Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of cancer in Barrett's esophagus is multifactorial. Gastroesophageal reflux seems to be important in the initiation of Barrett's esophagus, but its role in promoting carcinogenesis has yet to be established. Diet, lifestyle and carcinogens, especially the nitrates, may be important in the development of carcinogenesis, and require further investigation. Inhibition of reflux-stimulated inflammatory changes, for example by inhibiting cyclooxygenase, holds promise for decreasing cancer progression. Similarly, dietary and lifestyle modification used in the management of reflux may also help to prevent the development of esophageal cancer. The molecular changes that are associated with the development of cancer in Barrett's esophagus offer several potential areas of intervention to prevent and manage esophageal cancer. Limiting cell growth, increasing apoptosis of damaged cells, limiting cell invasion and angiogenesis factors could be useful to accomplish this goal. Having a greater understanding of the pathogenesis of this condition can only help to develop more management options in the future.
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PMID:Mechanisms of disease: Carcinogenesis in Barrett's esophagus. 1626 72

There are a wide variety of palliative treatments for esophageal cancer. The aim of most treatments is to maintain oral food intake, which should stabilize or even improve quality of life. Stent placement is currently the most widely used treatment modality for palliation of dysphagia from esophageal cancer. Stent placement offers a rapid relief of dysphagia, however, the rate of complications (late hemorrhage) and recurrent dysphagia (stent migration, tumor overgrowth) is relatively high. The scientific evidence to advocate the use of anti-reflux stents for the prevention of gastro-esophageal reflux is currently too low. Photodynamic therapy is mostly used in North America; however, due to the high costs of the treatment, the long-lasting side effects and the necessity of repeated treatments, it is not an ideal treatment for palliation of malignant dysphagia. Nd:YAG laser is a relatively effective and safe treatment modality, although laser treatment is also expensive, technically difficult and requiring repeated treatment sessions at 4-6 weeks intervals. Single dose brachytherapy compares favorably to stent placement in long-term effectiveness and safety. Effective treatment strategies are probably 12 Gy given in one fraction or 16 Gy given in two fractions. Palliative chemotherapy offers response rates in recent trials (including partial and complete responses) ranging from 35% to 50%. Whether palliative chemotherapy also results in a survival benefit is not established yet. For clinical trials on palliation of esophageal cancer, the measurement of quality of life is an important outcome measure. The cancer-specific EORTC QLQ-C30 and the esophageal cancer-specific EORTC-OES-18 are validated measures for establishing quality of life status. For the future, a multimodality approach with stent placement or brachytherapy in combination with chemotherapy may be indicated.
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PMID:Palliative therapy. 1629 91

Esophageal cancer development after previous atresia repair is extremely rare in young patients. We present the clinical course of a patient who developed an adenocarcinoma of the esophagus at the age of 22 years, after repair of a tracheoesophageal fistula with esophageal atresia in the neonatal period. She developed a stricture of the esophageal anastomosis requiring frequent dilatations. Six years after an antireflux procedure because of a difficult treatable severe gastroesophageal reflux, an advanced adenocarcinoma was detected at the site of the end-to-end anastomosis of the previous atresia.
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PMID:Development of an adenocarcinoma of the esophagus 22 years after primary repair of a congenital atresia. 1656 17

Concern over how best to manage individuals with Barrett's esophagus (BE) has grown because of the consistent rise in the incidence of esophageal adenocarcinoma. Since the 1970s, the rate of increase in incidence of esophageal adenocarcinoma has been greater than that for any other cancer in the US population. Patients with BE have increased risk for esophageal cancer, but the rate of progression and potential risk factors in progression remain poorly understood. Much remains to be learned about BE and its association with adenocarcinoma before effective surveillance or management strategies can be defined and implemented. In this article, the relationship between BE and gastroesophageal reflux disease, risk for adenocarcinoma, and prospects for molecular diagnosis are discussed.
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PMID:Barrett's Metaplasia: defining the problem. 1636 8

The incidence of esophageal cancer has increased dramatically in the Western population in the last 2 decades. In 1975, about three fourths of the esophageal neoplasms were squamous cell carcinomas and the remainder were adenocarcinomas. During the last 2 to 3 decades, this pattern has changed dramatically and the incidence of squamous cell carcinomas has declined while the incidence of adenocarcinomas has increased. The reason for this dramatic increase is not clear, but gastro esophageal reflux disease, obesity and Barrett's esophagus have been identified as risk factors. High grade dysplasia in Barrett's esophagus is a premalignant condition which can progress to invasive adenocarcinoma. In this article, we discuss the natural history of high grade dysplasia (HGD), difficulties in the diagnosis, the incidence of adenocarcinoma in resected specimens and the surgical aspects in the treatment of HGD, including minimally invasive esophagectomy.
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PMID:Surgical aspects of the patient with high-grade dysplasia. 1642 39

Although significant advancements have been made in the treatment of esophageal cancer, this aggressive malignancy commonly presents as locally advanced disease with a poor prognosis. Despite improvements in the detection of premalignant pathology, newer preventative strategies, and the development of more effective combination therapies, the overall incidence of esophageal carcinomas has risen. A clear association has been established between the development of esophageal cancer and Helicobacter pylori infection, gastroesophageal reflux disease, smoking, and heavy alcohol use. However, the growing number of newly diagnosed esophageal adenocarcinomas, despite widespread treatments with proton pump inhibitors and the eradication of H. pylori, leaves the medical community searching for more answers. There is a potential link between esophageal adenocarcinoma and obesity. Common presenting symptoms of esophageal cancer are dysphagia, odynophagia, and progressive weight loss. The initial assessment for patients with these symptoms is made with double-contrast barium esophagraphy. Treatment modalities include surgery, chemotherapy, radiation therapy, or a combination of modalities. Prevention strategies include smoking and alcohol cessation.
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PMID:Esophageal cancer: a review and update. 1683 35

Recent studies indicate that the prevalence of reflux esophagitis (RE) in China is increasing. RE is one of the most common esophageal complications associated with gastroesophageal reflux disease (GERD) and RE-Barrett's esophagus-esophageal adenocarcinoma (EAC) sequence has been considered as an histogenesis model for EAC in Western countries. RE is only present in a subset of patients with GERD, suggesting an altered susceptibility to RE may exist in these GERD individuals. However, the genetic changes related with high susceptibility to RE is largely unknown. The polymorphisms in glutathione S-transferases (GSTs) T1, M1 and P1 have been reported with high susceptibity to esophageal cancer in Chinese people. The present case-control study was thus undertaken to characterize the genetic polymorphisms of GSTs and their correlation with susceptibility to RE. One hundred and nine patients with RE, 97 patients with nonerosive reflux disease (NERD) and 97 normal controls were recruited in this study. All the subjects were from Beijing, China, and received endoscopic examination and questionnaires for RE. Genomic DNA was extracted from the lymphocytes of peripheral blood for each subject. Genotypes of the GSTM1 and GSTT1 genes were analyzed by a multiplex PCR method. A-->G polymorphism of codon 104 of the GSTP1 gene was detected using PCR-based restriction fragment length polymorphisms (RFLP). The variant GSTP1 genotypes (*A/*Bomicron*B/*B) was found with a high frequency in the case with RE (40%), and followed by NERD (25%) and normal control (22%). The differences were statistically significant (P < 0.05). The risk for RE increased 2.42-fold [odds ratio (OR); 95% confidence interval (95% CI), 2.42 (1.22-4.80)] in the subjects with variant GSTP1 genotype. The subjects with positive variant GSTP1 genotypes and negative H. pylori infection showed increasing tendency for risk of RE [OR (95% CI), 2.67 (1.06-6.70)]. However, the subjects with GSTT1 and GSTM1 polymorphisms did not show any correlation with high risk for RE or NERD. No significant interactions were identified between the variant GSTs and cigarette smoking, or alcohol drinking and subtype of RE. The present result suggests that GSTP1 genetic polymorphism may be one of the high susceptibility factors involved in the mechanisms of RE. H. pylori infection may play a protective role against RE.
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PMID:Genetic polymorphisms in glutathione S-transferases T1, M1 and P1 and susceptibility to reflux esophagitis. 1706 92

Esophageal cancer remains an important public health problem worldwide. Understanding and preventing the occurrence of this cancer are complicated by the fact that the 2 major histologic types, squamous cell carcinoma (SCC) and adenocarcinoma (ACE), differ substantially in their underlying patterns of incidence and key etiologic factors. The main characteristic that they share is a high mortality rate. Surveillance, Epidemiology, and End Results data for the United States show a 30% drop in incidence of SCC between 1973 and 2002, with declines greatest in black males, although incidence in this group remains high compared with other groups. Incidence of ACE has increased 4-fold over the same period, with a nearly 5-fold increase in white males. Alcohol and smoking are major, established risk factors for SCC. Gastroesophageal reflux disease is consistently associated with increased risk of ACE, whereas infection with Helicobacter pylori may reduce its incidence. Increasing body mass index is also strongly associated with ACE risk while showing no association or an inverse relationship with SCC. Diet affects both types of esophageal cancer, with a higher intake of fruits and vegetables associated with reduced incidence. Aspirin and other nonsteroidal antiinflammatory drugs are currently the most promising chemoprevention candidates for both cancer types. Lifestyle changes, such as weight loss and exercise, are additional ways in which the incidence of ACE might be reduced.
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PMID:Epidemiology and pathogenesis of esophageal cancer. 1718 92

Long-standing gastro-oesophageal reflux disease (GORD) can give rise to Barrett's oesophagus (BM), a metaplastic condition and precursor to oesophageal adenocarcinoma (AC). Oesophageal cancer was once rare but is now the 5th biggest cancer killer in the U.K. Reflux of bile acids into the oesophagus is implicated in the progression to BM as bile acids at pH 4 have been shown to induce c-myc expression, an oncogene upregulated in BM and AC. In the present study we investigated the role of the biopolymer alginate on bile acid induced molecular changes in oesophageal cell lines. OE21, OE33 and TE-7 oesophageal cell lines were exposed to 100 microM deoxycholic acid at pH 4 in the presence or absence of alginates. Levels of c-myc, E-cadherin, beta-catenin and Tcf signalling were determined by Real-Time PCR, Western blotting, immunofluoresence and reporter assays. All alginates tested were able to prevent the induction of c-myc by acidified deoxycholic acid in vitro. The upstream effects of acidified deoxycholic acid on E-cadherin, beta-catenin and Tcf signalling were also suppressed by alginate. Therefore, we have demonstrated that reflux of bile acids into the oesophagus initiates a potentially damaging molecular cascade of events using an in vitro model and that a biopolymer, alginate, can protect against these effects.
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PMID:The effect of alginates on deoxycholic-acid-induced changes in oesophageal mucosal biology at pH 4. 1747 68

Bile reflux may play a key role for esophageal carcinogenesis in reflux disease. In search for bile-specific effects, the animal model of esophageal cancer was applied in a mutagenesis assay. Big Blue transgenic mice were operated with microsurgical techniques. Seven had total gastrectomy with esophagojejunostomy creating esophageal reflux of bile and five had a sham operation. After 24 weeks, the mutation frequency (MF) was measured through standard Big Blue mutagenesis assay in the esophageal mucosa and the duodenum as control. Esophageal reflux resulted in esophagitis in the distal esophagus. The MF in esophageal mucosa was 1.6 times higher in animals with reflux than in sham-operated animals; it was identical in the duodenum. In conclusion, the mutagenic potential of bile reflux has been confirmed. However, mechanisms of carcinogenesis in the esophageal cancer model other than chronic inflammation could not be identified because of the only moderately increased MF.
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PMID:Carcinogenesis in reflux disease--in search for bile-specific effects. 1792 60


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