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Background DOG1 (ANO1; TMEM16A) is a voltage-gated calcium-activated chloride and bicarbonate channel. DOG1 is physiologically expressed in Cajal cells, where it plays an important role in regulating intestinal motility and its expression is a diagnostic hallmark of gastrointestinal stromal tumors (GIST). Data on a possible role of DOG1 in pancreatic cancer are rare and controversial. The aim of our study was to clarify the prevalence of DOG1 expression in pancreatic cancer and to study its association with parameters of cancer aggressiveness. Methods DOG1 expression was analyzed by immunohistochemistry in 599 pancreatic cancers in a tissue microarray format and in 12 cases of pancreatitis on large tissue sections. Results DOG1 expression was always absent in normal pancreas but a focal weak expression was seen in four of 12 cases of pancreatitis. DOG1 expression was, however, common in pancreatic cancer. Membranous and cytoplasmic DOG1 expression in tumor cells was highest in pancreatic ductal adenocarcinomas (61% of 444 interpretable cases), followed by cancers of the ampulla Vateri (43% of 51 interpretable cases), and absent in 6 acinus cell carcinomas. DOG1 expression in tumor associated stroma cells was seen in 76 of 444 (17%) pancreatic ductal adenocarcinomas and in seven of 51 (14%) cancers of the ampulla Vateri. Both tumoral and stromal DOG1 expression were unrelated to tumor stage, grade, lymph node and distant metastasis, mismatch repair protein deficiency and the density of CD8 positive cytotoxic T-lymphocytes in the subgroups of ductal adenocarcinomas and cancers of ampulla Vateri. Overall, the results of our study indicate that DOG1 may represent a potential biomarker for pancreatic cancer diagnosis and a putative therapeutic target in pancreatic cancer. However, DOG1 expression is unrelated to pancreatic cancer aggressiveness.

Martina Koch, Thomas Becker, Rainer Lueck, Michael Neipp, Juergen Klempnauer, Bjoern NashanKlinik fuer Allgemein-, Viszeral- und Transplantationschirurgie, Medizinische Hochschule Hannover, Hannover, GermanyAbstract: The interleukin-2 receptor antagonist basiliximab has proven in large clinical trials to be safe and effective to reduce acute rejections in the first year after renal transplantation. Since acute rejections are a risk factor for chronic graft loss, their effective reduction might have a positive effect on long term allograft survival. So far data is spares to prove this hypothesis and 10-year follow up on basiliximab induction therapy is not available. In our center, 41 patients were enrolled in the multicenter trial CHIB201 in 1995/96 comparing basiliximab vs no induction therapy after renal transplantation. We retrospectively analyzed the outcome of these patients after 10 years. The main reason for patient death with functioning graft were infectious complications (basiliximab: 3/20, placebo 1/19), 21% of all patients developed cancer without an obvious correlation to specific immunosuppression. Death censored 10-year graft survival was equivalent in both groups: 65% in the basiliximab and 68% in the placebo group with a mean s-creatinine-clearance of 60 and 44 ml/min. In this small study patient and graft survival was equivalent 10 years after transplantation comparing basiliximab induction therapy and placebo.Keywords: basiliximab, induction therapy, long term graft survival, renal transplantation