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

With regard to esophageal tumors, important reports on several topics have been published recently. 1) The place of endoscopic ultrasonography (EUS) as the best locoregional staging technique for cancer of the esophagus has been further consolidated. The addition of fine-needle aspiration makes EUS more sensitive than computed tomography (CT) and more accurate than CT or EUS alone for nodal staging. 2) High-resolution endoscopy with chromoendoscopy has been found to be very effective for mucosal lesions, but not for submucosal lesions. In combination with EUS, the sensitivity for submucosal tumors increases up to 60 %. 3) Autofluorescence-guided biopsy has been reported to be a good tool for detecting high-grade dysplasia. A narrow-band imaging system improved the overall accuracy for depth of invasion. 4) The incidence of hypopharyngeal cancer increases after resection for esophageal carcinoma. Patients with a scattered staining pattern after application of Lugol's solution are more prone to develop upper lesions. 5) Fluorescence imaging makes it possible to detect low-grade intraepithelial neoplasia in Barrett's mucosa, with fewer biopsies. 6) Patients with Barrett's esophagus with a length of over 3 cm had a significantly greater prevalence of dysplasia in comparison with those in the whom the Barrett's segment was shorter than 3 cm (23 % vs. 9 %, P = 0.0001). With regard to gastric tumors, 1) Helicobacter pylori eradication can significantly reduce the development of gastric cancer, but only in patients without precancerous lesions. 2) Intestinal metaplasia types II and III have been shown to have a higher rate of progression to low-grade dysplasia than type I. 3) With regard to screening in asymptomatic individuals, serum pepsinogen may represent an alternative to conventional fluoroscopy methods. 4) In patients who have undergone esophagectomy for esophageal cancer, annual follow-up endoscopies are vital for detecting early secondary gastric cancer and ulcerations in which curative treatment is possible. 5) High-resolution endoscopy allows more precise diagnosis of early gastric cancer. The presence of irregular minute vessels and variations in vessel caliber were found to be specific of early gastric cancer. The small regular pattern of sulci and ridges was observed significantly more frequently in differentiated carcinoma than in undifferentiated carcinoma. 6) Infrared-ray electronic endoscopy combined with indocyanine green injection appears to be effective in detecting sentinel nodes that contain metastases in patients with gastric cancer. 7) Gastric adenocarcinoma was found to show specific changes in the fluorescence spectra emitted, in comparison with normal gastric mucosa. However, there was wide variation in the emitted autofluorescence spectra in gastric cancer with signet-ring cells in comparison with normal mucosa.
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PMID:Diagnosis of esophagogastric tumors. 1565 54

A miniaturized confocal microscope was developed that could be integrated in the distal tip of a conventional colonoscope. With this technique, denoted confocal endomicroscopy, subsurface analysis of the gut mucosa and in-vivo histology during ongoing endoscopy are possible in full resolution by point scanning laser analysis. The diagnostic spectrum of confocal endomicroscopy is expanding from screening and surveillance for colorectal cancer to Barrett's esophagus, Helicobacter pylori-associated gastritis, and gastric cancer. The new detailed images seen with confocal laser endomicroscopy allow a unique look on cellular structures at and below the surface of the gut. This review describes the optical and diagnostic possibilities of confocal laser endomicroscopy.
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PMID:Confocal laser endomicroscopy. 1627 35

Endomicroscopy becomes possible due to the integration of a miniaturized confocal microscope in the distal tip of a conventional endoscope. Endomicroscopy enables subsurface analysis of the gut mucosa and in vivo histology during ongoing endoscopy in full resolution by point scanning laser fluorescence analysis. Cellular, vascular and connective structures can be seen in detail. Graduation of cellular changes with endomicroscopy allows an immediate in-vivo diagnosis of different gastrointestinal diseases. The diagnostic spectrum of confocal endomicroscopy is currently expanding from screening and surveillance for colorectal cancer towards Barrett's esophagus, Helicobacter pylori associated gastritis and early gastric cancer. The new detailed images seen with confocal laser endomicroscopy are unequivocally the beginning of a new era where this optical development will allow a unique look on cellular structures and functions at and below the surface of the gut.
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PMID:[Endomicroscopy--technology with future]. 1634 78

The upper gastrointestinal (GI) cancers have various carcinogenic pathways and precursor lesions, such as dysplasia for esophageal squamous cell carcinoma, Barrett esophagus for esophageal adenocarcinoma, and intestinal metaplasia for the intestinal-type of gastric cancer. Recently, many epigenetic events in carcinogenic pathways have been revealed, along with genomic and genetic alterations. This information has provided deeper insight into an understanding of the mechanisms of upper GI carcinogenesis. Moreover, detection methods of aberrant methylation have been applied to clinical fields to stratify high-risk groups, detect early cancer, and to predict clinical outcomes. In this review, a variety of information is summarized regarding gene hypermethylation in esophageal and gastric cancer.
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PMID:CpG island hypermethylation in progression of esophageal and gastric cancer. 1636 78

Helicobacter pylori infection is recognized as the major cause of gastritis and gastric cancer; however, its role in the development of gastroesophageal reflux disease and Barrett's adenocarcinoma is unclear. The expression of NF-kappaB, AP-1, and COX-2 may be important in inflammation and tumorigenesis in the esophagus. The aim of this study was to examine the effect of live H pylori or H pylori extract (HPE) on these factors in the esophageal epithelial cell lines SKGT-4 and OE33. NF-kappaB and AP-1 activity were assessed by gel shift assay and COX-2 by Western blotting. Coculture of SKGT-4 and OE33 with live H pylori and HPE induced NF-kappaB and AP-1 DNA-binding activity, and also decreased IkappaB-alpha levels. Treatment with the specific MEK1/2 MAPK inhibitor PD98059, but not the p38 MAPK inhibitor SB203580, inhibited NF-kappaB and AP-1 activity. The antioxidant vitamin C inhibited H pylori-induced NF-kappaB activation, but increased AP-1 expression. Moreover, HPE induced COX-2 expression and IL-8 production, and PD98059 inhibited COX-2 expression, ERK1/2 phosphorylation, and IL-8 production. These data demonstrate that both live H pylori and HPE induce NF-kappaB and AP-1 expression in esophageal epithelial cells. The induction of such transcription factors may play a role in the specific immune response within Barrett's mucosa and may indirectly cause inflammation of the gastric cardia and the distal esophagus.
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PMID:Helicobacter pylori extract induces nuclear factor-kappa B, activator protein-1, and cyclooxygenase-2 in esophageal epithelial cells. 1662 21

H. pylori infection is a major pathogen inducing gastric mucosal inflammation and causing dysregulation of normal acid inhibitory regulatory mechanisms. The overall effect on gastric acid secretion is dependent on the location and severity of inflammation. Eradication results in healing of gastric mucosal inflammation, healing of peptic ulcers, prevention of new peptic ulcers, prevention or reduction in gastric cancer risk and in transmission of the infection. Neither H. pylori infection nor H. pylori eradication causes gastroesophageal reflux disease (GERD). H. pylori eradication also does not impede anti-secretory drug therapy of GERD. Misunderstandings of the negative association between H. pylori infection and GERD and/or Barrett's esophagus and misuse of the epidemiologic concept of ''protection'' led to considerable confusion and likely resulted in some patients receiving poor care. Current evidence is consistent with the notion that H. pylori should be eliminated whenever the organism is found. However, H. pylori infection has become increasing difficult to cure in part due to the emergence of antimicrobial resistance. In Western countries, triple therapy consisting of a proton pump inhibitor, amoxicillin and clarithromycin no longer achieves adequate eradication rates and will soon need to be abandoned. When used, legacy triple therapy should be given for 14 days. Fluorquinolones may temporarily be useful: 10-14 day duration is superior to 7 days. However, worldwide resistance is rapidly increasing. Other potential replacement therapies and strategies are discussed including sequential therapies, high-dose proton pump inhibitor plus amoxicillin, and new quadruple therapies.
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PMID:Current understandings of Helicobacter pylori, peptic ulcer and gastroesophageal reflux disease. 1697 68

In surgical therapy for upper gastrointestinal cancer, adequate lymphadenectomy together with R0 resection of the primary tumour is one of the most important prognostic factors which can be influenced by the surgeon. Recommendations for localization- and stage-adapted lymphadenectomy can be made according to histopathologic and anatomic investigations of the patient collectives of large centres. After neoadjuvant radiochemotherapy in cancer of the cervical oesophagus, the absence of lymph nodes on the resected specimen seems to be of less prognostic value. In squamous cell cancer of the suprabifurcal oesophagus, radical lymphadenectomy is recommended. Despite significant morbidity, in specialized centres this procedure yields good results with low mortality. For infrabifurcal oesophageal cancer, two-field lymphadenectomy during the so-called Ivor-Lewis operation is the method of choice. Locally advanced Barrett carcinoma is also an indication for classic two-field lymphadenectomy together with abdominothoracic oesophagectomy and creation of a stomach tube with intrathoracic anastomosis. The lymphadenectomy should however include the area of retroperitoneal lymphatic drainage at the pedicle of the left kidney. Submucosal cancer in this area can be treated with luminal limited resection of the oesophagogastric junction with adequate lymphadenectomy. Adenocarcinoma of the cardia and subcardial gastric cancer including the cardia both require lymphadenectomy analogous to that performed in gastric cancer, with special attention paid to the retroperitoneal lymphatic drainage towards the left kidney pedicle. For therapy of gastric cancer, a systematic D2 lymphadenectomy should always be performed.
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PMID:[Lymphadenectomy with tumors of the upper gastrointestinal tract]. 1733 37

Epigenetic alterations, represented by aberrant DNA methylation, are deeply involved in human cancers. In gastric cancers, tumor-suppressor genes are inactivated more frequently by promoter methylation than by mutations. We recently showed that H. pylori infection, a potent gastric carcinogenic factor, induces methylation of specific genes in the gastric mucosae. When the methylation levels were analyzed in the gastric mucosae of healthy volunteers, cases with a single gastric cancer, and cases with multiple gastric cancers, who have increasing levels of risks for gastric cancers, there was a significant increasing trend in the methylation levels among the individuals without current H. pylori infection. This finding unequivocally showed the presence of an epigenetic field for cancerization. The degree of the field defect was measured more conveniently using methylation levels of marker genes than using those of tumor-suppressor genes. The presence of an epigenetic field for cancerization has been indicated for liver, colon, Barrett's esophageal, lung, breast, and renal cancers. Since decreased transcription is involved in the specificity of methylated genes, it is likely that specific genes are methylated according to carcinogenic factors. These findings emphasize the usefulness of DNA methylation as a marker for past exposure to carcinogens and future risk of cancer development.
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PMID:Epigenetic field for cancerization. 1739 62

We have previously reported that H. pylori infection prevents reflux esophagitis (RE) and Barrett's esophagus (BE) by decreasing gastric acid secretion. Gastroesophageal (GE) junction adenocarcinoma, including Barrett's adenocarcinoma, has been thought to be a complication of gastroesophageal reflux disease. However, the relationship between H. pylori infection, gastric acid secretion and GE junction adenocarcinoma had not yet been investigated in Japan. We demonstrated that the status of gastric acid secretion was higher in patients with GE junction adenocarcinoma than in patients with early gastric cancer (EGC), and that the level was the same in patients with RE and those with BE. We also found that the prevalence of H. pylori infection in patients with GE junction adenocarcinoma was significantly lower than that in patients with EGC, although not as low as that in patients with RE and BE, suggesting that preservation of gastric acid secretion may be important for the development of GE junction adenocarcinoma in Japanese people, regardless of the presence of H. pylori infection.
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PMID:The prevalence of Helicobacter pylori infection and the status of gastric acid secretion in patients with gastroesophageal junction adenocarcinoma in Japan. 1745 Apr 43

Hereditary diffuse gastric cancer and tylosis are autosomal dominant cancer susceptibility syndromes. Accumulating evidence also suggests a genetic contribution to Barrett's esophagus and adenocarcinoma, traditionally considered acquired disorders. In this article we review the current knowledge on the genetic mechanisms underlying hereditary diffuse gastric cancer, tylosis, and Barrett's esophagus. Hereditary diffuse gastric cancer is a paradigm for hereditary cancer susceptibility syndromes with E-cadherin implicated as the dominant oncogene in up to one-third of cases. Tylosis in contrast remains the paradox as whilst the putative abnormality has been localized to the long arm of chromosome 17, sequencing of this region has failed to reveal a disease causing mutation. In the case of Barrett's esophagus and adenocarcinoma, although a validated specific disease-associated gene is yet to be identified, the increasing body of evidence of a possible genetic link is paving the way for subsequent prognostic studies such as AspECT (Aspirin Esomeprazole Chemoprevention Trial). For the clinician these advances in understanding are already having implications for practice in terms of improved screening and the stratification of management strategies. As the mechanisms continue to be defined, there is the real possibility that these mechanisms could be exploited or subverted in the design of new therapies. In the meantime, however, clinicians should undertake rigorous biopsy programs to ensure early invasive lesions are detected.
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PMID:Genetics of gastroesophageal cancer: paradigms, paradoxes, and prognostic utility. 1792 1


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