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

Two randomized nutrition intervention trials were conducted in Linxian, an area of north central China with some of the world's highest rates of esophageal and stomach cancer and a population with a chronically low intake of several nutrients. One trial used a factorial design that allowed us to assess the effects in nearly 30,000 participants of daily supplementation with four nutrient combinations: retinol and zinc; riboflavin and niacin; vitamin C and molybdenum; and beta-carotene, alpha-tocopherol, and selenium. The second trial provided daily multiple vitamin-mineral supplementation or placebo in 3318 persons with esophageal dysplasia, a precursor to esophageal cancer. After supplements were given for 5.25 y in the general population trial, small but significant reductions in total [relative risk (RR) = 0.91] and cancer (RR = 0.87) mortality were observed in subjects receiving beta-carotene, alpha-tocopherol, and selenium but not the other nutrients. The reductions were greater in women than men, and in those under compared with over the age of 55; however, differences by sex or age were not significant. After multiple vitamin and mineral supplements were given for 6 y in the smaller dysplasia trial, reductions in total (RR = 0.93) and cancer (RR = 0.96) mortality were observed but these were not significant. The largest reductions were for cerebrovascular disease mortality, but the effects differed by sex: a significant reduction was observed in men (RR = 0.45) but not women (RR = 0.90). Restoring adequate intake of certain nutrients may help to lower the risk of cancer and other diseases in this high-risk population.
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PMID:The Linxian trials: mortality rates by vitamin-mineral intervention group. 749 42

Most countries with adequate statistical infrastructure have registered declines in gastric cancer mortality and incidence rates. Such a trend is dominated by the most frequent variant, namely the so-called intestinal type of adenocarcinoma, usually ulcerated and occupying predominantly the antrum and the antrum-corpus junction. This variant is considered the endstage of a prolonged precancerous process with gradual progression from (a) chronic active gastritis to (b) multifocal atrophic gastritis to (c) intestinal metaplasia, first resembling the phenotype of the small intestine and later that of the colon, to (d) dysplasia and (e) finally to invasive carcinoma. Major trends in dietary habits, namely lower intake of salt and increased and more frequent consumption of fresh fruits and vegetables, have been linked to the decline. In parallel with those trends, improved sanitation and more adequate housing may be responsible for the declining rates of infection with Helicobacter pylori, the major cause of chronic active gastritis. A decline in the frequency of papillary adenocarcinoma of the oxyntic mucosa, associated with the pernicious anaemia syndrome, appears to have taken place much earlier. Although the frequency of the pernicious anaemia syndrome seems to have remained at similar levels, its complications in terms of papillary adenocarcinoma have decreased in populations of northern European extraction. This may be related to time trends in dietary habits. The secular decline in diffuse carcinoma has been either of much less magnitude or non-existent. Few clues are available on this tumour variant. It is somewhat predominant in women, in subjects of blood group A phenotype, and less frequent in older subjects. Cell lines derived from diffuse carcinomas lack functional calcium dependent adhesion molecules ("cadherins"). Recent increases in incidence rates have been registered for adenocarcinoma of the gastric cardia. This increase parallels that of lower oesophageal adenocarcinoma, frequently linked with Barrett's oesophagus, reflux oesophagitis, a history of duodenal ulcer and gastric hypersecretion. New developments in molecular biology are being used to study the process of gastric carcinogenesis. There is hope that specific molecular alterations may provide better understanding of the different variants of gastric carcinoma and their secular trends.
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PMID:Gastric cancer. 753 41

Gastric carcinoma is the world's overall second most common cancer. Besides obvious environmental factors, recent epidemiological studies and a better knowledge of Helicobacter Pylori biological properties revealed that the microorganism is involved in the first steps of gastric carcinogenesis as proposed by the Correa model (from normal gastric tissue through superficial gastritis, multifocal atrophic gastritis, intestinal metaplasia and dysplasia to carcinoma). Significant correlation between the prevalence of H. pylori infection and incidence of gastric carcinoma (mainly the intestinal type) in various geographical areas has been reported. The high prevalence of HP in pre-neoplastic states and in cases of early gastric cancer indicates the infection would precede the development of gastric cancer. HP-related chronic inflammation of gastric mucosa with increased mucosal cell proliferation, deficit in local ascorbic acid concentration, topical ammonia toxicity are putative mechanisms that overexpose a weakened gastric mucosa to environmental carcinogens.
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PMID:Gastric carcinoma: the Helicobacter pylori trail. 757 79

Serum micronutrient levels and their relationship to precancerous gastric lesions were studied in 600 subjects aged 35-64 years living in high-risk area of gastric cancer in Linqu County, Shandong Province. Serum micronutrient levels in local residents were 0.54 micrograms/ml, 0.29 micrograms/ml, 3.14 micrograms/ml, 9.62 micrograms/ml, 30.2 micrograms/L, 924 micrograms/L, 1 016 micrograms/L, and 42.0 micrograms/L for vitamin A, beta-carotene, vitamin C, vitamin E, selenium, zinc, copper and ferritin, respectively. Serum levels of beta-carotene, vitamin C and ferritin, and ratio of serum levels of zinc and copper correlated inversely to severity of pathological changes in gastric mucous membrane. With increase of serum level of beta-carotene or vitamin C, odds ratios (OR) of intestinal dysplasia and metaplasia lowered to 0.8, 0.6 and 0.9, 0.5, respectively, and with increase of those of both beta-carotene and vitamin C, their OR lowered further to 0.16, with patients of chronically atrophic gastritis as controls. It indicated maybe beta-carotene and vitamin C played a strong contributing role in protecting from development of precancerous gastric lesions.
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PMID:[Relationship between serum micronutrients and precancerous gastric lesions]. 758 56

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

Porfimer sodium (Photofrin II) is a photosensitizer which distributes selectively to tumor tissues, and causes tumor cell death by combination with light irradiation. Photodynamic therapy (PDT) by combination of porfimer sodium and laser was developed as a new cancer therapy. Tumor selectivity of porfimer sodium are based on the following reasons; 1) high affinity for lipoprotein, especially, low density lipoprotein (LDL), 2) elevation of LDL receptor activity in cancer tissue, and 3) lack or imcompleteness of lymphatic system in cancer tissue. Porfimer sodium is activated by laser irradiation at 630 nm, which can reacts with tissue oxygen to produce highly reactive excited siglet oxygen (1O2). This highly reactive molecule is subsequently capable of killing tumor cells through oxidation of cellular component like mitochondrial enzymes. In addition, this highly reactive intermediate causes destruction of the tumor capillaries, which accelerates tumor cell death. The growth suppression or lethal damage to tumor cells by PDT of porfimer sodium and excimer dye laser were observed in experimental tumor models. In human clinical trials, the rates of complete response (CR) for roentgenographically occult lung cancer, stage I lung cancer, superficial esophageal cancer, superficial gastric cancer and carcinoma in situ or dysplasia of the cervix were 84.8%, 50.0%, 90.0%, 87.5% and 94.4%, respectively. The major side effects were cutaneous symptoms e.g. photosensitivity, pigmentation, increasing GOT, GPT but these symptoms were not severe. PDT using porfimer sodium and excimer dye laser must be clinically useful for the treatment of inoperable early cancer or conservation of organ functions.
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PMID:[Porfimer sodium (Photofrin-II)]. 766 80

The second British Stomach Cancer Group trial was a prospective randomised controlled trial of adjuvant radiotherapy or cytotoxic chemotherapy after gastrectomy for adenocarcinoma. It recruited between 1981 and 1986. No survival advantage has been demonstrated for the patients receiving either type of adjuvant therapy compared with those undergoing surgery alone. We report on 436 patients randomised into the trial together with 203 patients, who did not fulfil the trial criteria, referred to the trial. A univariate (log-rank) analysis of pathological factors obtained from the local referring centres showed that tumour size, macroscopic type, number os sites involved, depth of invasion, involvement of resection lines and lymph nodes and histological grade were significant determinants of survival. Histological review by two experienced histopathologists found that the Lauren classification and histological grade, but not the Ming classification, were significant prognostic factors. The degree of lymphocytic and eosinophilic infiltration and presence of dysplasia assessed by one of the pathologists showed a significant correlation with survival. However, inter-observer correlation for these histological parameters and grade was poor. Multivariate analysis identified only depth of invasion, resection line and nodal involvement as significant independent pathological variables influencing survival. This study confirms the need for expert preparation of the resected specimen to obtain the important information on depth of invasion and nodal status and also reveals some variation in histological assessment, particularly grading, in gastric carcinoma.
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PMID:Pathological prognostic factors in the second British Stomach Cancer Group trial of adjuvant therapy in resectable gastric cancer. 773 9

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

Abnormalities of the tumour suppressor gene p53 have been shown in approximately 60% of advanced gastric adenocarcinomas and it has been suggested that the immunohistochemical finding of increased p53 expression is a prognostic marker in gastric cancer. No studies of early (T1) tumours have been reported. Over expression of p53 protein in 95 early gastric carcinomas and in adjacent mucosa was investigated using immunohistochemistry with antibody CM1. Thirty five per cent of the tumours were positive. The frequency of p53 positivity in tumours of tubular histological type (46%) was significantly higher than that in signet ring tumours (10%) (p = 0.006), and neoplasms that invaded deeply into the submucosa were more frequently positive (45%) than others (30%). Five of eight (62%) T1 tumours with lymph node metastases showed immunoreactive p53. In signet ring tumours, immunopositivity correlated with the frequency of DNA aneuploidy. p53 Over expression was also found in 15% of 26 examples of high grade dysplasia in mucosa adjacent to invasive tumours. No positivity was found in intestinal metaplasia or in normal mucosa. The findings show that immunocytochemically demonstrable over expression of p53 correlates with other morphological markers of aggressiveness in T1 gastric adenocarcinoma. The increasing frequency of p53 immunoreactivity in the sequence of high grade dysplasia-->early gastric cancer-->advanced gastric cancer supports the view that abnormalities of p53 are related to tumour progression in gastric carcinogenesis.
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PMID:Expression of p53 in early (T1) gastric carcinoma and precancerous adjacent mucosa. 782 4

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


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