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)

Barrett's carcinoma occurred in 66 of 331 patients with adenocarcinomas of the esophagus or gastroesophageal junction. Only 32 (46%) of these patients had a history of gastroesophageal reflux. A history of alcohol and tobacco abuse was absent in 50% and 47.5%, respectively. The mean length of Barrett's metaplasia was 7.37 cm. Operability was 98.5% and resectability 95.5%. No postoperative or hospital deaths occurred. Pathologic staging was as follows: stage 0 and I, 38.3%; stage II, 20.6%; stage III, 22.2%; and stage IV, 19%. Overall survivals were 80.5% at 1 year, 62.7% at 2 years, and 58.2% at 5 years. Five-year survival for patients with stage I disease was 100%; for stage II, 87.5%; for stage III, 22.2%; and for stage IV, 0%. Thirty-four (51.5%) patients were under surveillance for a related or unrelated condition before diagnosis of their carcinoma; only nine (26.5%) had diseased lymph nodes. In 32 the diagnosis was made at their first medical contact, and 78% of them had diseased lymph nodes. Five-year survival without nodal metastasis was 85.3% and significantly better than for patients with metastasis, 38.3% (p = 0.0033). Of the 66 patients, 19 (28.7%) had a biopsy-proved history of Barrett's metaplasia before malignancy developed. Mean time interval between diagnosis of metaplasia and degeneration was 3.8 years (89.5% > 1 year). Over the surveillance period, the length of metaplastic Barrett's esophagus remained unchanged in all patients. Barrett's ulceration was present from the beginning in 14 patients, and three patients never had an ulcer. Intestinal metaplasia was seen in 18 patients. Resected specimens revealed severe dysplasia in 16 patients. Of the 19 patients, 73.7% had stage I disease. Our data suggest that close endoscopic monitoring and systematic biopsies of the smallest irregularities in the metaplastic mucosa may result in early detection of carcinoma. In this respect, patients with an ulcer within a zone of intestinal metaplasia seem to be at risk. Early detection increases substantially the chances for cure by diminishing the risks of lymph node involvement. Resection remains the treatment of choice in Barrett's adenocarcinoma including high-grade dysplasia, because mortality can be kept low with excellent to very good functional results in the majority of the patients provided the intervention is performed by experienced teams.
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PMID:Surgical treatment of Barrett's carcinoma. Correlations between morphologic findings and prognosis. 815 27

Smoking and alcohol consumption predispose to oesophageal mucosal damage and exacerbates gastro-oesophageal reflux. The alcohol and smoking habits of patients with severe oesophagitis (n = 24), Barrett's columnar lined oesophagus (CLO) (n = 58), and adenocarcinoma arising in CLO (n = 23) were studied. There was no significant difference between the age (median 67, 64, and 65 years respectively) or duration of symptoms (median 10 years) in each group. Patients with benign CLO were significantly more likely to be non-smokers and non-drinkers, or both than patients with both severe oesophagitis and adenocarcinoma (p < 0.001). Of those who smoked or drank, patients with CLO had a smoking history of a median 15 pack years (range 2-60 pack years), which was less than both the severe oesophagitis (median 45.5, range 5-150 pack years) (p < 0.01), and adenocarcinoma groups (median 55.25, range 4-200 pack years) (p < 0.001). Patients with adenocarcinoma had smoked for more years in total (median 38.5, range 4-54 years) than patients with CLO (median 29.5, range 6-55 years) (p < 0.01). Patients with severe oesophagitis (median 38.5, range 27-55 years) and adenocarcinoma patients had a similar long history of smoking both of which were greater than CLO patients (p < 0.003). Half of the severe oesophagitis group drank more than 40 units/week and six more than 100 units/week (median 40, range 1-->100 units/week), whereas CLO patients who drank did so more moderately (median 10, 1-100 units/week) (p < 0.02). Adenocarcinoma patients also had a somewhat greater alcohol intake than CLO patients, median 15 (1-100 units/week) (p<0.02). Smoking and alcohol consumption do not predispose to the development od metaplastic columnar lined oesophagus in patients with severe gastro-oesophageal reflux but are strongly associated with the development of adenocarcinoma in patients with established Barrett's oesophagus.
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PMID:The role of smoking and alcohol in metaplasia and cancer risk in Barrett's columnar lined oesophagus. 831 2

Barrett esophagus was found in seven members of a single family. Two of these patients also had adenocarcinoma of the gastroesophageal junction. Among family members who did not have Barrett epithelium, one had esophageal ulcerations with dysplasia in squamous epithelium and another had an esophageal stricture. The pattern of involvement suggests autosomal dominant inheritance of Barrett esophagus and/or gastroesophageal reflux disease in this family, with a strong predisposition for adenocarcinoma of the esophagus.
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PMID:Familial Barrett esophagus and adenocarcinoma of the gastroesophageal junction. 834 64

Barrett's esophagus (i.e. columnar epithelial metaplasia in the distal esophagus) is an acquired condition that in most patients results from chronic gastroesophageal reflux. It is a disorder of the white male in the Western world with a prevalence of about 1/400 population. Due to the decreased sensitivity of the columnar epithelium to symptoms, Barrett's esophagus remains undiagnosed in the majority of patients. Gastroesophageal reflux disease in patients with Barrett's esophagus has a more severe character and is more frequently associated with complications as compared with reflux patients without columnar mucosa. This appears to be due to a combination of a mechanically defective lower esophageal sphincter, inefficient esophageal clearance function, and gastric acid hypersecretion. Excessive reflux of alkaline duodenal contents may be responsible for the development of complications (i.e., stricture, ulcer, and dysplasia). Therapy of benign Barrett's esophagus is directed towards treatment of the underlying reflux disease. Barrett's esophagus is associated with a 30- to 125-fold increased risk for adenocarcinoma of the esophagus. The reasons for the dramatic rise in the incidence of esophageal adenocarcinoma, which occurred during the past years, are unknown. High grade dysplasia in a patient with columnar mucosa is an ominous sign for malignant degeneration. Whether an esophagectomy should be performed in patients with high grade dysplasia remains controversial. Complete resection of the tumor and its lymphatic drainage is the procedure of choice in all patients with a resectable carcinoma who are fit for surgery. In patients with tumors located in the distal esophagus, this can be achieved by a transhiatal en-bloc esophagectomy and proximal gastrectomy. Early adenocarcinoma can be cured by this approach. The value of multimodality therapy in patients with advanced tumors needs to be shown in randomized prospective trials.
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PMID:Barrett's esophagus: pathogenesis, epidemiology, functional abnormalities, malignant degeneration, and surgical management. 835 51

Barrett's oesophagus is a pre-malignant condition with an increased risk of adenocarcinoma. The prevalence of adenocarcinoma in Barrett's oesophagus is about 10% but its true incidence in the general population is unknown. The development of adenocarcinoma in Barrett's oesophagus is a multi-step process. Gastro-oesophageal reflux symptoms are absent in many Barrett's patients and both Barrett's oesophagus and adenocarcinoma are usually but not always diagnosed simultaneously. When a carcinoma is identified, the treatment of choice is resection. Three-stage oesophagectomy is considered the most appropriate procedure. The prognosis of Barrett's carcinoma is dismal and the survival rate is related to stage of the tumour. However, encouraging results have been reported in the past 5 years. Endoscopic surveillance for Barrett's oesophagus is still a controversial topic but for some high-risk subgroups of patients regular surveillance is advocated. At the present time, dysplasia is the best available indicator of malignancy in Barrett's oesophagus.
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PMID:Malignant Barrett's oesophagus. 842 76

Earlier studies with monoclonal antibody (mcAb) DD9E7 have identified a family of nonspecific cross-reacting antigen (NCA)-related antigens that are highly expressed in human pancreatic adenocarcinoma. To analyse the molecular nature of these glycoproteins further, a lambda gt11 expression library has been constructed from the GER pancreatic adenocarcinoma cell line and screened with an NCA sequence-specific oligonucleotide probe. Sequence analysis and restriction enzyme mapping of the clones isolated have shown that they are all homologous with the NCA-50 protein core sequence rather than other related members of the carcinoembryonic antigen/NCA gene family. With use of the same probe, a 2.5-kb mRNA transcript, characteristic of NCA-50, was found in pancreatic adenocarcinoma tumour samples. This study suggests that the 80- to 115-kDa glycoproteins, which we had previously identified in pancreatic adenocarcinomas with NCA-specific mcAb DD9E7, are the result of aberrant glycosylation of the NCA-50 protein core following cell transformation.
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PMID:The protein core of the NCA-related pancreatic adenocarcinoma-associated antigen (DD9-Ag) is NCA-50. 846 91

A clinico-pathological study was carried out in two series of patients in order to determine: the prevalence of adenocarcinoma in Barrett's oesophagus in patients undergoing surgical resection for columnar cancer of the oesophagus, the incidence of Barrett's oesophagus in patients with complications of gastro-oesophageal reflux, and the subsequent cancer development in 3-20 years follow-up of such patients, compared with others who had no Barrett's oesophagus. Group 1 consisted of 264 patients with adenocarcinoma of the oesophagus undergoing resection and reconstruction; 18 (6.8%) had concomitant carcinoma and Barrett's oesophagus. These were predominantly male (male/female ratio 8/1) and had worse long-term survival than the other adenocarcinomas. Group 2 consisted of 782 patients with complications of gastro-oesophageal reflux, 26 (3.3%) of whom were found to have Barrett's oesophagus. When followed up for a period of up to 20 years, 4 (15.4%) of these developed cancer in the mean period of 11.5 years (1 case per 74 person-years). This is highly significant compared with 4 others (0.5%) who developed cancer amongst the 756 remaining patients in group 2 with no Barrett's oesophagus, in the mean interval of 8 years 2 months (1 case per over 1500 person-years). Of the 18 patients with Barrett's stricture, 4 (22%) developed cancer at a mean interval of 11.5 years representing one case per 51.7 person-years indicating a higher risk of cancer development in patients with Barrett's stricture compared with other patients with complications of gastro-oesophageal reflux with/without columnar epithelial-lined oesophagus and no stricture. Anti-reflux operation has not protected our patients with Barrett's oesophagus against cancer development.
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PMID:Adenocarcinoma and Barrett's oesophagus. A clinico-pathological study. 846 Nov 44

We describe an oesophageal tumour composed of choriocarcinoma, hepatoid adenocarcinoma, small cell carcinoma and tubular adenocarcinoma. The choriocarcinomatous areas and hepatoid adenocarcinomatous areas contained beta human chorionic gonadotropin-positive cells and alpha fetoprotein-positive cells, respectively. The small cell carcinomatous areas contained cells positive for serotonin or adrenocorticotrophic hormone, while the tubular adenocarcinomatous areas contained cells positive for carcinoembryonic antigen. Non-neoplastic gastric type columnar epithelium was found directly adjoing the tumour at the oral side. This tumour, with its unprecedented histology combination of tissues may have originated in Barrett's oesophagus, although we could not confirm a history of chronic gastro-oesophageal reflux.
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PMID:Combined choriocarcinoma, hepatoid adenocarcinoma, small cell carcinoma and tubular adenocarcinoma in the oesophagus. 854 32

Complications of Barrett's esophagus include ulceration, stricture, hemorrhage, perforation, and the development of malignancy. Barrett's esophagus and adenocarcinoma may be diagnosed simultaneously and that gastroesophageal reflux symptoms may be absent in many cases. Although endoscopic surveillance is justified, no agreement on the frequency can be made. Survival of patients with adenocarcinoma in Barrett's esophagus depends on the stage at diagnosis.
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PMID:Barrett's esophagus: a review. 855 27

Barrett's esophagus (BE) is a metaplastic change of the squamous esophageal epithelium to columnar gastric or intestinal-like epithelium. BE is associated with long-standing gastroesophageal reflux disease and carries an increased risk for dysplasia and adenocarcinoma. Little if any is known regarding the differentiation state of esophageal metaplasia and its relationship to carcinogenesis. In this study, we investigated the potential of villin, a cytoskeletal protein, and Ep-CAM, a glandular epithelial glycoprotein, to serve as markers for enterocytic differentiation in BE at the molecular level. Endoscopic mucosal biopsy samples of normal esophagus, BE, stomach and duodenum were collected from 23 patients with BE. Biopsies were analyzed for villin and Ep-CAM expression by immunoblotting, and in some cases for the presence of microvilli by electron microscopy. By mapping of BE segments in 6 patients, correlations were also made between the histologic evidence of metaplasia and villin expression. Villin was uniformly expressed in all duodenal samples but was not detected in normal esophagus and stomach. In BE biopsies, villin expression was limited to the subset of patients whose adjacent biopsies showed microvilli by electron microscopy. In several patients studied, however, the expression of villin and the epithelial glycoprotein Ep-CAM differed among various regions of esophageal metaplasia within the same patient. Mapping studies failed to reveal any correlation among histologic evidence of metaplasia, dysplasia and villin expression and confirmed the multifocal heterogeneity of villin expression in BE. Preliminary data of 4 adenocarcinoma patients studied showed that villin expression was absent in 3 and very low in 1 patient. Ep-CAM was highly expressed in all adenocarcinoma patients. Our results show that BE represents a complex epithelium with significant heterogeneity in antigen expression and ultrastructural morphologic features. This molecular heterogeneity supports the presence of different stages of differentiation within the same epithelium.
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PMID:Multifocal heterogeneity in villin and Ep-CAM expression in Barrett's esophagus. 860 65


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