Laparoscopic ischemic conditioning of the stomach prior to esophagectomy.

Several complications after esophagectomy with gastric pull-up are associated with ischemia within the gastric conduit. The aim of this study is to assess the feasibility of laparoscopic ischemic preconditioning of the stomach prior to thoracotomy, esophagectomy, and gastric pull-up with an intrathoracic anastomosis. A retrospective review of 24 consecutive patients between October 2008 and July 2011 with esophageal adenocarcinoma (stage I-III) undergoing laparoscopic gastric ischemic conditioning prior to esophagectomy was conducted. Conditioning included laparoscopic ligation of the left and short gastric arteries, celiac node dissection, and jejunostomy tube placement. Formal resection and reconstruction was then performed 4-10 days later. Of the 24 patients, 88% received neoadjuvant chemotherapy/radiation therapy. Twenty-three of the 24 patients underwent successful laparoscopic ischemic conditioning and subsequent esophagectomy. Total mean number of lymph nodes harvested was 21.8 (±8.0), and a mean of 5.3 (±2.4) celiac lymph nodes identified. There were no conversions to an open procedure. Length of stay was 3.8 (±4.8) days with a median length of stay of 2 (1-24) days. Three patients experienced anastomotic leak, six patients experience delayed gastric emptying, and two patients developed anastomotic stricture. There were no surgical site infections. R0 resection was achieved in all patients who underwent laparoscopic ischemic conditioning followed by esophagectomy. Laparoscopic ischemic conditioning of the gastric conduit has been shown to be feasible and safe.

Phorbol 12,13 dibutyrate behaves in a tumor-inhibitory manner in esophageal adenocarcinoma cell lines.

Esophageal cancer is an extremely lethal human disease. Relatively little is known about the molecular mechanisms leading to esophageal cancers, nor the signaling pathways activated to maintain and augment the tumor growth. Esophageal cancer cell lines were evaluated to assess the effect of phorbol 12,13 dibutyrate on protein kinase C activity, indirectly using protein kinase D (formerly known as protein kinase C-µ), Akt activity, and cell proliferation. Treatment of esophageal cancer cell lines with the phorbol ester phorbol 12,13 dibutyrate led to a rapid and dramatic increase in the activation of protein kinase D. In addition, administration of phorbol 12,13 dibutyrate also decreased the phosphorylation of Akt. Interestingly, in the OE19 esophageal adenocarcinoma cell line, treatment with phorbol 12,13 dibutyrate also led to inhibition of cell growth. All the phorbol ester effects observed were reversible by combined treatment with a protein kinase C inhibitor, implicating protein kinase C in the cells' response to the phorbol ester. Overall, these studies suggest that protein kinase D (e.g. protein kinase C-µ) may behave as a tumor suppressor in some esophageal cancer samples, serving to inhibit Akt activity and block cell growth.