Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Barrett's esophagus is the premalignant lesion for adenocarcinoma of the esophagus and the esophagogastric junction. The incidence of esophageal adenocarcinoma has been rapidly rising in the Western world over the last two decades, and Barrett's esophagus is the only known premalignant lesion for this cancer. Esophageal adenocarcinoma develops through the metaplasia-dysplasia sequence with progression from no dysplasia, low grade dysplasia, high grade dysplasia, and ultimately to esophageal adenocarcinoma. The diagnosis and management of high grade dysplasia (HGD) in patients with Barrett's esophagus is extremely controversial. Patients with HGD within Barrett's esophagus are at the highest risk for development of esophageal adenocarcinoma if concurrent adenocarcinoma doesn't already exist. Given the high likelihood of metastatic disease and poor prognosis associated with invasive cancer, detection of HGD within Barrett's esophagus is considered by many as the final endpoint requiring definitive therapy in the form of surgical resection. However, other limited data seem to suggest that a number of patients with HGD may actually regress or persist and not develop cancer, thus suggesting a less aggressive approach for management. Finally with the advent of local endoscopic therapy, reversal therapy is being studied in patients with HGD and may be validated for this major indication. Currently, surgery remains the goal standard and the most definitive therapy for HGD. This articles critically reviews the risks and benefits associated with each approach of managing HGD.
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PMID:Controversies in Barrett's esophagus: management of high grade dysplasia. 1121 52

Oesophageal adenocarcinoma is believed to arise from metaplastic mucosa in the distal oesophagus, a condition also known as Barrett's oesophagus (BE). BE develops as a result of injury caused by refluxing gastric and duodenal contents and is associated with increased risk of malignant transformation. Matrix metalloproteinases (MMPs) have been implicated in all aspects of tumour progression; tumour growth, basement membrane degradation, invasion and metastatic spread. Using in situ hybridization, we investigated the expression patterns of collagenases-1 and -3, stromelysin-2, matrilysin, metalloelastase and TIMPs-1 and -3 in BE, adenocarcinoma and lymph-node metastases. Matrilysin was expressed abundantly in 12/15 tumours and in 4/6 lymph-node metastases and its expression correlated with the histological aggressiveness of tumour. Matrilysin and metalloelastase were upregulated already in BE. Stromelysin-2 and collagenase-3 expression was detected only in a few tumours. Collagenase-1 was expressed by cancer and stromal cells in 9/15 tumours. Tumour-infiltrating macrophages expressed metalloelastase in 13/15 cancers. TIMPs-1 and -3 were expressed in 12/15 and 11/15 tumours, respectively. Laminin-5 and tenascin were abundantly expressed at the invasive front of poorly differentiated tumours, but not in BE. Our results indicate that matrilysin is the principal MMP expressed by tumour cells in oesophageal adenocarcinoma, and further studies are needed to investigate whether matrilysin or tenascin-C could be used as a predictive marker for progression of BE to cancer.
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PMID:Upregulation and differential expression of matrilysin (MMP-7) and metalloelastase (MMP-12) and their inhibitors TIMP-1 and TIMP-3 in Barrett's oesophageal adenocarcinoma. 1148 70

We investigated the feasibility of using carbon-11 choline (CHOL) positron emission tomography (PET) for the staging of oesophageal cancer, in comparison with fluorine-18 fluorodeoxyglucose (FDG) PET, using histopathological findings as the gold standard. Eighteen patients were studied: 16 patients with cancer of the oesophagus or gastro-oesophageal junction and two with in situ carcinoma/high-grade dysplasia. PET imaging was performed 5 min (CHOL) or 90 min (FDG) after injection of 370 MBq of the tracer. PET images were analysed by two independent and blinded physicians using visual and standardised uptake value (SUV) analysis. PET results were compared with surgical and histopathological findings. FDG-PET was able to detect all (100%) of the 16 malignant primary lesions, while CHOL-PET detected 73%. In situ carcinoma ( n=1) and high-grade dysplasia ( n=1) were not visualised with either tracer. Diffuse uptake of the tracers was noted in areas of Barrett's oesophagitis. Twelve patients had locoregional metastases (N1) that were not detected with either FDG or CHOL. Six patients had additional distant nodal (M1a) metastases; four of six (66%) were visualised by FDG, and three of five (60%) by CHOL-PET. On a lesion basis, FDG-PET detected 10/12 non-regional metastases (sensitivity 83%), while CHOL-PET detected 5/12 (sensitivity 42%). Haematogenous distant metastases (M1b) were positive on FDG-PET in three of four patients, and on CHOL-PET in two of four. SUV values were significantly higher for FDG (FDG 6.6+/-3.5, CHOL 5.5+/-2.5, P=0.04). CHOL-PET is able to visualise oesophageal carcinoma and its metastases, but appears to be inferior to FDG-PET. Presumably this is the result of lower tumoural uptake and considerable non-specific uptake of CHOL in liver, stomach wall, pancreas and small intestine. Further studies are needed to confirm these data.
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PMID:Carbon-11 choline or FDG-PET for staging of oesophageal cancer? 1173 25

Alpha-fetoprotein (AFP)-producing esophageal tumors are extremely rare. We report herein the case of a 51-year-old man found to have an AFP-producing adenocarcinoma arising from esophageal proper mucosa. The patient presented for investigation of dysphagia, and esophagogram and endoscopy revealed a lesion about 2 cm in size with a depressed center surrounded by low nodular protrusions in the lower esophagus. The preoperative serum AFP concentration was elevated to 52.4 ng/ml. A subtotal esophagectomy was performed, and macroscopic examination of the resected specimen revealed a superficial protruding lesion. Histopathological studies showed a poorly differentiated adenocarcinoma with a single lymph node metastasis. The tumor had infiltrated the submucosal layer, but there was no evidence of lymphatic or venous invasion. Immunohistochemical study revealed tumor cells positive for AFP. There were no findings of Barrett's epithelium or any mucosal changes due to reflux esophagitis. An elevated AFP level 2 years after the operation led us to suspect tumor recurrence; however, diagnostic imaging studies showed no evidence of a recurrence or metastases. The serum AFP levels responded well to chemotherapy with transient decreased levels, but continued to rise until finally, 5 years after the operation, adenocarcinoma cells were detected in the pleural effusion. Thus, careful monitoring of the serum AFP levels at regular intervals could be a useful marker to indicate recurrence of esophageal carcinoma.
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PMID:Alpha-Fetoprotein-producing esophageal adenocarcinoma: report of a case. 1175 90

The need for radical subtotal esophagectomy and extensive lymphadenectomy in patients with early Barrett cancer, i.e. T1 tumors, is increasingly questioned. Based on the principles of surgical oncology, the precancerous nature of Barrett esophagus, and the high rate of lymph node metastases in patients with T1b tumors, the minimal extent of the procedure for early Barrett cancer must include the entire segment of the distal esophagus covered by intestinal metaplasia and a regional lymphadenectomy. In adequately selected patients this can be achieved by a limited surgical procedure with transhiatal resection of the distal esophagus and jejunum interposition, but not by endoscopic mucosal ablation or endoscopic mucosa resection. The high recurrence rates after endoscopic interventions does not support the use of these techniques in operable patients.
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PMID:[Endoluminal therapy of neoplastic changes in the gastrointestinal tract: Barrett esophagus--from the viewpoint of the surgeon]. 1182 35

Several case reports have emphasized that esophageal carcinoid tumors are associated with a poor prognosis. To expand our knowledge about the pathology and biologic behavior of these rare tumors, we reviewed the clinicopathologic and immunohistochemical findings of four cases of primary esophageal carcinoid. The age of the patients ranged from 48 to 82 years (mean 63 years; median 61 years). The lower segment of the esophagus was involved in two cases and the mid segment was involved in one case. The sizes of the tumors ranged from 0.3 cm to 3.5 cm. Two tumors were confined to the lamina propria and two invaded into the muscular wall. Two tumors appeared polypoid, whereas the remaining two were incidental findings and associated with adenocarcinoma arising in a background of Barrett esophagus. The adenocarcinoma was superficially invasive in one case, whereas it penetrated the muscular wall in the other. All four carcinoid tumors were immunoreactive with chromogranin and synaptophysin. There was focal expression of serotonin in two cases, glucagon in one case, and pancreatic polypeptide in one case. Endocrine cell hyperplasia was noted in both the Barrett esophagus and the invasive adenocarcinoma. One patient died secondary to postoperative pneumonia. Three patients are alive and disease free at 1, 6, and 23 years status post therapy. None of the patients had metastatic disease. These findings show that esophageal carcinoids are associated with a favorable prognosis. They arise in two settings: (1) a single large polypoid tumor or (2) an incidental finding and in association with adenocarcinoma arising in the background of Barrett esophagus. The presence of endocrine cell hyperplasia in the Barrett mucosa and the adenocarcinoma supports the hypothesis that these lesions arise from a common stem cell.
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PMID:Carcinoid tumor of the esophagus: a clinicopathologic study of four cases. 1191 32

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.
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PMID:Results of surgical therapy in patients with adenocarcinoma of the esophagus and cardia. 1195 79

The incidence rate of adenocarcinoma of the esophagogastric junction (AEG) is increasing in association with the epidemiologic rise in distal esophageal adenocarcinoma and gastric cardial (AEG type III) tumors. The overall survival rate is poor in most patients with AEG because lymph node or visceral metastases are frequently present at the time patients become symptomatic. A few patients are identified early in the disease because of screening for gastroesophageal reflux and Barrett's esophagus. Early stage AEG (T1N0 or T2NO, carcinoma in situ, or severe dysplasia ) can in many instances be cured with surgery alone. Ablative treatments for early stage AEG, including endoscopic fulguration by cautery and laser or photodynamic therapy, are investigational at this time. Locoregionally advanced AEG (T3, T4, N1, or M1a ) without distant systemic metastases (M1b) has a poor overall survival rate with surgery alone or definitive chemotherapy and radiation therapy without surgery. Analysis of the use of multimodality treatment strategies for locoregionally advanced AEG types I and II have demonstrated improved survival rates in two small phase III trials with preoperative concurrent chemoradiotherapy followed by surgical resection. In contrast, three small phase III trials with preoperative concurrent or sequential chemoradiotherapy in patients with predominantly squamous cell carcinoma did not demonstrate any clear survival advantage. Additionally, a randomized phase III study evaluating preoperative chemotherapy without radiation therapy in esophageal cancer (predominantly adenocarcinoma) has demonstrated no survival benefit. In light of these results, additional large randomized phase III studies are needed to confirm the potential benefit of preoperative concurrent chemoradiotherapy. At the present time, preoperative chemoradiotherapy remains investigational. For locoregionally advanced gastric adenocarcinoma, including AEG type III, postoperative concurrent 5-fluorouracil (5-FU)-based chemoradiotherapy is associated with improved survival as demonstrated in a recently completed random assignment trial (INT 0116). As a result, surgery with postoperative chemoradiotherapy has recently become the standard of care for patients with AJCC stage II and III gastric adenocarcinoma (including patients with AEG type III). Metastatic AEG (M1b) should be treated with palliative chemotherapy (in good performance patients) or supportive care (poor performance) in asymptomatic patients. Radiation therapy and endoscopic stent placement (expandable wire mesh) can be used to palliate dysphagia in patients with M1b disease. The development of expandable stents and improved radiotherapy has obviated surgical bypass to palliate patients with symptomatic, metastatic AEG.
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PMID:Gastroesophageal junction adenocarcinoma. 1205 46

The Barrett esophagus as the premalignent lesion for adenocarcinoma of the esophagus and the esophagogastric junction is of widespread interest. Endoscopy and histology are the diagnostic basis. Methylen blue staining and high-resolution endoscopes facilitate the diagnosis of Barrett esophagus. Use of a high resolution endoluminal ultrasound probe and optical coherence tomography are new methods for evaluating the local depth invasion of the Barrett mucosa. Accurate pretherapy staging for esophageal carcinoma is important for a stage--directed therapy. After endoscopy and histology the endoscopic ultrasound is the method of choice for local regional staging of esophageal carcinoma. Computed tomography and positron emission tomography were shown to be especially useful in detection of distant metastases.
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PMID:[Barrett esophagus--esophageal carcinoma: diagnosis]. 1207 Oct 89

Barrett's metaplasia develops in 6-14% of individuals with gastroesophageal reflux. Barrett's adenocarcinomas are increasing in epidemic proportions for as yet unknown reasons, approximately 0.5-1% of patients with Barrett's will develop adenocarcinoma. Heartburn duration and frequency (but not severity), male gender, and Caucasian race are major risk factors for developing cancer. Obesity and smoking are weak risk factors. Survival is determined by depth of tumor invasion (stage). Once invasion of the muscularis propia occurs, the vast majority of patients will have developed widespread metastasis, even when clinical staging studies are negative. No currently available therapy results in prolonged survival once metastases develop. Thus, the more widespread use of effective surveillance strategies is the only currently available means for reducing the morbidity and mortality associated with Barrett's adenocarcinoma.
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PMID:Barrett's esophagus: clinical characteristics. 1213 12


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