most, if not nearly all, cases of infection. H. pylori infection has declined rapidly in developed countries, which probably has contributed to declines in duodenal ulcer disease and gastric cancer. The full health implications of the potential elimination of infection are unknown.
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PMID:Recent developments in the epidemiology of Helicobacter pylori. 1103 73

Infection with Helicobacter pylori has been recognized as a risk factor for gastric cancer, although it is still unclear whether strains of this organism behave as carcinogens. We have studied 30 H. pylori clinical isolates from 15 patients with gastric cancer and 15 patients with other gastroduodenal diseases. Bacterial pellet and supernatant fluid of broth cultures were tested for mutagenicity by means of the Ames test using the pre-incubation technique. The average Ames ratio was 1.111 in the bacterial pellet and 1.312 in the supernatant of strains from the gastric-cancer group, and 0.858 and 0.950 in those from the non-gastric-cancer group, respectively. The strains from the gastric-cancer group had a significantly higher ratio than those from the non-gastric-cancer group, although all results were below the cut-off ratio of the Ames test, and were thus regarded as having no mutagenicity. The Ames ratio of the supernatant was higher than that of the bacterial pellet in both groups. The results indicate that all of the H. pylori strains tested revealed no mutagenicity, but the difference in Ames ratio between strains might reflect differences in genotoxicity between the strains.
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PMID:Mutagenicity of Helicobacter pylori in the Ames test using Salmonella typhimurium TA100. 1109 32

Prevalence rates and risk factors for H. pylori infection have been reported in many countries over the past year. Infection patterns in developed and developing countries are very different. Very high infection rates in developing countries with high incidence of gastric cancer were described, however, African enigma is still under controversy. The main risk factors for H. pylori infection are fecal-oral and oral-oral spread because H. pylori has not been detected to any extent in the environment. Recently, in childhood, main risk factors for transmission may be the contact with own father with H. pylori infection in Japan. Re-infection are very rare in adults, but not uncommon in childhood. Prevalence of H. pylori infection is reviewed.
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PMID:[Epidemiology of H. pylori infection]. 1121 91


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