ObjectiveTo identify factors that have contributed to reduced rates of death and complications after esophageal resection in a 17-year period at a tertiary referral center. Summary Background DataThere has been an evolving refinement in surgical technique and perioperative management of patients undergoing esophageal resection at Queen Mary Hospital during the past two decades. As of the end of 1998, there had been no hospital deaths among the last 105 consecutive resections performed for esophageal squamous cancer. MethodsThe results of esophageal resection for squamous cell carcinoma were analyzed using a prospective esophageal database. A longitudinal study was performed to compare and analyze rates of death and complications for three consecutive time periods. ResultsThe study group comprised 710 patients who underwent one-stage esophageal resection between 1982 and 1998. A transthoracic esophagectomy was the preferred approach in 590 patients (83%). The overall hospital death rate was 11%. The leading causes of hospital death were pulmonary complications (45.5%) and progression of malignant disease (21.5%); anastomotic leakage accounted for 9% of deaths. During the study period, the hospital death rate decreased from 16% to 3.2%, and the incidence of postoperative respiratory failure decreased from 15.5% to 6.5%. Perioperative factors that correlated with the decreased death rate over time were the increased postoperative use of epidural analgesia and bronchoscopy (for clearance of pulmonary secretions), a decrease in history of smoking, and a decrease in surgical blood loss of more than 1,000 mL. ConclusionsIn this series of predominantly transthoracic esophagectomies, there has been a decline in the hospital death rate to less than 5%. These results are largely attributable to factors aimed at reducing postoperative pulmonary complications.

Calcium-dependent cell adhesion molecules (cadherins) are involved in maintaining the epithelial structure of a number oftissues including the mammary gland. In breast and other tumor types. loss of E-cadherin expression has been seen in high grade tumors and correlates with increased invasiveness. Here we show high levels of expression of N-cadherin in the most invasive breast cancer cell lines which was inversely correlated with their expression of E-cadherin. A stromal cell line also expressed N-cadherin in accordance with its fibroblastic morphology. N-cadherin localized to areas of cell-cell contact in all cells that expressed it. Calcium-dependent intercellular adhesion of N-cadherin-expressing breast cancer and stro-ma1 cells was specifically inhibited by an anti N-cadherin monoclonal antibody. In addition, N-cadherin promoted the interaction of invasive breast cancer cells with mammary stromal cells; in contrast, E-cadherin expressing cell lines did not co-aggregate with stromal cells. The combined results suggest a functional role for N-cadherin in cohesion of breast tumor cells which, in addition promotes their interaction with the surrounding stromal cells. thereby facilitating invasion and metastasis.

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