Genes and viruses in hepatobiliary neoplasia

Reeves, Mark E.; DeMatteo, Ronald P.

doi:10.1002/1098-2388(200009)19:2<84::aid-ssu2>3.0.co;2-0

Cited by 32 publications

(14 citation statements)

References 98 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A US cohort of individuals found HBV nucleic acids in ICC. Furthermore, recent studies show that HBV has been suggested to be involved in the pathogenesis of ICC through the inflammatory process (Tomimatsu et al, 1993;Reeves and DeMatteo, 2000;Liu et al, 2003). These strongly support the notion that HBV can be associated with ICC even in the absence of cirrhosis (Perumal et al, 2006) and further support the potential role of HBV infection in the pathogenesis of biliary cancers.…”

Section: Discussionmentioning

confidence: 99%

The Metabolic Syndrome and Risk Factors for Biliary Tract Cancer: A Case-control Study in China

Wu¹,

He²,

Yu³

et al. 2012

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

Objectives: Recent data show that the metabolic syndrome may play a role in several cancers, but the etiology for biliary tract cancer is incompletely defined. The present aim was to evaluate risk factors for biliary tract cancer in China. Methods: A case-control study in which cases were biliary tract cancer patients referred to Peking Union Medical College Hospital (PUMCH). Controls were randomly selected from an existing database of healthy individuals at the Health Screening Center of PUMCH. Data on the metabolic syndrome, liver diseases, family history, and history of diabetes and hypertension were collected by retrospective review of the patients' records and health examination reports or by interview. Results: A total of 281 patients (102 intrahepatic cholangiocarcinoma (ICC), 86 extrahepatic cholangiocarcinoma (ECC) and 93 gallbladder carcinoma (GC)) and 835 age-and sex-matched controls were enrolled. HBsAg + /anti-HBc + (P=0.002), history of diabetes (P=0.000), cholelithiasis (P=0.000), TC (P=0.003), and HDL (P=0.000) were significantly related to ICC. Cholelithiasis (P=0.000), Tri (P=0.001), LDL (P=0.000), diabetes (P=0.000), Apo A (P=0.000) and Apo B (P=0.012) were significantly associated with ECC. Diabetes (P=0.017), cholelithiasis (P=0.000) and Apo A (P=0.000) were strongly inversely correlated with GC. Conclusion: Cholelithiasis, HBV infection and metabolic symptoms may be potential risk factors for the development of biliary tract cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

The Metabolic Syndrome and Risk Factors for Biliary Tract Cancer: A Case-control Study in China

Wu¹,

He²,

Yu³

et al. 2012

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

show abstract

“…Despite recent discoveries in the field of molecular biology, such as the frequent inactivation of tumor suppressor genes (p53, APC, smad 4, bcl2, p16), the finding of mutations in oncogenes (k ras, c myc, c erb 2, c neu), and chromosomal aneuploidy detected in up to 25% of cases, there is no established clinical role for such tests as of yet (12).…”

mentioning

confidence: 99%

The Value of Serum CA 19-9 in Predicting Cholangiocarcinomas in Patients with Primary Sclerosing Cholangitis

et al. 2005

View full text Add to dashboard Cite

CA 19-9 has been used with questionable accuracy to aid diagnosis of cholangiocarcinoma complicating primary sclerosing cholangitis. We aimed to characterize the test properties of CA 19-9 and of a change in CA 19-9 over time in predicting cholangiocarcinoma. Charts of 208 patients were reviewed. Fourteen patients had cholangiocarcinoma. Median CA 19-9 was higher with cholangiocarcinoma (15 vs. 290 U/ml, p < 0.0001). A cutoff of 129 U/ml provided: sensitivity 78.6%, specificity 98.5%, adjusted positive predictive value 56.6% and negative predictive value 99.4%. The median change over time was 664 U/ml in cholangiocarcinoma compared to 6.7 U/ml in primary sclerosing cholangitis alone (p < 0.0001). A cutoff of 63.2 U/ml for change in CA 19-9 provided: sensitivity 90%, specificity 98% and positive predictive value 42%. Only 2 patients with cholangiocarcinoma were the candidates for curative therapy. In conclusion, the positive predictive value of an elevated CA 19-9 was 56.6%; only advanced cases were detected by this method.

show abstract

“…It is well known that HBV leads to HCC. HCC incidence clearly correlates with HBV infection as 80% of HCC occur in HBV-infected patients (8). Some studies on HBV-induced HCC focus on the integration of HBV DNA (9-11), HBx (12,13), the PreS2 activators (14), and the immune systemmediated chronic inflammation of the liver (15)(16)(17).…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B virus DNA-induced carcinogenesis of human normal liver cells by virtue of nonmethylated CpG DNA

Xu²,

Chen³

et al. 2009

Oncol Rep

View full text Add to dashboard Cite

Abstract. Hepatitis B virus has been linked to the pathogenesis and carcinogenesis of hepatocellular carcinoma. Components of viruses have been identified within pathological specimens of hepatocellular carcinoma tissue. We characterized the in vitro response of human normal liver cells (L-02 cells) to components of infectious agents related to toll-like receptors. Immortalized human normal liver cells (L-02 cells) exhibited increased proliferation in response to exposure to CpG DNA. This molecule is a well-characterized surrogate for DNA viruses, which are common in the liver. Our experiments show that L-02 cells and some hepatoma cell lines such as HepG2, HuH7, Hep3B, express TLR 9 (CpGspecific). CpG DNA, HBV DNA, DNA of HBV middle envelope protein (MP) containing a number of CpG, supernatant of HepG2.2.15 (HepG2 cells transfected HBV) excreting HBV DNA and extraction of nucleic acids from HepG2.2.15 supernatant can all activate NF-κB. In addition, L-02 cells were less susceptible to TNF-·-induced apoptosis as measured by Annexin V-FITC staining when stimulated with CpG. mRNA of DNA methyltransferase 1 (DNMT-1) and BCL-2 was increased when L-02 cells were stimulated with CpG DNA. Our study has identified a possible novel mechanism that indicates how CpG DNA of HBV DNA may contribute to the malignant transformation of benign liver cells.

show abstract

Genes and viruses in hepatobiliary neoplasia

Cited by 32 publications

References 98 publications

The Metabolic Syndrome and Risk Factors for Biliary Tract Cancer: A Case-control Study in China

The Metabolic Syndrome and Risk Factors for Biliary Tract Cancer: A Case-control Study in China

The Value of Serum CA 19-9 in Predicting Cholangiocarcinomas in Patients with Primary Sclerosing Cholangitis

Hepatitis B virus DNA-induced carcinogenesis of human normal liver cells by virtue of nonmethylated CpG DNA

Contact Info

Product

Resources

About