Helicobacter species ribosomal DNA in the pancreas, stomach and duodenum of pancreatic cancer patients.
OBJECTIVE
To determine whether gastric and enteric Helicobacter species are associated with pancreatic cancer.


METHODS
Patients with exocrine pancreatic cancer (n = 40), neuroendocrine cancer (n = 14), multiple endocrine neoplasia type 1 (n = 8), and chronic pancreatitis (n = 5) were studied. Other benign pancreatic diseases (n = 10) and specimens of normal pancreas (n = 7) were included as controls. Pancreatic tissue specimens were analyzed by Helicobacter-specific PCR-assay and products were characterized by denaturing gradient electrophoresis and DNA-sequencing. From a subset of the pancreatic cancer patients, gastric and/or duodenal tissue as well as gallbladder and ductus choledochus tissue were analyzed. Gallbladder and choledochus samples were included as controls. Stomach and duodenum samples were investigated to analyze whether a gastric helicobacter might disseminate to the pancreas in pancreatic cancer patients. Pancreatic specimens were analyzed by Bacteroides-specific PCR for detecting the translocation of indigenous gut microbes to the diseased pancreas.


RESULTS
Helicobacter DNA was detected in pancreas (tumor and/or surrounding tissue) of 75% of patients with exocrine cancer, 57% of patients with neuroendocrine cancer, 38% of patients with multiple endocrine neoplasia, and 60% of patients with chronic pancreatitis. All samples from other benign pancreatic diseases and normal pancreas were negative. Thirty-three percent of the patients were helicobacter-positive in gastroduodenal specimens. Surprisingly, H. bilis was identified in 60% of the positive gastroduodenal samples. All gallbladder and ductus choledochus specimens were negative for helicobacter. Bacteroides PCR-assay was negative for all pancreatic samples.


CONCLUSIONS
Helicobacter DNA commonly detected in pancreatic cancer suggests a possible role of the emerging pathogens in the development of chronic pancreatitis and pancreatic cancer.
Nilsson
Hans-Olof
HO
Department of Laboratory Medicine, Division of Medical Microbiology, Lund University, Solvegatan 23, S-223 62 Lund, Sweden. hans-olof.nilsson@med.lu.se
Stenram
Unne
U
Ihse
Ingemar
I
Wadstrom
Torkel
T
D000328:Adult; D000368:Aged; D001439:Bacteroides / Q000235:genetics / Q000502:physiology; D018278:Carcinoma, Neuroendocrine / Q000209:etiology / Q000235:genetics / Q000382:microbiology*; D016022:Case-Control Studies; D003135:Common Bile Duct / Q000737:chemistry / Q000382:microbiology; D004275:DNA, Ribosomal / Q000032:analysis* / Q000235:genetics; D004386:Duodenum / Q000737:chemistry* / Q000382:microbiology; D005260:Female; D005704:Gallbladder / Q000737:chemistry / Q000382:microbiology; D016998:Helicobacter / Q000235:genetics* / Q000502:physiology; D016481:Helicobacter Infections / Q000150:complications / Q000235:genetics; D006801:Humans; D008297:Male; D008875:Middle Aged; D018761:Multiple Endocrine Neoplasia Type 1 / Q000209:etiology / Q000235:genetics / Q000382:microbiology*; D010179:Pancreas / Q000737:chemistry* / Q000382:microbiology; D010190:Pancreatic Neoplasms / Q000209:etiology / Q000235:genetics / Q000382:microbiology*; D016133:Polymerase Chain Reaction; D013270:Stomach / Q000737:chemistry* / Q000382:microbiology
D004275:DNA, Ribosomal