Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Humans are exposed to preformed N-nitroso compounds (NOC), but also to a wide range of precursors and nitrosating agents which can react in vivo to form potentially carcinogenic NOC and diazo compounds. Nitrite, nitrate and nitrosating agents can also be synthesized endogenously in enzymic reactions mediated by bacteria, activated macrophages and neutrophils. The latter two cell types generate, via the enzyme nitric oxide synthase, the nitric oxide radical that is involved in cytotoxicity, and is believed to be involved in formation of carcinogenic nitrosamines, DNA base deamination and oxidative damage. Thus endogenous NOC formation, DNA damage and gene mutations in humans could occur at various sites of the body such as the stomach and chronically infected or inflamed organs. Sensitive procedures to estimate the exposure of humans to NOC have been developed and applied in ecological and cross-sectional studies. These have shown that inhabitants of high-risk areas for stomach and esophageal cancer, patients with urinary tract infections (at risk for bladder cancer) and Thai subjects infected with liver fluke (at risk for cholangiocarcinoma) had significantly higher exposure to endogenous NOC. Clinical studies have examined the model of stomach carcinogenesis based on intragastric nitrosation, but the precise roles of bacterial overgrowth and of Helicobacter pylori infection in NOC synthesis and/or inducing oxidative stress in stomach mucosa remain to be clarified. Together these results support the role of NOC and other nitrite-derived mutagens in human cancer etiology, in particular when exposure starts early in life and persists over a long period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endogenously formed N-nitroso compounds and nitrosating agents in human cancer etiology. 133 85

Infection by bacteria, parasites or viruses and tissue inflammation such as gastritis, hepatitis and colitis are recognized risk factors for human cancers at various sites. Nitric oxide (NO) and other oxygen radicals produced in infected and inflamed tissues could contribute to the process of carcinogenesis by different mechanisms, which are discussed on the basis of authors' studies on liver fluke infection and cholangiocarcinoma development. A similar mechanism could apply to other suspected and known cancer-causing agents including Helicobacter pylori infection (stomach cancer) or asbestos exposure (lung mesothelioma). Studies on the type of tissue and DNA damage produced by NO and by other reactive oxygen species are shedding new light on the molecular mechanisms by which chronic inflammatory processes may initiate or enhance carcinogenesis in humans.
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PMID:Chronic infections and inflammatory processes as cancer risk factors: possible role of nitric oxide in carcinogenesis. 751 36

Chronic gastritis may favour the development of gastric cancer more as a condition than as precancerous lesion. Since, in most cases, it is pathologically correlated with Helicobacter pylori infection, it is reasonable to postulate at least an indirect role for this organism in the pathogenesis of gastric cancer. H. pylori, however, is only one of the risk factors involved, in that additional factors (excess salt, cigarette smoking, deficiency of foodstuffs with an antioxidizing effect) may facilitate the malignant transformation of chronic atrophic gastritis into intestinal-type gastric cancer. Gastric carcinogenesis therefore presents itself as a multifactorial, multistage process, furthered by the occurrence of precancerous lesions which are usually interrelated (type-III intestinal metaplasia, severe dysplasia) and by functional alterations such as achlorhydria, which, though it is not enough in itself to cause gastric cancer, promotes abnormal intragastric bacterial development, a condition which may be followed by abnormal intragastric formation of cancerogenous nitroso compounds. The existence of a close correlation between both gastric cancer and H. pylori infection and low socio-economic and hygienic status of the population lends further strength to the hypothesis that an "H. pylori factor" is involved in gastric carcinogenesis. Consequently, to reduce the risk of gastric cancer, various strategies have been devised to prevent H. pylori infection (improvement in socio-environmental conditions, anti-H. pylori vaccine) and/or to eradicate the organism (by means of therapeutic regimens including antimicrobial agents, which, however, can be implemented only in patients who have not developed diffuse atrophy and/or dysplasia, in whom H. pylori may no longer be detectable). Definitive proof of the real extent of the relationship between H. pylori and gastric cancer and of the efficacy of therapeutic and preventive measures can be provided only by controlled trials in populations with a high prevalence of chronic non-atrophic gastritis which are difficult to organize.
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PMID:Chronic gastritis, intestinal metaplasia, dysplasia and Helicobacter pylori in gastric cancer: putting the pieces together. 759 47

The study of gastric cancer is important in clinical medicine as well as in public health. Environmental factors play an important role in gastric carcinogenesis and thus primary prevention is feasible after improvement of these factors. The 5-year survival rate of resected early gastric cancer is over 90% and this provides an excellent paradigm for secondary prevention. Though its mortality rate has declined since 1970, gastric cancer remains common and carries a high mortality in Taiwan where about 2,000 patients die of gastric cancer annually. The age-adjusted mortality is 16.54 and 8.16/100,000 for male and female, ranking the third and fourth cancer death respectively. Epidemiologic data disclose a positive association between gastric cancer and some dietary factors in Taiwan. However, the role of Helicobacter pylori infection and hereditary susceptibility should be elucidated in the future. Endoscopy with biopsy is an excellent method of the diagnosis of gastric cancer. However, its invasiveness makes it impractical as a screening tool and thus the proportion of early gastric cancer to gastric cancer remains as low as 30% in most reports. The value of lymph node dissection remains controversial although surgery is one of the most effective methods of eradicating gastric cancer. Overall, the 5 year survival rate is 24.5% to 54%. Laser therapy is usually reserved for patients with high operative risk and specific types of gastric cancer. To improve the survival results, development of a simple and economic screening program based on the epidemiologic results and utilization of noninvasive examinations such as serologic markers to diagnose and treat gastric cancer at its earliest stage deserves further study.
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PMID:[Gastric cancer in Taiwan]. 771 65

Recent epidemiologic evidence indicates that Helicobacter pylori infection increases the risk for gastric carcinoma. Infection with H. pylori leads to chronic gastritis, which usually persists for life unless treated with antimicrobial drugs. Because the great majority of gastritis patients never develop neoplasias, research concerning those who do may provide clues about carcinogenesis. In affluent populations, H. pylori infection leads to nonatrophic gastritis, predominantly involving diffusely the antrum (diffuse antral gastritis), the basic lesion seen in patients with duodenal ulcer, which has not been associated with increased risk for gastric carcinomas. In populations with high gastric cancer risk, H. pylori infection is associated with multifocal atrophic gastritis, which frequently advances to intestinal metaplasia, occasionally to dysplasia, and rarely to carcinoma. H. pylori infection increases the rate of proliferation of the gastric epithelial cells and decreases the gastric secretion of ascorbic acid, processes that may modulate the process of carcinogenesis. Infection with H. pylori is characterized by infiltration of lymphocytes, polymorphonuclear leukocytes, and macrophages in the gastric mucosa. There is considerable interest in investigating oxygen radicals originating in white blood cells and the possibility that they induce mutations with carcinogenic potential in the gastric epithelium.
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PMID:Helicobacter pylori and gastric carcinogenesis. 776 38

A nested case-control study was carried out to investigate the association between Helicobacter pylori infection and gastric cancer risk in Taiwan. A total of 29 patients newly affected with gastric cancer and 220 healthy controls matched with cases on age, sex and residence were selected from a cohort of 9,775 men recruited from 1984 through 1986. Frozen serum samples collected at recruitment examination were tested for IgG antibodies against Helicobacter pylori by an enzyme-linked immunosorbent assay. The average interval between serum collection and cancer diagnosis was 3.1 years. Gastric cancer cases had a higher seropositive prevalence (69%) than matched controls (59%) giving an odds ratio of 1.6 (95%) confidence interval = 0.7-2.6). Compared with previous nested case-control studies, Helicobacter pylori infection in early childhood may be a risk factor for gastric cancer. However, a long induction period seems required for gastro-carcinogenesis associated with Helicobacter pylori infection.
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PMID:A nested case-control study on the association between Helicobacter pylori infection and gastric cancer risk in a cohort of 9775 men in Taiwan. 776 44

The association between Helicobacter pylori infection and gastric cancer remains controversial. A community-based serosurvey was carried out in Taiwan to investigate the association. Serum IgG antibodies against Helicobacter pylori were examined in 728 subjects randomly selected from three townships with different gastric cancer mortality rates. The overall seropositivity of Helicobacter pylori was 54.7% (398/728) with no gender difference (males: 54.5%; females: 54.8%). The seroprevalence of Helicobacter pylori progressively increased with age in all three study townships. The age-specific seropositivity of Helicobacter pylori correlated well with age-adjusted gastric cancer mortality in the three townships. The difference in seropositivity was more profound in younger age groups. The ecological study in Taiwan suggests an association between Helicobacter pylori infection and gastric cancer. Helicobacter pylori infection in early childhood may be a key issue; in addition, a long induction time appears to be required for gastric carcinogenesis.
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PMID:Ecological study of association between Helicobacter pylori infection and gastric cancer in Taiwan. 785 Dec 3

Recently many reports have shown a strong association between Helicobacter pylori infection in the stomach and recurrent peptic ulcer. Moreover, prospective cohort serological studies showed that H. pylori infected individuals have significantly increased rate of gastric cancer in the USA. H. pylori is a gram-negative spiral organism which has urease activity and produces ammonia and CO2 from urea, and nestles in the gastric pits and overlaying mucus gel layer. Many diagnostic methods of H. pylori infection are available; ie bacterial culture, 13C-urea breath test, histology, serum IgG antibody against H. pylori. We developed a new method, ie tissue IgA antibody against H. pylori and detection of H. pylori DNA in the gastric juice by PCR method. Triple therapies with metronidazole, bismuth compounds, and amoxicillin or tetracyclin are difficult to use in Japan because of their sever side effects. Thus, new methods with proton pump inhibitor (PPI) and amoxicillin have been introduced. We treated 14 patients of whom were H. pylori positive-active peptic ulcer with 30 mg/day of lansoprazole, a new PPI, plus 1,500 mg/day of amoxicillin for 2 weeks and 8 (57%) patients were eradicated. Gastric carcinogenesis are multi-steps and multifactorials process. Hypothetical sequence of intestinal type of gastric cancer is that superficial gastritis-->atrophic gastritis-->intestinal metaplasia-->dysplasia-->gastric cancer and H. pylori infection may play a role in the early stage of the sequence. We examined mucosal IgA antibody against H. pylori in chronic gastritis and intestinal metaplasia detected by the Tes-Tape method in 25 resected specimens after gastrectomy for gastric cancer. Positivity rates of tissue H. pylori IgA antibody were lower in the mucosa of intestinal metaplasia than in non-metaplastic gastric mucosa and were negative in carcinoma. Causal relationship between H. pylori infection and gastric cancer is not proven and factors other than H. pylori infection are also important in the gastric carcinogenesis. Finally we introduce 2 reports: (1) NIH Consensus Conference: Helicobacter pylori in peptic ulcer disease (JAMA. 1994; 272: 65-69). The consensus panel concluded that 1. ulcer patients with H. pylori infection require treatment with antimicrobial agents in addition to antisecretory drugs whether on first presentation with the illness or on recurrence; 2. the value of treating nonulcerative dyspepsia patients with H. pylori infection remains to be determined; and 3. the interesting relationship between H. pylori infection and gastric cancer requires further exploration. (2) World Health Organization: Working Group Meeting (Reported in World Congress of Gastroenterology, Los Angeles, 1994). H. pylori plays a causal role in the chain of events leading to cancer of the stomach. Group I: definite carcinogen.
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PMID:[Helicobacter pylori in peptic ulcer and gastric cancer]. 785 88

The association between gastric adenocarcinoma and Helicobacter pylori infection remains controversial. A seroprevalence study of Helicobacter pylori infection in 143 patients with gastric adenocarcinoma and a control group of 823 subjects randomly selected from four areas in Taiwan, was carried out to elucidate the association. The overall seropositivity of Helicobacter pylori in gastric adenocarcinoma patients (62.9%) was higher than in controls (54.4%), but the difference was not statistically significant (p > 0.05). The seropositivity of early gastric adenocarcinoma (61.5%) was not significantly different from that of advanced gastric adenocarcinoma (63.2%). Various demographic factors such as sex, blood type, cigarette smoking, tumor histology and location were not associated with the seroprevalence of Helicobacter pylori. The age-specific seroprevalence of Helicobacter pylori tended to be higher in younger patients and decreased after the age of 60 years in gastric adenocarcinoma, in contrast to a stepwise increase of seropositivity in controls. This suggests that Helicobacter pylori infection in early life may be a contributory factor in gastric carcinogenesis.
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PMID:Helicobacter pylori infection in early and advanced gastric adenocarcinoma: a seroprevalence study in 143 Taiwanese patients. 811 47

We compared the gastric mucosa lesions of 63 direct relatives of 24 patients with gastric carcinoma with those observed in 151 dyspeptic patients and in seven members of a family with familial gastric carcinoma of diffuse type. We found a higher prevalence of Helicobacter pylori infection (96.8%) and gastritis (98.4%) in the relatives of patients with sporadic carcinoma than in the dyspeptic patients. One-third of the individuals of the former group displayed chronic atrophic gastritis and intestinal metaplasia. Dysplasia was only observed in the group of cancer patient relatives. The relatives of patients with intestinal carcinoma showed a higher prevalence of chronic atrophic gastritis (40.0%), incomplete intestinal metaplasia (22.9%) and dysplasia (5.7%) than the relatives of patients with diffuse carcinoma (10.0%, 0.0% and 0.0%, respectively). The only striking feature that emerged from the comparison of relatives of patients with sporadic gastric carcinoma with the members of the family with familial gastric carcinoma was the significantly higher prevalence of hyperplastic lesions (100%) in the latter group. These results reinforce the existence of two main pathways of carcinogenesis of gastric mucosa, one leading to intestinal carcinoma via chronic atrophic gastritis and intestinal metaplasia and the other leading to diffuse carcinoma via hyperplastic changes.
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PMID:Characteristics of the gastric mucosa of direct relatives of patients with sporadic gastric carcinoma. 849 May 43


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