Advanced non-polypoid colorectal adenomas and early-stage carcinomas can be safely and effectively resected by endoscopic mucosal resection.

A growing body of evidence suggests that oxygen radicals are generated in all forms of experimental pancreatitis at an early stage of disease. Moreover, first indirect observations assume that also in human acute recurrent and chronic pancreatitis oxygen free radicals are generated and add to the damages seen. The source of the enhanced production of oxygen radicals remains still unclear. Experimentally, the efficiency of scavenger treatment varies between three different models, whereby these differences depend more on the design of the experimental models than on the form of pancreatitis which was induced. Antioxidant treatment with radical scavengers should therefore interrupt these deleterious pathomechanisms or at least mitigate the damages normally seen. Most studies, however, pretreated the experimental animals before inducing acute pancreatitis, which does not mirror the clinical reality. Patients, however, are admitted after onset of the disease. Therefore, well-defined, controlled clinical studies are needed to validate the involvement of oxygen radicals in acute and chronic pancreatitis and the effect of scavenger treatment in patients with pancreatitis.

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The GI tract surgeon must accumulate competent endoscopic experience. His responsibility for GI diseases focuses on surgical treatment using minimal access surgical techniques including surgical endoscopy in preoperative, intraoperative, and postoperative settings. This major assignment is a challenge not only for GI tract surgeons in the near future.

Caspase-1 (interleukin-1L L-converting enzyme) is reported to play an important role in the regulation of apoptosis. We investigated the inhibition of caspase-1 by the cell permeable caspase-1 inhibitor Ac-AAVALLPAVLLALLAP-YVAD.CHO in pancreatic carcinoma cells. Inhibition of caspase-1 induced a non-apoptotic/`necrotic-like' cell death in AsPC-1, BxPC-3, MiaPaCa-2 and Panc-1 cells. Expression levels of bcl-2 and bax were up-regulated in caspase-1 inhibitor-treated cells while that of bcl-x L remained unaltered. Our observations support our previous findings that caspase-1 is potentially involved in antiapoptotic processes in pancreatic carcinoma. ß