Hepatitis B virus status and the risk of pancreatic cancer

Yang, Shengli; Cao, Shiyi; Yin, Xiaoxv; Xie, Jun; Tu, Xiaochen; Xu, Jing; Xu, Xing; Dong, Xiaoxin; Lu, Zuxun

doi:10.1097/cej.0b013e32835b6a21

Cited by 35 publications

(25 citation statements)

References 22 publications

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“…37 Subsequently, between the end of 2012 and the beginning of 2013, at least three meta-analyses have been published confirming that both viruses are risk factors for the development of pancreatic cancer. [38][39][40] Further evidence supports the results of these epidemiological studies.…”

Section: Introductionsupporting

confidence: 79%

Pancreatic carcinoma development: new etiological and pathogenetic evidence

Fiorino¹,

Reggiani

Pontoriero

et al. 2013

Ital J Med

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Pancreatic adenocarcinoma (PAC) is a very aggressive cancer with a poor prognosis. To date, the causes and pathogenetic mechanisms involved in the development of this malignancy remain largely unknown. Therefore, additional studies are required to improve our knowledge of the events that occur during the process of pancreatic carcinogenesis. The purpose of this article is to describe the most recent evidence, concerning the possible risk factors and mechanisms that may contribute to determine the development of PAC, as well as models, such as the tensegrity model, that may explain this complex process. Available studies suggest that approximately 15-20% of human malignancies are somehow associated with chronic infection. Some epidemiological research has shown that some infectious agents represent risk factors for PAC. In particular, several reports showed that the infection caused by some micro-organisms, including helicobacter pylori and some bacterial species of oral microbiota, as well as by viral agents, such as human immunodeficiency virus (HIV), and hepatitis B (HBV) and C (HCV) viruses, is associated with an increased probability of developing PAC. For the first time, observational studies and meta-analyses have suggested that HBV and HCV, two hepatotropic viruses with oncogenic properties, may be also risk factors for PAC. However, the small number of available reports, nearly all performed in Asian populations, limits their validity to these ethnic groups. Therefore, additional studies focusing on populations of different geographical areas and enrolling larger series of patients are required to confirm this association. Furthermore, an accurate description and a better understanding of the events and of the pathogenetic mechanisms involved in the process of pancreatic carcinogenesis, as proposed by the tensegrity model, might be a useful approach to effectively deal with this pathology.

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Section: Introductionsupporting

confidence: 79%

Pancreatic carcinoma development: new etiological and pathogenetic evidence

Fiorino¹,

Reggiani

Pontoriero

et al. 2013

Ital J Med

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Section: Obi and Risk Of Other Malignanciesmentioning

confidence: 99%

“…Wang et al conducted a meta-analysis involving 5883 patients with pancreatic cancer 73. They demonstrated that the RR for development of pancreatic cancer was 1.76 (95% CI = 1.05-2.93) in anti-HBc-positive but anti-HBs-negative individuals, and concluded that OBI may increase the risk of pancreatic cancer 73. In patients with hematological malignancies, the presence of OBI cannot be ignored because HBV reactivation may occur in patients with OBI undergoing immunosuppressive therapy or chemotherapy, where it is often associated with the fulminant course of hepatitis, as well as in those with HBsAg positivity 4,9,11.…”

Section: Obi and Risk Of Other Malignanciesmentioning

confidence: 99%

Clinical Significance of Occult Hepatitis B Infection in Progression of Liver Disease and Carcinogenesis

Nishikawa¹,

Osaki²

2013

J. Cancer

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Occult hepatitis B infection (OBI) is defined as long-lasting persistence of hepatitis B virus (HBV) DNA in the liver of patients with hepatitis B surface antigen (HBsAg)-negative status, with or without serological markers of previous exposure (antibodies to HBsAg and/or to hepatitis B core antigen). Over the past two decades, significant progress has been made in understanding OBI and its clinical implications. OBI as a cause of chronic liver disease in patients with HBsAg-negative status is becoming an important disease entity. In conditions of immunocompetence, OBI is inoffensive in itself and detection of HBV DNA in the liver does not always indicate active hepatitis. However, when other factors that cause liver damage, such as hepatitis C virus infection, obesity and alcohol abuse are present, the minimal lesions produced by the immunological response to OBI might worsen the clinical course of the underlying liver disease. Several lines of evidence suggest that OBI is associated with progression of liver fibrosis and the development of hepatocellular carcinoma in patients with chronic liver disease. The major interest in OBI is primarily associated with the growing, widely discussed evidence of its clinical impact. The aim of this review is to highlight recent data for OBI, with a major focus on disease progression or carcinogenesis in patients with chronic liver disease.

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“…Recently, there have been an increasing number of epidemiological studies on the association between the well-known oncogenic virus, HBV, and PDAC, although the relationship between the two remains unclear. The majority of these studies determined that HBV infection was an independent risk factor and prognostic factor for PDAC patients, and suggested a unique subtype of PDAC with a worse prognosis [3,8,[10][11][12][13][14][15][16][17][18][19]. However, other studies found no association between HBV infection and PDAC [20][21][22][23][24].…”

Section: Introductionmentioning

confidence: 98%