Minithoracotomy combined with mechanically stapled bronchial and vascular ligation for anatomical lung resection.

BACKGROUND: The most appropriate approach to anatomic pulmonary resection has been debated with the advance of minimally invasive techniques and especially the common use of mechanical staplers. Video assisted surgery and muscle-sparing thoracotomy are established options of surgical approach for lung resection. We utilize a combined technique of vertical muscle sparing minithoracotomy and mechanical closure of the hilum structures to accomplish lung resection. METHODS: From December 1995 through January 2002, 713 patients (mean age, 65 +/- 11, 44.6% male) underwent anatomic pulmonary resection including 64 pneumonectomies, 514 lobectomies, and 135 formal segmental resections. Pulmonary resection was approached though a direct access, vertical, minithoracotomy (< 10 cm), and vascular ligation was performed with port-access endostapling instrumentation. Full mediastinal lymph node sampling was performed for primary lung cancer. RESULTS: The average operative time was 55 minutes for lobectomy-formal segmentectomy and 62 minutes for pneumonectomy. An average of 3.6 staple applications were utilized to ligate the pulmonary vasculature (n = 2548 for 713 patients). Operative vascular complications included 5 minor intimal fractures, 1 posterior segmental arterial avulsion, and 1 staple misfiring for an adverse event rate during stapler application of 0.27%. Only one conversion to standard thoracotomy was necessary to control bleeding from the pulmonary vein. There were no intraoperative deaths. CONCLUSIONS: Vertical minithoracotomy is a safe and expedited approach for anatomic lung resection. Direct visualization for dissection and effective pulmonary hilum mechanical closure with staplers were demonstrated. This approach is a reasonable option when a complete video-assisted surgery seems to be hazardous and a full open thoracotomy could represent an additional morbidity.

MAPK and PI3K inhibition reduces proliferation of Barrett's adenocarcinoma in vitro.

BACKGROUND: Esophageal adenocarcinoma often arises from Barrett's esophagus. Mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) play critical roles in cell survival. We hypothesized that inhibition of these pathways in Barrett's adenocarcinoma would decrease cell proliferation and alter apoptosis in vitro. MATERIALS AND METHODS: Two Barrett's-associated adenocarcinoma cell lines, SEG-1 (wild-type p53) and BIC-1 (mutant p53), were treated with MAPK (U0126) and PI3K (LY294002) inhibitors at 20 microm concentrations. After 24 and 72 h, cell viability was measured by MTT assay. Apoptosis and necrosis were evaluated by the Annexin V-FITC assay. Statistical analysis was performed by ANOVA. RESULTS: LY294002 and U0126 treatment produced significant reductions (range 15.7 to 62.0%, P < 0.05) in cellular proliferation at both 24 and 72 h in the SEG-1 cells. BIC-1 cell viability was reduced (39.3 to 56.4%, P < 0.05) at 72 h. Both early and late apoptotic activity were significantly increased (P < 0.05) in the SEG-1 cells using both inhibitors. Necrosis was significantly reduced (P < 0.05) using both inhibitors. No changes in either early or late apoptosis or necrosis were observed in the BIC-1 cells. CONCLUSIONS: Herein, we report significant antiproliferative effects against Barrett's adenocarcinoma by MAPK and PI3K inhibition in vitro. Pro-apoptotic mechanisms prevail in the wild-type p53 cells. Further investigation is warranted to advance the clinical treatment of this devastating disease.