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Objective: To assess the accuracy of pretreatment staging and the potential of using endosonographic findings to select patients for curative or palliative resection by comparing the preoperative endosonographic and computed tomographic (CT) findings with the histology of the surgical specimen. Methods: Forty-two patients referred to our clinic with esophageal carcinoma underwent preoperative upper endoscopy with biopsy, endosonography, thoracic CT, and abdominal CT. Based on endoscopic ultrasonographic findings, patients with early-stage disease underwent enbloc esophagogastrectomy, whereas those with advanced disease had a palliative transhiatal esophagectomy. Exceptions included patients with poor physiologic reserve who were treated by the transhiatal route. Results: In eight patients, we were unable to pass the ultrasonographic endoscope. Seven of these eight had transmural tumors with nodal involvement on histologic study. Tumor length, based on endosonographic measurements, was correctly predicted in 34 patients (85%). Extent of wall penetration was accurately predicted in 26 (76%) of the 34, and regional lymph node status was accurately predicted in 28 (82%) of the 34. Of the patients with sonographic wall penetration, 80% had histologic evidence of one or more positive nodes. Using the WNM staging system, endoscopic ultrasonography correctly staged the cancer in 68% of the patients. Three patients were treated with an inappropriate procedure. Conclusion: Endosonography is a reliable method for the preoperative staging and selection of patients for curative or palliative resection. Endosonographic wall penetration appears to be a critical factor in determining tumor spread. (Arch Surg. 1994;129:534-539)

Objectives: The role of fundoplication in patients with pure type II paraesophageal hiatal hernia remains controversial. Conventional thinking suggests that because the lower esophageal sphincter is located within the abdomen, it is competent, and fundoplication is unnecessary. Few studies have used objective evaluation to guide the addition of an antireflux procedure. Methods: Fifteen consecutive patients with type II paraesophageal hernia were treated between May 1991 and July 1994. All had radiographic criteria of pure type II hernias. Preoperative evaluation included upper intestinal endoscopy, esophageal manometry, and 24-hour ambulatory pH monitoring. The lower esophageal sphincter was considered incompetent if any of the following criteria were present: a resting pressure less than 7 mm Hg, an overall sphincter length less than 2 cm, or an intraabdominal length less than 1 cm. Primary symptoms responsible for surgery were related to the hernia in 73% of patients: dysphagia or postprandial abdominal pain in six patients, abdominal distension or vomiting in four patients, and bleeding in one patient. Symptoms typical of gastroesophageal reflux were present in four patients: heartburn and regurgitation in two each. Results: Objective evidence of gastroesophageal reflux was present in the majority of patients. Five patients (31%) had evidence of esophageal injury: esophagitis in three patients, stricture in one, and esophageal ulcer in one. In 11 of 15 patients (69%), pathologic esophageal acid exposure was detected by 24-hour pH monitoring. Twelve patients (75%) had a defective lower esophageal sphincter, usually the result of an inadequate intraabdominal length (8/12, 66%). Hernia reduction, crural closure, and Nissen fundoplication were performed in 14 patients (one patient awaits surgery). Symptomatic relief was excellent in all cases. No patient has had hernia recurrence at an average of 14 months' follow-up (range 2 to 39 months). Conclusion: Objective evaluation reveals that gastroesophageal reflux accompanies type II paraesophageal hernia in a high proportion of patients, usually because of an incompetent lower esophageal sphincter. Appropriate treatment includes reduction of the hernia, crural closure, and fundoplication in most, if not all, patients. (J Thorac C ardiovasc S urg 1996;111:655-61)

Objective: This study was undertaken to investigate the role of the angiogenic factors vascular endothelial growth factor and basic fibroblast growth factor in the development and progression of Barrett esophagus and adenocarcinomas of the esophagus and gastroesophageal junction. Methods: Vascular endothelial growth factor and basic fibroblast growth factor messenger RNA expression levels, relative to the control gene encoding β-actin, were measured by using a quantitative reverse transcription-polymerase chain reaction method (ABI 7700 Sequence Detector system) in specimens of Barrett intestinal metaplasia (n = 16), dysplasia (n = 11), adenocarcinoma (n = l 5), and matching normal squamous esophageal tissues (n = 35). Vascular endothelial growth factor and basic fibroblast growth factor protein expression and CD31+ microvessel density were assessed by means of immunohistochemistry in 25 tissue sections that included representative areas for each of these Barrett stages. Results: Expression levels were significantly increased in adenocarcinoma compared with in either normal squamous mucosa (P

Background High expression of Bmi-1, a key regulatory component of the polycomb repressive complex-1, has been associated with many solid and hematologic malignancies including esophageal squamous cell carcinoma. However, little is known about the role of Bmi-1 in esophageal adenocarcinoma. The aim of this study is to investigate the amplification and high expression of Bmi-1 and the associated clinicopathologic characteristics in esophageal adenocarcinoma and squamous cell carcinoma. Methods The protein expression level of Bmi-1 was detected by immunohistochemistry (IHC) from tissue microarrays (TMA) constructed at the University of Rochester from using tissues accrued between 1997 and 2005. Types of tissues included adenocarcinoma, squamous cell carcinoma and precancerous lesions. Patients’ survival data, demographics, histologic diagnoses and tumor staging data were collected. The intensity (0–3) and percentage of Bmi-1 expression on TMA slides were scored by two pathologists. Genomic DNA from 116 esophageal adenocarcinoma was analyzed for copy number aberrations using Affymetrix SNP 6.0 arrays. Fisher exact tests and Kaplan-Meier methods were used to analyze data. Results By IHC, Bmi-1 was focally expressed in the basal layers of almost all esophageal squamous mucosa, which was similar to previous reports in other organs related to stem cells. High Bmi-1 expression significantly increased from squamous epithelium (7%), columnar cell metaplasia (22%), Barrett’s esophagus (22%), to low- (45%) and high-grade dysplasia (43%) and adenocarcinoma (37%). The expression level of Bmi-1 was significantly associated with esophageal adenocarcinoma differentiation. In esophageal adenocarcinoma, Bmi-1 amplification was detected by DNA microarray in a low percentage (3%). However, high Bmi-1 expression did not show an association with overall survival in both esophageal adenocarcinoma and squamous cell carcinoma. Conclusions This study demonstrates that high expression Bmi-1 is associated with esophageal adenocarcinoma and precancerous lesions, which implies that Bmi-1 plays an important role in early carcinogenesis in esophageal adenocarcinoma.