title: Polymorphisms of UDP-glucuronosyltransferase 1A7 are not involved in pancreatic diseases.
abstract: BACKGROUND
  Xenobiotic mediated cellular injury is thought to play a major role in the pathogenesis of pancreatic diseases. Genetic variations that reduce the expression or activity of detoxifying phase II biotransformation enzymes such as the UDP-glucuronosyltransferases might be important in this respect. Recently, a UGT1A7 low detoxification activity allele, UGT1A7*3, has been linked to pancreatic cancer and alcoholic chronic pancreatitis.
  
  
  OBJECTIVE
  To investigate whether UGT1A7 polymorphisms contribute to the risk of pancreatitis and pancreatic cancer.
  
  
  METHODS
  Genetic polymorphisms in the UGT1A7 gene were assessed in a large cohort of patients with different types of pancreatitis and pancreatic cancer originating from the Czech Republic (n = 93), Germany (n = 638), Netherlands (n = 136), and Switzerland (n = 106), and in healthy (n = 1409) and alcoholic (n = 123) controls from the same populations. Polymorphisms were determined by melting curve analysis using fluorescence resonance energy transfer probes. In addition, 229 Dutch subjects were analysed by restriction fragment length polymorphism.
  
  
  RESULTS
  The frequencies of UGT1A7 genotypes did not differ between patients with acute or chronic pancreatitis or pancreatic adenocarcinoma and alcoholic and healthy controls.
  
  
  CONCLUSIONS
  The data suggest that, in contrast to earlier studies, UGT1A7 polymorphisms do not predispose patients to the development of pancreatic cancer and pancreatitis.
authors.forename: M
authors.initials: M
authors.lastname: Verlaan
authors.forename: J P H
authors.initials: JP
authors.lastname: Drenth
authors.forename: K
authors.initials: K
authors.lastname: Truninger
authors.forename: M
authors.initials: M
authors.lastname: Koudova
authors.forename: H-U
authors.initials: HU
authors.lastname: Schulz
authors.forename: M
authors.initials: M
authors.lastname: Bargetzi
authors.forename: B
authors.initials: B
authors.lastname: Künzli
authors.forename: H
authors.initials: H
authors.lastname: Friess
authors.forename: M
authors.initials: M
authors.lastname: Cerny
authors.forename: A
authors.initials: A
authors.lastname: Kage
authors.forename: O
authors.initials: O
authors.lastname: Landt
authors.forename: R H M
authors.initials: RH
authors.lastname: te Morsche
authors.forename: J
authors.initials: J
authors.lastname: Rosendahl
authors.forename: W
authors.initials: W
authors.lastname: Luck
authors.forename: R
authors.initials: R
authors.lastname: Nickel
authors.forename: J
authors.initials: J
authors.lastname: Halangk
authors.forename: M
authors.initials: M
authors.lastname: Becker
authors.forename: M
authors.initials: M
authors.lastname: Macek
authors.forename: J B M J
authors.initials: JB
authors.lastname: Jansen
authors.forename: H
authors.initials: H
authors.lastname: Witt
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism; D000328:Adult; D015331:Cohort Studies; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D014453:Glucuronosyltransferase / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010182:Pancreatic Diseases / Q000201:enzymology*; D010195:Pancreatitis / Q000201:enzymology; D011110:Polymorphism, Genetic; D015262:Xenobiotics
chemical_list: D015262:Xenobiotics; D014453:Glucuronosyltransferase; C107611:UDP-glucuronosyltransferase, UGT1A7