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Background: Pancreatic ductal HCO3 secretion is critically dependent on the cystic fibrosis trans- membrane conductance regulator chloride channel (CFTR) and the solute-linked carrier 26 member 6 anion transporter (SLC26A6). Deterioration of HCO3 secretion is observed in chronic pancreatitis (CP), and CFTR mutations increase CP risk. Therefore, SLC26A6 is a reasonable candidate for a CP susceptibility gene, which has not been investigated in CP patients so far. Methods: As a first screening cohort, 106 subjects with CP and 99 control subjects with no pancreatic disease were recruited from the Hungarian National Pancreas Registry. In 60 non-alcoholic CP cases the entire SLC26A6 coding regionwas sequenced. In the Hungarian cohort variants c.616G > A (p.V206M) and c.1191C > A (p.P3971⁄4) were further genotyped by restriction fragment length polymorphism analysis. In a German replication cohort all exons were sequenced in 40 non-alcoholic CP cases and variant c.616G > A (p.V206M) was further analyzed by sequencing in 321 CP cases and 171 controls. icine, University of Szeged, 62 545 200; fax: þ36 62 545

Genetic investigations in chronic pancreatitis and pancreatic cancer