Low frequency of Helicobacter DNA in benign and malignant liver tissues from Baltimore, United States

Perumal Vivekanandan, Michael Torbenson

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)213-216
Number of pages4
JournalHuman Pathology
Volume39
Issue number2
DOIs
StatePublished - Feb 1 2008
Externally publishedYes

Fingerprint

Helicobacter
Baltimore
Hepatocellular Carcinoma
Liver
DNA
Helicobacter Infections
Geographic Locations
Neoplasms
Cholangiocarcinoma
Hepatitis C
Helicobacter pylori
Liver Diseases
Alcohols
Polymerase Chain Reaction

Keywords

  • Cholangiocarcinoma
  • Helicobacter
  • Hepatocellular carcinoma

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Low frequency of Helicobacter DNA in benign and malignant liver tissues from Baltimore, United States. / Vivekanandan, Perumal; Torbenson, Michael.

In: Human Pathology, Vol. 39, No. 2, 01.02.2008, p. 213-216.

Research output: Contribution to journalArticle

@article{4343b83da37647c596ee127a69f9e5a0,
title = "Low frequency of Helicobacter DNA in benign and malignant liver tissues from Baltimore, United States",
abstract = "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.",
keywords = "Cholangiocarcinoma, Helicobacter, Hepatocellular carcinoma",
author = "Perumal Vivekanandan and Michael Torbenson",
year = "2008",
month = "2",
day = "1",
doi = "10.1016/j.humpath.2007.06.003",
language = "English (US)",
volume = "39",
pages = "213--216",
journal = "Human Pathology",
issn = "0046-8177",
publisher = "W.B. Saunders Ltd",
number = "2",

}

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 - 2008/2/1

Y1 - 2008/2/1

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

UR - http://www.scopus.com/inward/record.url?scp=38149104066&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=38149104066&partnerID=8YFLogxK

U2 - 10.1016/j.humpath.2007.06.003

DO - 10.1016/j.humpath.2007.06.003

M3 - Article

C2 - 17949788

AN - SCOPUS:38149104066

VL - 39

SP - 213

EP - 216

JO - Human Pathology

JF - Human Pathology

SN - 0046-8177

IS - 2

ER -