[Roentgenologic studies of the esophagogastric junction in infants with esophagogastric junction insufficiency].
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Esophageal Diseases↗
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Results for “ESOPHAGOGASTRIC JUNCTION”
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Adenocarcinoma of the esophagogastric junction: a summary of responses to a questionnaire on adenocarcinoma of the esophagus and the esophagogastric junction in Japan.
Adenocarcinoma of the esophagogastric junction is recognized as a distinct clinical entity; however, the choice of surgical approaches is controversial. To analyze the results of surgery among patients with adenocarcinoma of the esophagus (type I) and the cardia (type II) based on Siewert's classification in Japan, surgical procedures, histopathologic characteristics, and outcome were re-evaluated according to the TNM classification in 1263 patients with adenocarcinoma of the esophagus (type I) and the cardia (type II) through a questionnaire sent to the members of the Japanese Society of Esophageal Diseases. One hundred and thirty-four (10.6%) patients had type I tumors and 1129 (89.4%) patients had type II tumors. There were significant differences in sex distribution and associated intestinal metaplasia in the esophagus between patients with type I and type II tumors. Although different surgical approaches were performed, the overall 5-year survival rate was 53% without any difference between the two groups. The significant prognostic factors in general linear models were R category, pN category, and differentiation, but not pT category. There was no difference in survival between patients with stage IIB and III disease. The survival rate of the patients who underwent a transhiatal approach was similar to that of those undergoing a transthoracic approach. The results suggest that Siewert's classification (type I and type II) is useful in planning treatment strategy for adenocarcinoma of the esophagogastric junction. Lymph node metastasis was the most important prognostic factor, and staging based on the number of lymph node metastases or the extent of lymph node metastasis is necessary.
Adenocarcinoma↗
[Scanning and translucent electron microscopic observations on squamo-glandular junctions in the esophagogastric junction].
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Desmosomes↗
Adjuvant (cisplatin, etoposide, and 5-fluorouracil) chemotherapy after curative resection of gastric adenocarcinomas involving the esophagogastric junction.
Gastric adenocarcinomas involving the esophagogastric junction represent a particular therapeutic problem because they lie in the border area between two body cavities: the thorax and the abdomen. The prognosis of gastric adenocarcinomas involving esophagogastric junction is poor because there is widespread lymphatic metastasis, making curative resection difficult. Even in patients with localized disease who are potentially curable, the 5-year survival rate is approximately 20% with curative resection only, somewhat lower than for those with cancer elsewhere in the stomach. The authors conducted a pilot study to evaluate the safety and possible efficacy of adjuvant chemotherapy with cisplatin, etoposide, and 5-fluorouracil (PEF) after curative resection of gastric adenocarcinoma involving esophagogastric junction. Three cycles of adjuvant PEF chemotherapy with cisplatin (20 mg/m2/day intravenously on days 1-5), etoposide (100 mg/m2/day intravenously on days 1, 3, and 5), and 5-fluorouracil (800 mg/m2/day continuous intravenous infusion on days 1-5) were given every 3 weeks after curative resection of gastric adenocarcinoma involving the esophagogastric junction. Between November 1989 and June 1995, a total of 50 patients with postoperative stage II, IIIA, or IIIB disease entered this trial. In 14 of 50 patients (28%), the disease recurred during the follow-up of 4-83 months (median 26 months). Disease-free survival was 4-83+ months (median 48 months), and the actuarial 5-year disease-free survival rate was 48% (95% CI: 41% to 55%). Overall survival was 4-83+ months (median 62 months), and the actuarial 5-year survival rate was 54% (95% CI: 40% to 68%). The prognostic factor analysis showed that the postoperative N stage and the interval between surgery and chemotherapy affected disease-free survival and overall survival. The toxicities of PEF adjuvant chemotherapy were leukopenia, nausea/vomiting, and alopecia, but they were mostly mild and reversible except in one patient who died because of treatment-related sepsis. Adjuvant chemotherapy with three cycles of PEF regimen was well tolerated and seems to be a promising treatment for gastric adenocarcinoma involving the esophagopstric junction, in comparison with previous treatments. To define the efficacy of adjuvant PEF chemotherapy for gastric adenocarcinoma involving esophagogastric junction, prospective randomized trials are warranted.
Adenocarcinoma↗
Screening of molecular biomarkers ASPN and LBH and construction of a prediction nomogram for the progression of esophagogastric junction adenocarcinoma.
BACKGROUND: Esophagogastric junction adenocarcinoma (EGJA) is an aggressive malignancy of the digestive system with poor prognosis. Early diagnosis and accurate prediction of tumor progression remain major clinical challenges. This study aimed to identify and validate molecular biomarkers and construct a precise diagnostic model, providing a scientific basis for individualized treatment. METHODS: Differentially expressed genes (DEGs) associated with EGJA were identified using The Cancer Genome Atlas (TCGA) database. Quantitative real-time polymerase chain reaction (qRT-PCR) was then performed for further screening. The protein expression levels of ASPN and LBH were validated by immunohistochemistry in both tumor and adjacent non-tumor tissues. A nomogram was constructed by integrating clinical and pathological features, and its performance and clinical utility were assessed using receiver operating characteristic (ROC) curves and decision curve analysis (DCA). RESULTS: Immunohistochemistry demonstrated that the protein expression of ASPN was significantly upregulated in tumor tissues, with expression levels increasing with tumor stage. Conversely, LBH was downregulated in tumor tissues and decreased with advancing stages. The predictive model achieved an area under the curve (AUC) value of 0.977, indicating excellent diagnostic and prognostic performance. DCA confirmed the clinical net benefit of the model. CONCLUSIONS: ASPN and LBH are critical molecular biomarkers for EGJA. The nomogram combining these two markers enables accurate distinction between early and advanced-stage tumors, offering significant support for early diagnosis of EGJA.
ASPN↗
[Pancreas like acinar glands in the esophagogastric junctional mucosa].
Esophagogastric material resected for malignancy, obtained from 52 adult patients, was examined histologically. In a longitudinal examination of 32 total gastrectomies, intramucosally located pancreatic acinar cell-like cells (PALC) were observed frequently (10 of 12 patients, p < 0.05) only in the uppermost one-sixth part, especially in a 10 mm-long zone around the squamocolumnar junction (SCJ). Entire sampling of the junctional mucosa revealed no significant difference in frequency of occurrence of PALC between esophageal and gastric cancer groups (13 of 20 patients, 20 of 31 patients, respectively). In 59 sections examined precisely, 43 sections showed zonal atrophy of the gastric glands. More than half of these zones (25 of 44 zones) did not overlap with 4 mm-long SCJ zones. In the latter zones, stratified columnar epithelia, epithelial islands, and PALC were observed more frequently, although intestinal metaplasia was not. These data suggested that the occurrence of PALC is correlated with the anatomical site, i.e. SCJ, but not with such ill conditions, i.e. atrophic gastritis or gastric cancer. PALC in the SCJ may be orthotopic.
Adenocarcinoma↗
[Limited surgical resection versus local endoscopic therapy of early cancers of the esophagogastric junction].
BACKGROUND: Adenocarcinomas of the esophagogastric junction (especially Barrett's cancers) are increasingly diagnosed at early stages. The current standard treatment - radical resection with extensive lymphadenectomy - has been challenged. Limited resection or endoscopic mucosal ablation have been proposed as less invasive alternatives. METHODS: Available data regarding limited surgical resections and endoscopic interventional procedures are evaluated with respect to short- and long-term results (mortality, morbidity, oncologic adequacy, quality of life). RESULTS: Limited resection of the esophagogastric junction has been proven as safe (low morbidity and mortality) and oncologically adequate procedure (low rate of recurrence/excellent long-term survival) with good quality of life. The procedure meets the oncological requirements (R0-resection, complete resection of potentially tumor-infiltrated lymph nodes and the entire precancerous Barrett's esophagus). Reconstruction with interposition of a pedicled isoperistaltic jejunal loop prevents reflux and is crucial for achieving good postoperative quality of life. In contrast, endoscopic mucosal resection (EMR) carries the risk of high recurrence rates (at least 30 %). This has to be regarded as an effect of the frequent incomplete resection, multicentric tumor growth, the persistence of precancerous Barrett's mucosa and persistence of gastroesophageal reflux. Consequently, from the oncological view point, EMR is only suited for unicentric mucosal tumors (T1a) in short segments of Barrett's esophagus. Reliable preoperative identification of such tumors is, however, currently not possible. CONCLUSION: For adequately selected patients with early Barrett's cancer, limited resection of the esophagogastric junction is an appropriate procedure. Endoscopic mucosa resection (EMR) might gain importance as staging tool.
Adenocarcinoma↗
Epidemiology of adenocarcinoma of the esophagogastric junction.
The incidence of adenocarcinoma of the esophagogastric junction has increased rapidly in the later half of the twentieth century in the United States and most western countries. Although squamous cell carcinoma of the esophagus used to predominate, adenocarcinoma of the distal esophagus and esophagogastric junction now accounts for more than half of new diagnoses in western countries. There also has been a shift from the development of distal gastric cancers to ones in a more proximal location. These recent epidemiologic shifts have led to controversy regarding the etiology and treatment of adenocarcinoma of the esophagogastric junction. Uncertainty still exists with regards to nomenclature and classification, risk factors, treatment, and screening and surveillance of esophagogastric adenocarcinoma. This article examines the epidemiology and etiologies of adenocarcinoma of the esophagogastric junction.
Adenocarcinoma↗
Lymph node micrometastases in patients with adenocarcinoma of the esophagogastric junction.
Recurrences of adenocarcinoma of the esophagogastric junction are frequent even in patients who are classified as pN0 after radical resection, suggesting that occult nodal metastases may have been missed on routine histologic examination. Immunohistochemical analysis using antibodies to cytokeratin was retrospectively performed in 1301 lymph nodes from 46 patients who underwent surgical resection for adenocarcinoma of the esophagogastric junction through a laparotomy and a right thoracotomy. Compared to routinely stained sections, the total number of metastatic lymph nodes was significantly (P = 0.0001) increased when both serial sectioning and anticytokeratin immunohistochemical analysis were performed. Overall 6 (33.3%) of the 18 patients previously considered N0 were recategorized as N1 for the presence of micrometastases to lesser curvature nodes. Three of these patients had recurrent disease within the first year of follow-up. Both the probability of survival or no recurrence and the disease-free survival were significantly greater in patients in whom the ratio of invaded to removed lymph nodes was less than 0.2. Anticytokeratin analysis identified occult nodal metastases in one third of our patients with adenocarcinoma of the esophagogastric junction. This modified tumor staging and had an impact on overall and disease-free survival.
Adenocarcinoma↗
[Does incidence of carcinoma of the esophagogastric junction increase?].
The incidence of carcinoma of the esophagogastric junction was evaluated based on data from the Japanese Esophageal Cancer Registry during the periods 1976-1994 and the Japanese Gastric Cancer Registry during 1963-1989. Although the number of cases of carcinoma of the esophagogastric junction had increased, the incidence was evaluated to have decreased. On the other hand, there are some reports that the incidence of carcinoma of the esophagogastric junction and the cardia have increased in the USA and western European countries. The trend is controversial and it is necessary to evaluate the location of lesions accurately. Possible explanations for the increasing trend etc. therefore are smoking and alcohol intake, Helicobacter pylori infection, hiatal hernia. To determine the incidence of carcinoma of the esophagogastric junction more reliably, the nationwide cancer registry program should continue.
Esophageal Neoplasms↗
Adenocarcinoma of the esophagogastric junction.
Adenocarcinoma of the esophagogastric junction (EGJ) has increased rapidly in incidence in the latter half of the twentieth century. The increase in incidence has affected white men between the ages of 40 and 60 disproportionately. Understanding the etiology and improving treatment requires careful classification of EGJ tumors. A recent consensus conference recognized three types of EGJ adenocarcinomas: distal esophageal, cardia, and subcardia gastric. Distal esophageal adenocarcinomas are associated with Barrett's esophagus. Helicobacter pylori infection may play a role in some adenocarcinomas of the subcardia, but the association is unproven. Therapy for all types of EGJ tumors is surgical, but multimodal forms of treatment are commonly used because of the advanced stage at which these tumors often present. Several endoscopic options exist for primary therapy of early-stage tumors and for palliation.
Adenocarcinoma↗
[Cancer at the esophagogastric junction].
The definition of cancer at the esophagogastric junction has been discussed for over 30 years. Although at present, two classifications advocated by Nishi or Siewert have been used, these classifications are still controversial from the viewpoints of anatomy, physiology, histology, diagnosis and treatment. We should analyze a large number of patients based on the same definition of cancer at the esophagogastric junction. Adjustment of the Japanese rules for cancer of the esophagus and stomach is necessary, and a treatment strategy should be established for cancer at the esophagogastric junction.
Adenocarcinoma↗
Prevalence and risk factors associated with specialized intestinal metaplasia at the esophagogastric junction.
BACKGROUND/AIMS: Specialized intestinal metaplasia around the esophagogastric junction is considered to be premalignant. The aim of this study was to examine prospectively the prevalence of metaplasia and to correlate its presence with clinical, endoscopic and histological findings. METHODOLOGY: In 101 symptomatic patients (40 women, 61 men; mean age: 55 yr, range: 20-79 yr), biopsies were taken from gastric type mucosa just distal to the esophagogastric junction. They were stained with hematoxylin and eosin and alcian blue-periodic acid Schiff for the detection of specialized intestinal metaplasia and inflammation of the cardiac mucosa (carditis) and with Warthin-Starry for H. pylori presence. RESULTS: Metaplasia was detected in 27 patients (26.7%). Multiple logistic regression analysis revealed that metaplasia was associated significantly with age (odds ratio, 2.8; 95% confidence interval, 1.2-6.6), endoscopic suspicion of short segment Barrett's esophagus (odds ratio, 3.6; 95% confidence interval 2.2-6.9), detection of H. pylori (odds ratio, 2.8; 95% confidence interval, 1.1-7) and presence of carditis (odds ratio, 6.4; 95% confidence interval, 2.8-16.8). CONCLUSIONS: The prevalence of specialized intestinal metaplasia around the esophagogastric junction is high in symptomatic patients. Age, endoscopic evidence of short segment Barrett's esophagus and histological presence of H. pylori and carditis are independent risk factors associated with its presence.
Adenocarcinoma↗
The pattern of metastatic lymph node dissemination from adenocarcinoma of the esophagogastric junction.
BACKGROUND: The incidence of adenocarcinoma of the esophagogastric junction is rapidly increasing, and the extent of lymphadenectomy for such tumors remains controversial. The aim of this study was to identify the pattern of dissemination by examination of all lymph nodes retrieved from resected tumors of the esophagogastric junction. METHODS: The endoscopic and pathologic reports of patients who underwent RO resection for adenocarcinoma of the esophagogastric junction between January 1996 and November 1999 were examined. Patients with type 1 tumors (distal esophagus) underwent subtotal esophagectomy with 2-field lymphadenectomy. Patients with type 2 (gastric cardia) tumors underwent transhiatal D2 total gastro-esophagectomy. Lymph node groups were dissected from the main specimens and examined separately. RESULTS: One hundred and four type 1 and 48 type 2 tumors were studied. Median nodal recovery was 23 lymph nodes (type 1, 22 lymph nodes; type 2, 23 lymph nodes). Seventy-eight percent of the type 1 tumors with nodal metastases had dissemination in both the abdomen and mediastinum. The common abdominal sites were the paracardiac and the left gastric stations. Within the mediastinum, paraesophageal, paraaortic and tracheobronchial metastases were more often encountered. Type 2 tumors had positive lymph nodes most frequently in the left and right paracardiac, lesser curve (N1 group), and left gastric (N2 group) territories. Nodal status correlated with increasing depth of tumor invasion (P =.002). CONCLUSIONS: The pattern of nodal dissemination for cardia tumors concurs with that described by other studies. The current definition of nodal fields in the abdomen and mediastinum for esophageal tumors relates to experience with squamous carcinomas. Our results demonstrate a different pattern of dissemination for junctional esophageal adenocarcinomas. The nodal stations to be resected in radical lymphadenectomies for such tumors should be redefined.
Adenocarcinoma↗
The location and frequency of intestinal metaplasia at the esophagogastric junction in 223 consecutive autopsies: implications for patient treatment and preventive strategies in Barrett's esophagus.
The frequency of intestinal metaplasia at the esophagogastric junction is as high as 36% in endoscopy studies; the majority of cases (approximately 67%) occur in short segments of esophageal columnar mucosa. The validity of these studies has been questioned, however, because of heterogenous underlying diseases prompting endoscopy. To determine the frequency and origin of intestinal metaplasia at the esophagogastric junction, we histologically evaluated the entire esophagogastric junction for the presence of intestinal metaplasia using Alcian blue/periodic acid-Schiff mucin stains in 223 consecutive autopsies. Precise localization of the Z line in relation to the esophagogastric junction and tongues of esophageal columnar-appearing mucosa were noted in each case. Mean patient age was 47 years; 69% of patients were male, and 63% were white. Twenty five of 223 cases (11%) had intestinal metaplasia at the esophagogastric junction. Only 2 of 25 cases (8%) had intestinal metaplasia in the esophagus; the remaining 23 cases (92%) had intestinal metaplasia in the gastric cardia. Male gender, advanced age, white ethnic origin, and short tongues of esophageal columnar mucosa were not associated with gastric cardia intestinal metaplasia. An association of distal gastric intestinal metaplasia (P < .01) and chronic gastritis (P < .01) with gastric cardia intestinal metaplasia suggests a role for Helicobacter pylori infection in this process. The frequency of intestinal metaplasia at the esophagogastric junction in an unselected autopsy population is low (11%) even after exhaustive histologic evaluation using Alcian blue mucin stains. Furthermore, intestinal metaplasia is confined to the gastric cardia in more than 90% of cases with no association to male gender, white ethnic origin, advanced age, or the presence of short segments of esophageal columnar-appearing mucosa at endoscopy. These results demonstrate that caution is warranted when applying the findings of endoscopy studies to the development of preventive and screening strategies aimed at identifying Barrett's esophagus in an asymptomatic general population.
Adolescent↗
The significance and etiology of intestinal metaplasia of the esophagogastric junction.
Biopsies from the vicinity of the esophagogastric junction occasionally show foci of intestinal metaplasia. Whether these biopsies represent Barrett's esophagus in all cases is controversial and of clinical importance because patients with Barrett's esophagus are at significantly increased risk for developing esophageal adenocarcinoma. Recent evidence suggests that intestinal metaplasia of the gastric cardia is also quite common. Although prospective data are relatively sparse, it has been suggested that the risk of progressing to dysplasia and adenocarcinoma is significantly lower for intestinal metaplasia of the gastric cardia when compared with esophageal intestinal metaplasia (Barrett's esophagus). Immunohistochemical stains for cytokeratins 7 and 20 may be useful in more precisely localizing the site of intestinal metaplasia in biopsy specimens taken from the vicinity of the esophagogastric junction. Correlation of all clinical, endoscopic, histologic, and immunohistochemical data may be used by the gastroenterologist to determine the likely source of the intestinal metaplasia and whether the patient should be followed by endoscopic surveillance.
Adenocarcinoma↗
Hiatus hernia and intrathoracic migration of esophagogastric junction in gastroesophageal reflux disease.
The prevalence and clinical presentation of reducible and irreducible hiatus hernia were investigated within a gastro-esophageal reflux disease patient population. Reflux symptoms and esophagitis data were collected on 791 patients. The barium swallow was used to assess the esophagogastric junction. Clinical and endoscopic findings were tested to predict radiographic findings. The esophagogastric junction was normal in 17% of patients, 53% had a sliding hiatus hernia with a reducible esophagogastric junction; in 23% it was irreducible although axial, and 8% had massive incarcerated hiatus hernia. The presence of reducible sliding hiatus hernia did not influence clinical presentation. Axial irreducibility presented with long-standing severe symptoms and esophagitis in 80% of cases. Clinical and endoscopic findings predicted axial irreducibility in 52% of cases. In conclusion, sliding hiatus hernia with an reducible esophagogastric junction does not influence the severity of gastroesophageal reflux disease. An irreducible esophagogastric junction is associated with long-standing severe gastroesophageal reflux disease. Clinical and endoscopic findings may only be indicative of axial esophagogastric junction irreducibility; thus barium swallow should be part of the work-up.
Esophagogastric Junction↗
Cancer of the esophagogastric junction.
In the Western world, there has been an alarming rise in the incidence and prevalence of adenocarcinoma arising at the esophagogastric junction during recent decades. Epidemiological, clinical and pathological data support a sub-classification of adenocarcinomas arising in the vicinity of the esophagogastric junction (AEG) into adenocarcinoma of the distal esophagus (Type I), true carcinoma of the cardia (Type II) and subcardial carcinoma (Type III). While most, if not all, adenocarcinomas of the distal esophagus arise from areas with specialized intestinal metaplasia, which develop as a consequence of chronic gastroesophageal reflux, the etiology and pathogenesis of true carcinoma of the gastric cardia and subcardial gastric cancer is not clear at present. Although a subgroup of true carcinomas of the gastric cardia may also develop within short segments of intestinal metaplasia at the esophagogastric junction, a causal relation between these tumors and gastroesophageal reflux has been difficult to establish. Irrespective of the etiology, a complete removal of the primary tumor and its lymphatic drainage has to be the primary goal of any surgical approach to adenocarcinoma of the esophagogastric junction. Our experience in the management of more than 1000 such patients during the past 18 years suggests that an individualized therapeutic strategy oriented by tumor type and stage results in survival rates superior to those reported with a more indiscriminate approach. This individualized strategy prescribes a transmediastinal esophagectomy with lymphadenectomy in the lower posterior mediastinum and along the celiac axis for Type I tumors, extended total gastrectomy with transhiatal resection of the distal esophagus and D2 lymphadenectomy for Type II and Type III tumors, a limited resection of the esophagogastric junction and distal esophagus with interposition of a pedicled jejunal segment for uT1N0 tumors, and neoadjuvant chemotherapy followed by resection for uT3/T4 tumors. Extensive preoperative staging is essential to allow correct selection of the appropriate therapeutic strategy using this tailored approach.
Adenocarcinoma↗