Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumor-specific immunity to carcinoma of the colon, pancreas and stomach was assayed by tube LAI. Cancers of the colon, pancreas and stomach, were shown to possess organ-type specific neoantigens. In 115 patients with colon cancer, 100%, 75%, 61% with Dukes' A, B and C cancer were LAI positive, respectively. Even a microfocus of in situ cancer in a colon adenoma was sufficient to stimulate measurable tumor-specific immunity in the host. In Dukes' D cancer, 25% of patients with widespread metastasis were positive, whereas 100% with solitary lesions were positive. Reactive leukocytes from patients with colon cancer did not react to extracts of normal bowel mucosa or villous adenoma from LAI-negative patients. Leukocytes from 19% (3 of 16) of patients with colon adenomas reacted to the extract of colon cancer but not normal colon mucosa. Moreover, the LAI-positive response of the patients with colon adenomas or colon cancer is directed to a colon cancer TSA which is linked to beta2-microglobulin. These studies suggest that some colon adenomas express TSA before morphological evidence of cancer. It is not known if the acquisition of a cell surface TSA is an irreversible step toward unrestrained growth and metastasis. In pancreatic cancer, 100% of patients with cancers less than 5 cm and without metastasis were LAI positive, whereas 29% were positive when the cancer was greater than 5 cm or had metastasized. In Patients with stomach cancer, 100% with Stage II and 46% with Stage III and IV cancer were LAI-positive. Leukocytes from patients with other GIT cancers and from patients with inflammatory bowel disease or pancreatitis did not react with extracts of colon, stomach or pancreatic cancer. Leukocytes from patients with metastatic cancer, usually did not react in the tube LAI assay because their surfaces were coated in vivo with TSA. LAI reactivity was present when CEA was not detectable and when CEA levels were elevated LAI activity was often absent. The present study suggests that the automated tube LAI shows sufficient promise to warrant studies to determine its efficacy for the diagnosis of GIT cancers.
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PMID:Tube leukocyte adherence inhibition (LAI) assay in gastrointestinal (GIT) cancer. 37 89

Tumor-associated trypsin inhibitor (TATI) is a 6 K dalton protease inhibitor, that was isolated from urine of a patient with ovarian cancer. In our experience, mean serum level of TATI in healthy subjects (n. 120), is 13 micrograms/l (range 5.1-42 micrograms/l). The cut-off point is established in 32 micrograms/l (mean +/- 3 SD). We have examined 357 patients with gastrointestinal diseases: 98 gastric cancer, 50 colon cancers, 52 pancreatic cancers, 32 chronic pancreatitis, 38 IBD, 28 colon polyps, 40 gastric ulcers and 25 non-neoplastic biliary tree diseases. TATI may be a good tumor marker only in gastric cancer. Elevated levels of TATI also occur in obstructive hepatobiliary disease and active pancreatitis or IBD.
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PMID:[Determination of tumor-associated trypsin inhibitor (TATI) in subjects with gastrointestinal diseases. Preliminary data]. 271 42

Radiolabeled sucralfate has been utilized by several investigators to evaluate peptic ulcer, active inflammatory bowel disease, esophageal ulcer, and gastric cancer. A review of the available literature indicates that radiolabeled sucralfate has been used to evaluate peptic ulcer and active inflammatory bowel diseases with high sensitivity and specificity. Other possible uses of radiolabeled sucralfate which have been less thoroughly studied and for which data are inadequate to accurately determine sensitivity and specificity include the detection of gastric cancer and esophageal ulceration.
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PMID:Radiolabeled sucralfate: a review of clinical efficacy. 331 60

Plasma retinol was determined by reverse-phase high-performance liquid chromatography in healthy subjects and patients with digestive diseases. The plasma retinol in the healthy control was independent of age (80.5 +/- 17.16 micrograms/dl). On the other hand, the amount of retinol in patient groups was lower than in the healthy control group. It was 30.96 +/- 7.16 micrograms/dl in patients with liver cancer, 38.02 +/- 11.63 micrograms/dl in those with chronic pancreatitis and pancreatic cancer, 45.36 +/- 12.63 micrograms/dl in a patient group with inflammatory bowel disease, 66.25 +/- 7.27 micrograms/dl in the patients of early gastric cancer, and 66.44 +/- 10.10 micrograms/dl in the group with biliary stone. These results and many biological aspects of retinol in human made it clear that, the special attention should be paid to the fluctuation of plasma retinol amount. This was considered to play an important role in causing complications associated with digestive diseases.
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PMID:Determination of plasma retinol by high performance liquid chromatography, and its significance in digestive diseases. 371 60

This paper reports the results of a survey of gastro-enterologists' opinions and attitudes at the Stockholm, Sweden, Seventh World Congress (June 1982), elicited via a standard questionnaire in three languages. Respondents' replies were compared with those from the previous (Sixth) World Congress (Madrid 1978) on a variety of topics. As regards peptic ulcer, little change has occurred in the last four years concerning surgery, though highly selective vagotomy has become more common for duodenal ulcer. As regards drugs in routine use, this survey confirms the considerable rise in the proportion of centres prescribing H2 receptor blockers (from 48% in 1978 to 81% in 1982). As regards inflammatory bowel disease, there has been little change overall in surgical procedures though 'small' procedures have grown in popularity (such as diverting ileostomy), largely at the expense of colectomy. Most physicians would now recommend some form of cancer surveillance both for ulcerative colitis and Crohn's disease, the most popular modality being clinical examination plus sigmoidoscopy at 6-12 month intervals, with colonoscopy or barium enema every two years. As regards GI cancer detection, endoscopy is now the modality of choice both for gastric cancer and colo-rectal cancer. Finally, the majority of respondents confirm that they frequently encounter ethical problems both in connection with routine practice and research. By and large ethical committees were felt to be ineffective, and guidance on ethical matters (absent in many centres!) rarely takes a structured form. This last finding possibly lends weight to the O.M.G.E.'s intention to provide such guidance via its newly founded Ethical Committee.
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PMID:Sampling gastro-enterologists' opinions and attitudes at two world congresses. 614 11

The ultrasonic diagnosis "cockade sign" in patients with unexplained abdominal complaints was investigated by means of endoscopy and X-ray studies of the gastrointestinal tract. The following final diagnoses were established: gastric cancer in 24 patients (16,2%), colonic carcinoma in 31 patients (21%), intraabdominal tumor without infiltration of the GI-tract in 19 patients (12,8%), inflammatory bowel disease in 35 patients (23,6%). In 39 patients (26,4%) no inflammatory or neoplastic process of the GI-tract could be found. Most of these patients were suffering of a spastic colon. If a tumor of the gastrointestinal tract can be made visible by ultrasonography, this may shorten the diagnostic procedure. However, ultrasonic investigation of the abdomen cannot exclude an abdominal inflammatory or neoplastic process. Therefore, it is only useful as a screening procedure.
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PMID:[Clinical relevance of the "cockade phenomenon" in abdominal ultrasonic diagnosis]. 684 87

Helicobacter pylori (H. pylori) is the most common cause of peptic ulcers, and is considered as carcinogenic with respect to gastric cancer and MALT lymphoma. The role of H. pylori in other gastroduodenal diseases like atrophic gastritis and functional dyspepsia has been investigated in hundreds of works, but little is done about what role H. pylori may play in non gastric diseases. Gastro-esophageal reflux disease does not seem to be related to H. pylori but Barrett's esophagus might be. Inflammatory bowel diseases tend to be reverse correlated with H. pylori. In coronary heart disease some studies have shown a connection, others not. Diabetes is not likely to be H. pylori-associated and nor do liver diseases with exception for cirrhosis, where a correlation is possible. Respiratory diseases are little examined but bronchiectasis might have a correlation with H. pylori. A small series of children, who had died in sudden infant death, showed a high rate of H. pylori infection.
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PMID:Non-gastric effects of H. pylori infection: a literature review with respect to non gastric diseases which might be associated with H. pylori infection. 1002 62

The diagnostic value of pyruvate-kinase type tumor M2 (Tumor M2-PK) has been investigated in different tumors, and showed interesting results in cases of renal cancer, pancreatic cancer, lung cancer and some cases of gastric cancer. In this study we investigated EDTA-plasma of 68 patients with gastrointestinal cancer, 22 patients with inflammatory bowel disease (IBD) and 60 healthy controls. Sensitivity of Tumor M2-PK was 70.6% for all GI-tumors, that of CA19-9 was 55.4% and that of CEA was 53.3%. In pancreatic cancer CA19-9 showed the best sensitivity. In oesophageal/gastric cancer Tumor M2-PK was most sensitive and in colorectal cancer CEA and Tumor M2-PK showed the best results. The specificity of Tumor M2-PK was 90-96, 7%. In IBD some individuals showed elevated Tumor M2-PK levels but there was no correlation to CRP or to the clinical activity score. The results indicated that Tumor M2-PK might be a valuable marker in gastrointestinal cancer.
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PMID:Tumor M2-pyruvate kinase: a promising tumor marker in the diagnosis of gastro-intestinal cancer. 1132 48

Approximately 50% of humanity is infected with Helicobacter pylori. It is a life-long infection that elicits a marked host inflammatory response; however, natural infection fails to yield protective immunity. Rather than providing protection, the chronic inflammatory response associated with natural infection contributes to tissue damage and the pathogenesis of gastroduodenal disease, including atrophic gastritis, peptic ulcer, and gastric cancer. While bacterial factors are important triggers of inflammation, many subjects infected with strains bearing putative virulence factors remain free from disease. Recent genetic studies have implicated the host's immune and inflammatory responses, suggesting that disease results from an interaction between bacterial and environmental factors in genetically susceptible hosts. Other digestive diseases, including celiac disease and inflammatory bowel disease, mimic this paradigm, where it appears that luminal triggers only manifest disease in subjects with the right combination of host and environmental factors. Since infection with H. pylori is relatively common, it is possible to study the impact of a specific etiologic agent on the pathogenesis of disease in humans. This approach has illuminated the complexity of the pathogenic mechanisms, but the advances achieved to date may provide some hints regarding the pathogenesis of chronic inflammatory diseases elsewhere in the digestive tract.
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PMID:Helicobacter pylori infection as a model for gastrointestinal immunity and chronic inflammatory diseases. 1154 18

Epidemiologic evidence strongly suggests that improved standards of living are associated with an increased incidence of immune system-mediated disease. Allergy, autoimmunity, and within the focus of our laboratory, idiopathic inflammatory bowel disease, most notably Crohn's disease and ulcerative colitis, and progression of chronic gastritis to gastric cancer, are all mediated by proinflammatory immune responses induced by known or unknown antigens. A popular theory, known as the 'hygiene hypothesis' (1), suggests that improved health standards achieved through sanitation and vaccination, may in part be responsible for the apparent increase in immune system-mediated disease due to decreasing microbial and parasitic infections in humans, particularly in children. As antigenic exposure of children to infectious agents, especially parasites, has rapidly decreased, it is suspected that normally protective counter-regulatory Th2-type immune responses fail to develop, increasing the risk for aberrant pro-inflammatory responses in otherwise genetically pre-disposed individuals. This hypothesis has stimulated significant interest in development of animal models of Th1- and Th2-mediated disease to test this paradigm. This review illustrates some of the exciting evidence that Th1-mediated pathology in mouse models of helicobacter disease and diabetes is ameliorated by concurrent anti-inflammatory Th2 responses to parasite antigens and that initial application of these principles is benefiting human patients. The results from developing animal models of human disease not only support the hygiene hypothesis but also have led to novel therapies using parasite antigens to stimulate anti-inflammatory Th2-type responses to restore homeostasis in patients with aberrant Th1-type immune-mediated disease.
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PMID:Th1-mediated pathology in mouse models of human disease is ameliorated by concurrent Th2 responses to parasite antigens. 1496 4


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