TY - JOUR
T1 - Low frequency of Helicobacter DNA in benign and malignant liver tissues from Baltimore, United States
AU - Vivekanandan, Perumal
AU - Torbenson, Michael
PY - 2008/2
Y1 - 2008/2
N2 - Helicobacter DNA has been reported in hepatocellular carcinoma tissues in several studies from varying geographic locations, raising the possibility that Helicobacter infection may contribute to the pathogenesis of hepatocellular carcinoma. Other known risk factors for hepatocellular carcinoma show significant geographic variability, but whether the same holds for Helicobacter is unknown. We studied the prevalence of Helicobacter DNA in a US cohort of hepatocellular carcinoma, where the prevalence of Helicobacter infection is low in the general population. Liver tissues from 57 individuals were examined. Thirty-five individuals had paired tumor/nontumor samples, including 21 cases of hepatocellular carcinoma, for a total of 92 samples studied. Both Helicobacter genus and Helicobacter pylori species-specific polymerase chain reaction was performed. Helicobacter DNA was detected in 5 (9%) of 57 cases, all in nonneoplastic cirrhotic liver tissues from individuals with hepatitis C infection (n = 4) or alcohol liver disease (n = 1). Tissues from 22 hepatocellular carcinomas and 10 cholangiocarcinomas were all negative as were tissues from 8 benign primary hepatic tumors. In conclusion, Helicobacter DNA was detectable in 9% of liver tissues in this cohort but was not found in primary benign or malignant liver tumors. These findings indicate that Helicobacter infection is unlikely to be etiologically associated with hepatocellular carcinoma in this cohort. If Helicobacter infection does contribute to the development of hepatocellular carcinoma in general, then significant regional variability must exist.
AB - Helicobacter DNA has been reported in hepatocellular carcinoma tissues in several studies from varying geographic locations, raising the possibility that Helicobacter infection may contribute to the pathogenesis of hepatocellular carcinoma. Other known risk factors for hepatocellular carcinoma show significant geographic variability, but whether the same holds for Helicobacter is unknown. We studied the prevalence of Helicobacter DNA in a US cohort of hepatocellular carcinoma, where the prevalence of Helicobacter infection is low in the general population. Liver tissues from 57 individuals were examined. Thirty-five individuals had paired tumor/nontumor samples, including 21 cases of hepatocellular carcinoma, for a total of 92 samples studied. Both Helicobacter genus and Helicobacter pylori species-specific polymerase chain reaction was performed. Helicobacter DNA was detected in 5 (9%) of 57 cases, all in nonneoplastic cirrhotic liver tissues from individuals with hepatitis C infection (n = 4) or alcohol liver disease (n = 1). Tissues from 22 hepatocellular carcinomas and 10 cholangiocarcinomas were all negative as were tissues from 8 benign primary hepatic tumors. In conclusion, Helicobacter DNA was detectable in 9% of liver tissues in this cohort but was not found in primary benign or malignant liver tumors. These findings indicate that Helicobacter infection is unlikely to be etiologically associated with hepatocellular carcinoma in this cohort. If Helicobacter infection does contribute to the development of hepatocellular carcinoma in general, then significant regional variability must exist.
KW - Cholangiocarcinoma
KW - Helicobacter
KW - Hepatocellular carcinoma
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U2 - 10.1016/j.humpath.2007.06.003
DO - 10.1016/j.humpath.2007.06.003
M3 - Article
C2 - 17949788
AN - SCOPUS:38149104066
SN - 0046-8177
VL - 39
SP - 213
EP - 216
JO - Human Pathology
JF - Human Pathology
IS - 2
ER -