Published online Sep 7, 2022. doi: 10.3748/wjg.v28.i33.4812
Peer-review started: April 20, 2022
First decision: June 2, 2022
Revised: June 15, 2022
Accepted: August 16, 2022
Article in press: August 16, 2022
Published online: September 7, 2022
Processing time: 132 Days and 13.5 Hours
The etiology of pancreatic cancer is unclear. This limits possibilities for its prevention and effective treatment. Hepatitis B virus (HBV) is responsible for the development of hepatocellular carcinoma and different types of extrahepatic cancer, but its role in the etiology of pancreatic cancer is still being discussed.
The epidemiological relationship of previous HBV infection (PBI) with pancreatic cancer and identification of viral biomarkers within the tumor tissue may provide support for this. However, there is still a lack of such reports, especially from non-endemic regions for HBV infection.
In our study, we aimed to assess the prevalence of PBI and to identify viral biomarkers in patients with pancreatic ductal adenocarcinoma (PDAC) to support the role of the virus in the etiology of this cancer.
The data of 130 hepatitis B surface antigen-negative subjects were included in the final analysis (60 patients with PDAC confirmed by cytology or histology and 70 sex- and age-matched controls). All the participants were tested for HBV biomarkers in blood (antibody to hepatitis B core antigen, antibody to hepatitis B surface antigen and HBV DNA). Those with PDAC were tested for biomarkers in resected pancreatic tissues [HBV DNA, HBV pregenomic RNA and covalently closed circular DNA (cccDNA)]. Additionally, we performed immunohistochemistry staining of pancreatic tissues for hepatitis B virus X antigen and Ki-67 protein. Non-parametric statistics were used for the analysis.
We have established that 18/60 (30%) patients with PDAC and 9/70 (13%) participants in the control group (P = 0.029) were anti-hepatitis B core antigen-positive. HBV DNA was detected in 8 anti-hepatitis B core antigen-positive patients of PDAC (in 6 of them—in the pancreatic tumor tissue samples only) but in neither subjects of the control group. In 5 patients with PDAC we revealed signs of replicative competence of the virus (cccDNA with or without pregenomic RNA) in the pancreatic tumor tissue samples. Hepatitis B virus X antigen expression and active cells’ proliferation was revealed by immunohistochemistry in 4 participants with PDAC in the pancreatic tumor tissue samples.
PBI seems to be an underestimated cause of PDAC.
Larger studies are necessary to assess risks of PDAC in subjects with PBI and define HBV-associated mechanisms of carcinogenesis in them.