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

There is growing interest in the relationship between H. pylori infection and gastro-oesophageal reflux disease (GORD). However, this relationship is complex, as yet not fully elucidated, and probably based on a multiplicity of factors. The prevalence of H. pylori infection in patients with GORD is similar, more often lower than in matched controls. There is a negative correlation between H. pylori infection and the severity of GORD. There are many hypothetical mechanisms by which H. pylori infection may protect from the development of GORD. Conversely, there are many possible mechanisms by which H. pylori infection could theoretically foster the GORD. Patients after H. pylori eradication may develop GORD, and this seems to suggest a protective role of H. pylori infection, but other possible explanations include weight gain after H. pylori eradication, changes in dietary habits and smoking, and pre-existing GORD. H. pylori infected patients treated by various acid-inhibiting therapies such as proton pump inhibitors (PPIs), H2-receptors antagonists (H2-RA) or vagotomy, have an increase of their corpus gastritis severity, both in the activity of inflammation and in the density of organisms. Long-term therapy of GORD in H. pylori infected may lead to rapid progression of atrophic gastritis intestinal metaplasia and dysplasia, and increase the risk of developing gastric cancer. More recently it has been shown that H. pylori infection may interfere with the acid suppressive therapies used for treating GORD. In our opinion the progression of gastritis depends on the threshold of acid output at which H. pylori can 'flourish'. Recently interest is growing on gastric transitional zones and Helicobacter ecology. Any decrease of acid secretion changes the behaviour of H. pylori: the activity of gastritis improves in the antrum, but it deteriorates in the body. During proton pump inhibitor treatment, H. pylori redistribution occurs within the stomach, from an antral to a corpus or fundus prevalent pattern; corpus-fundus gastritis, exacerbated by PPI therapy, may result both in a diminished acid secretion and gastro-oesophageal reflux. The interest in Barrett's oesophagus is growing due to the associated risk of adenocarcinoma. The literature seems to demonstrate that the prevalence of H. pylori infection of the stomach in Barrett's oesophagus patients is not different from that exhibited by controls, roughly one-third of the subjects. Intestinal metaplasia of the gastric cardia seems to be equally frequent in patients with and without GORD. Finally, it appears unlikely that a causal relationship exists between H. pylori infection and Barrett's-associated adenocarcinoma.
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PMID:Review article: is Helicobacter pylori status relevant in the management of GORD? 1105 Apr 85

The incidence of esophageal tumors, and of adenocarcinoma in particular, has risen markedly in recent years in the developed countries. The use of a variety of histopathological and biological markers is now offering promising prospects for the future. Vertical tumor invasion, intratumoral microvessel density, antimucin monoclonal antibodies, flow cytometry, telomerase activity, and overexpression of cyclin D1 have been correlated with the staging and prognosis of esophageal carcinomas. By combining these markers with Lugol staining, a practical new method of staging esophageal tumors may become available in the coming years. As is well known, Barrett's mucosa is a preneoplastic condition. Discussions in the literature concerning short forms of Barrett's esophagus and their relationship to inflammation of the gastric cardia appear to describe two different scenarios--a gastroesophageal reflux condition for short forms of Barrett's esophagus, and an inflammatory phenomenon (perhaps unrelated to Helicobacter pylori infection) for inflammation of the gastric cardia. Cost-benefit studies of follow-up procedures in Barrett's esophagus have yet to be conducted, and considerable efforts--mainly using biological markers--are being made to identify those patients who are at greatest risk. Although the frequency of gastric tumors has declined in recent years, many as yet unclear aspects of these tumors have been studied. Technological progress has not led to substantial changes in the diagnostic procedures used, although autofluorescence methods and three-dimensional reconstruction have been analyzed. Laparoscopy, preferably combined with the use of ultrasound probes, may be a valuable tool for staging. The suggestion that endoscopy should be avoided in young patients (the "treat but do not scope" approach) has been seriously questioned, as it may lead to early cancer being overlooked. There is thought to be an intermediate stage of gastric cancer (between the early and advanced stages) in which the muscularis propria, but not the serosa, is invaded. Endoscopic ultrasonography is becoming increasingly established as a basic tool for the staging of gastric cancer. Gastric MALT lymphoma can be cured by H. pylori eradication therapy in many cases, but there is still uncertainty regarding the limitations of this approach.
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PMID:Diagnosis of esophagogastric tumors. 1120 80

Epidemiological evidence has clearly shown a highly significant relationship between Helicobacter pylori infection and the development of duodenal ulcer and distal gastric adenocarcinoma. Despite H. pylori being a common aetiological factor for both disorders, the two disease phenotypes are virtually mutually exclusive. This indicates that the host response to infection has a pivotal role in determining outcome; these disease phenotypes relate to the effect of infection on gastric acid secretion, duodenal ulcer being closely related to sustained acid secretion whereas gastric cancer follows gastric atrophy and impaired gastric acid secretion. Cancer at the oesophageal junction and that associated with Barrett's oesophagus is now the most rapidly increasing tumour in the gastrointestinal tract. The challenge for the next millennium, therefore, is to try and develop methods for identifying patients at risk of developing oesophagogastric cancer. A common feature in the pathogenesis of both gastric and oesophageal adenocarcinoma is inflammation presenting clinically as gastritis and oesophagitis. The pathway from gastritis to gastric atrophy, dysplasia and carcinoma is thought to be a multi-step process, probably triggered by free radicals within the gastric epithelium and increased exposure to luminal carcinogens. However, it has been unclear as to which aspect of the host response determines whether an individual will move along the neoplasia pathway. Recent work has shown that qualitative aspects of the immune environment in the stomach may account for a substantial part of the phenotypic divergence following H. pylori infection. Interleukin-1 beta polymorphisms relate closely to the propensity for an individual to develop distal gastric cancer and maybe useful for predicting risk in family members. In Barrett's oesophagus, we have recently shown that the immune environment may also be important in determining whether an individual will develop cancer. Although we did not find that Barrett's oesophagus was a profoundly inflammatory condition (unlike esophagitis in the squamous epithelium), where there was evidence of inflammation it was qualitatively different from that of oesophagitis in that a Th-2 response with increased expression of IL-4 predominated in Barrett's, whereas a Th-1 proinflammatory response characterised oesophagitis in squamous epithelium. It seems likely that the specific immune environment within Barrett's metaplasia may be an important driver towards dysplasia and carcinoma. Thus, the immune environment in the stomach and esophagus may be critical in determining whether an individual is at risk of developing neoplastic complications of H. pylori infection and gastroesophageal reflux. Identification of the genetic factors which underpin these responses may ultimately result in development of methods to identify individuals at high risk.
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PMID:Acid, helicobacter and immunity: a new paradigm for oesophagogastric cancer. 1159 70

We report a rare case of Barrett's adenocarcinoma asso-ciated with acquired eventration of the diaphragm in a 71-year-old woman. She initially developed dysphagia and epigastric discomfort in May, 1997. On July 9, she was referred to our Department of Surgery at the Ryukyus University Hospital for thorough examination and treatment. Esophageal adenocarcinoma and eventration of the diaphragm were revealed by exhaustive examinations, including chest X-ray, computed tomography, and magnetic resonance imaging, and proximal gastrectomy with reconstruction of jejunal interposition was performed, on August 8. Histologically, the tumor revealed that the adenocarcinoma arose from short-segment Barrett's esophagus (SSBE). It thus appears that eventration of the diaphragm may induce SSBE and Barrett's adenocarcinoma. We therefore recommend that periodic examinations of the esophagus and stomach be performed in patients with eventration of the diaphragm. Barrett's adenocarcinoma associated with acquired eventration of the diaphragm is reported. Patients with eventration of the diaphragm should undergo periodic examinations of the esophagus and stomach.
Gastric Cancer 1998 Dec
PMID:Barrett's adenocarcinoma associated with acquired eventration of the diaphragm. 1195 49

BACKGROUND: Adenocarcinoma of the esophagus and cardia is a challenging disease for the surgeon. Delay in diagnosis, nodal involvement, and incompleteness of resection have an adverse effect on long-term prognosis. Efforts are currently oriented to identify patients who may benefit from extensive resection.METHODS: Between November 1992 and May 1998, 218 patients with histologically proven adenocarcinoma of the distal esophagus or cardia were referred to our Department. In 6 patients (10.2%) cancer was discovered during endoscopic surveillance for Barrett's metaplasia. Overall, 147 patients (67%) underwent resection. An Ivor-Lewis approach was used in 121 patients; of these, 51 underwent an extended mediastinal lymph node dissection.RESULTS: Median cumulative survival was 25.9 +/- 3.1 months in patients undergoing resection, and 7 +/- 1.3 months in patients having palliation ( P < 0.01). Survival was significantly higher in patients with negative nodes than in those with lymph node metastases (54 +/- 12.9 versus 17 +/- 2.8 months; P < 0.01). Six of the 51 patients (11.8%) undergoing extended lym-phadenectomy had metastatic upper mediastinal nodes. Additional serial sections and immunohistochemistry were performed in 46 patients. In 6 of 18 patients (33.3%) with negative nodes at conventional hematoxylin-eosin examination, immunohistochemistry demonstrated micrometastases in the lesser curvature, paracardial, peripancreatic, or lower mediastinal nodes. Three of these patients had recurrent disease within the first year of follow-up.CONCLUSIONS: Early diagnosis remains the prerequisite for curative treatment of adenocarcinoma of the esophagus and cardia. Endoscopic surveillance appears to be warranted in patients with Barrett's metaplasia. When a curative resection is attempted, extended lymphadenectomy improves tumor staging and may prevent local recurrences. Serial sections and immunohistochemistry provide additional accuracy in the staging of the disease and may prove useful to select patients for adjuvant therapy.
Gastric Cancer 1999 Aug
PMID:Results of surgical therapy in patients with adenocarcinoma of the esophagus and cardia. 1195 79

Gastric cancer is one of the leading causes of cancer mortality in the world. Gastric adenocarcinomas account for more than 95% of gastric tumors, whereas gastrointestinal stromal tumors (GISTs) are the most common neoplasms of the rare gastric mesenchymal tumors. Although the incidence of mid-distal gastric adenocarcinomas is decreasing, the incidence of gastroesophageal junctional tumors and Barrett's adenocarcinomas is increasing for unknown reasons. The majority of gastric tumors are sporadic in nature. However, there are rare, inherited gastric cancer predisposition traits, such as germline p53 (Li-Fraumeni syndrome) as well as E-cadherin (CDH1) alterations in familial diffuse gastric cancers. Gastric cancer has been observed to be part of the spectrum of neoplasms associated with germline mismatch repair gene (MMR) alterations that give rise to the hereditary nonpolyposis colorectal cancer (HNPCC) entity. Comparative genomic hybridization analyses have identified several amplifications and losses of DNA copy numbers in gastric cancers. Loss of heterozygosity (LOH) studies have shown several chromosomal loci with significant allelic loss, thus indicating the possibility of harboring a tumor suppressor gene important in gastric tumorigenesis. Microsatellite instability (MIS) and associated alteration of the TGF-bIIR, IGFRII, BAX, E2F-4, hMSH3, and hMSH6 genes are found in a subset of gastric carcinomas. Cell adhesion molecule abnormalities such as those involving CDH1 may play an important role in diffuse-type gastric cancer development. Although, multiple somatic alterations have been described in gastric carcinomas at the molecular level, the significance of these changes in gastric tumorigenesis remains to be established in most instances. The critical molecular alterations in gastric cancers that may lead to advances in our armamentarium to combat this lethal disease remain to be fully characterized.
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PMID:Molecular biology of gastric cancer. 1197 14

Gastric intestinal metaplasia, an intermediate step in Correa's cascade of gastric carcinogenesis, is generally regarded as a pre-malignant lesion. Epidemiological studies suggest that patients with intestinal metaplasia have more than a 10-fold increased risk of developing gastric cancer. Within the subclassification of intestinal metaplasia, incomplete or type III intestinal metaplasia appears to be associated with even higher malignant potential. The topographical distribution of intestinal metaplasia may also have prognostic implications. Certain genetic and epigenetic alterations have been demonstrated in gastric intestinal metaplasia which straddle into gastric cancer. These findings suggest that genetic changes occur early in the multistep gastric carcinogenesis process. Unlike Barrett's oesophagus and colonic polyp, which have well-defined surveillance guidelines, there is no widely accepted surveillance programme for gastric intestinal metaplasia. An annual surveillance programme may allow early detection of gastric cancer, which theoretically may improve survival. It remains elusive whether the treatment of Helicobacter pylori infection may reverse gastric intestinal metaplasia or reduce the subsequent risk of cancer development. Further controlled studies with longer follow-up are needed to resolve this controversy. The role of chemo-prophylactic agents, e.g. cyclo-oxygenase-2 inhibitor, should be investigated.
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PMID:Review article: intestinal metaplasia and gastric carcinogenesis. 1214 69

Free radicals and reactive species produced in vivo can trigger cell damage and DNA modifications resulting in carcinogenesis. Dietary antioxidants trap these species limiting their damage. The present study evaluated the role of vitamins C and E in the prevention of potentially premalignant modifications to DNA in the human stomach by supplementing patients who, because of hypochlorhydria and possible depletion of gastric antioxidants, could be at increased risk of gastric cancer. Patients undergoing surveillance for Barrett's oesophagus (n 100), on long-term proton pump inhibitors were randomized into two groups: vitamin C (500 mg twice/d) and vitamin E (100 mg twice/d) for 12 weeks (the supplemented group) or placebo. Those attending for subsequent endoscopy had gastric juice, plasma and mucosal measurements of vitamin levels and markers of DNA damage. Seventy-two patients completed the study. Plasma ascorbic acid, total vitamin C and vitamin E were elevated in the supplemented group consistent with compliance. Gastric juice ascorbic acid and total vitamin C levels were raised significantly in the supplemented group (P=0.01) but supplementation had no effect on the mucosal level of this vitamin. However, gastric juice ascorbic acid and total vitamin C were within normal ranges in the unsupplemented group. Mucosal malondialdehyde, chemiluminescence and DNA damage levels in the comet assay were unaffected by vitamin supplementation. In conclusion, supplementation does not affect DNA damage in this group of patients. This is probably because long-term inhibition of the gastric proton pump alone does not affect gastric juice ascorbate and therefore does not increase the theoretical risk of gastric cancer because of antioxidant depletion.
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PMID:Dietary antioxidants and DNA damage in patients on long-term acid-suppression therapy: a randomized controlled study. 1220 36

Fluorescence endoscopy is a new technique which allows a better detection of non-visible malignant or premalignant lesions or, those which are difficult to detect. Exogenously applied sensitisers accumulate selectively in malignant lesions and induce fluorescence after illumination with light of adequate wavelength. However, also endogenous fluorophores, different located in malignant or benign lesions, induce a different autofluorescence in these lesions. Tissue fluorescence can be detected by optical sampling of the mucosa using fluorescence spectroscopy or by generating real time fluorescence images with specialised camera systems. Compared to point fluorescence spectroscopy the latter technique enables the screening of large surface areas of mucosa. Meanwhile, fluorescence endoscopy is a widely used technique in urology employing 5-aminolaevulinic acid sensitisation. In gastroenterology, this technique seems promising for the detection of early cancers or dysplasia in patients with Barrett's oesophagus or ulcerative colitis. Using different sensitisers, photodynamic therapy seems to be a promising option for patients with advanced oesophageal cancer and in the palliative treatment of non-resectable bile duct cancer, furthermore for patients with early gastric cancer and dysplasia in Barrett's oesophagus. Probably, by laser light fractionation or a combination of different sensitisers, an enhanced effect can be expected.
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PMID:Fluorescence endoscopy and photodynamic therapy. 1246 4

It has been suggested that certain histological criteria may serve to indicate a good prognosis in patients with esophageal carcinoma. These include absence of subepithelial extension of the carcinoma cells, stage no higher than m2, and no neoplastic involvement near the resection margin. As endoscopic mucosal resection is becoming an accepted treatment option in this type of tumor, prognostic parameters of this type are of particular interest. By contrast, when metastases are detected in the celiac lymph nodes, it implies that the tumor is unresectable and that palliative treatment is required. Endoscopic ultrasound (EUS)-guided fine-needle aspiration has been found to be the most cost-effective option in this setting. Although autofluorescence endoscopy is being tested as a new technique for endoscopic diagnosis, its value is at present unclear. However, such developments may lead to improved diagnosis in the future, particularly in relation to the initial stages of carcinoma. For the moment, EUS is still the most widely accepted method for early diagnosis and staging. Esophageal squamous-cell carcinoma appears to be commonly associated with head and neck cancer, but the cost-effectiveness of surveillance is a matter of controversy. With regard to Barrett's esophagus and adenocarcinoma, p53 staining in areas of low-grade dysplasia appears to be helpful for predicting progression to high-grade dysplasia. The prevalence of short-segment Barrett's esophagus increases with age, but the length of the segment does not increase with time; the length probably depends on individual conditions, not merely on elapsed time. Helicobacter pylori infection appears to be associated with intestinal metaplasia at the esophagogastric junction. However, the most recent data appear to suggest that this scenario (usually termed "carditis") may be different from intestinal metaplasia in the lower esophagus, related to acid reflux. A follow-up program might be able to detect Barrett's esophagus adenocarcinoma at earlier stages, but only a minority of Barrett's esophagus patients are likely to be detected before neoplasia has developed. Gastric cancer appears to develop in individuals with H. pylori infection, but not in uninfected persons. In addition, those with severe gastric atrophy, corpus-predominant gastritis, and intestinal metaplasia may be at greater risk for gastric cancer. This again raises the question of H. pylori eradication in asymptomatic individuals with infection, and surveillance of patients with severe intestinal metaplasia. The most recent data appear to support the notion that healing of MALT lymphoma depends not only on H. pylori eradication and on the stage of the tumor, but also on individual factors (possibly immunology-related).
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PMID:Diagnosis of esophagogastric tumors. 1251 Feb 24


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