Hepatitis B and C virus infections as possible risk factor for pancreatic adenocarcinoma

Fiorino, Sirio; Lorenzini, Stefania; Masetti, Michele; Deleonardi, Gaia; Grondona, Ana Gabriela; Silvestri, Tania; Chili, Elisabetta; Prete, Paola Del; Reggiani, Maria Letizia Bacchi; Cuppini, A; Jovine, Elio

doi:10.1016/j.mehy.2012.08.008

Cited by 18 publications

(12 citation statements)

References 268 publications

(395 reference statements)

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“…Viral infection is a common risk factor for multiple types of cancer. It has been estimated that chronic viral infection contributes to 15-20% of cancers, such as hepatitis B virus (HBV)-and hepatitis C virusrelated liver cancers, human papilloma virus-related cervical cancer, Epstein-Barr virus-related Burkitt lymphoma and nasopharynx cancer, and human immunodeficiency virus-related Kaposi's sarcoma and non-Hodgkin's lymphoma [3]. Complicated mechanisms including the induction of inflammation and genome disturbance are involved in virus-associated cancers [4,5].…”

Section: Introductionmentioning

confidence: 99%

“…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: 99%

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The hepatitis B virus X protein promotes pancreatic cancer through modulation of the PI3K/AKT signaling pathway

et al. 2016

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The hepatitis B virus X protein promotes pancreatic cancer through modulation of the PI3K/AKT signaling pathway

et al. 2016

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“…Moreover, there’re also investigations indicating that HBV infection is associated with a higher risk of some extrahepatic malignancies, including PC and non-Hodgkin’s lymphoma [11-15]. Some studies further presented a hypothetical mechanism of the development of PC with HBV infection: a multistep process from pre-neoplastic pancreatic lesions to invasive cancer resulted from persistent inflammation in the pancreas caused by HBV infection [16]. …”

Section: Introductionmentioning

confidence: 99%

The status of HBV infection influences metastatic pattern and survival in Chinese patients with pancreatic cancer

et al. 2013

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BackgroundIt has been proved that hepatitis B virus (HBV) infection alters the metastatic pattern and affects survival in colorectal cancer (CRC) and hepatocellular carcinoma (HCC), while the influence of HBV infection on metastatic pattern and survival in patients with pancreatic cancer (PC) has not been investigated yet.MethodsWe conducted an investigation to evaluate the impact of HBV infection on metastatic pattern and overall survival in PC. We collected the data of 460 PC patients treated in our hospital from 1999 to 2010. Serum HBV markers were tested with enzyme-linked immunosorbent assay. The impact of HBV infection on metastatic pattern and overall survival was analyzed.ResultsWe found that the incidence of synchronous liver metastasis was significantly higher in patients with HBsAg positive than those with HBsAg negative (46.0% vs 32.0%, P < 0.05), and higher in chronic HBV infection (CHB) group than both non HBV infection and resolved HBV infection group (61.1% vs 33.9%, P < 0.05, and 61.1% vs 28.7%, P < 0.05, respectively). What’s more, Kaplan-Meier analysis showed that CHB, resolved HBV infection and non HBV infection group had significant longer overall survival (OS) compared with inactive HBsAg carriers (IC) group (P=0.037, P=0.009, and P=0.019 respectively). But, in the multivariate analysis, only the CHB and non HBV infection group had significant better overall survival compared with IC group (P=0.010 and P=0.018 respectively).ConclusionsOur study found that HBV infection increased synchronous liver metastasis rate, and HBV infection status was an independent prognostic factor in PC patients.

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“…It is highly metastatic and the lack of early detection procedures makes it difficult to treat. Some reports hypothesized that there might be a correlation between pancreatic cancer and pathogenic infection involving HBV/ HCV [144]. Earlier, other groups ascertained significant association between HBV and pancreatic cancer [145,146].…”

Section: Inflammation and Extra Hepatic Manifestations As A Results Ofmentioning

confidence: 99%

HBV/HCV Infection and Inflammation

Zakaria¹,

Sankhyan²,

Ali³

et al. 2014

J Genet Syndr Gene Ther

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Liver is a key organ involved in the regulation of both systemic as well as local inflammatory responses. Hepatic inflammation is the hallmark of viral hepatitis caused by non-cytopathic Hepatitis B and C viruses (HBV and HCV). Both HBV and HCV induce several inflammatory responses, causing persistent liver injury, which manifests into progressive diseased state. This ultimately leads to fibrosis, cirrhosis and eventually hepatocellular carcinoma. The disease progression is mediated by a complex interplay of molecular pathways involving both viral and hepatic factors. The complex cellular crosstalk, involving pro-inflammatory cytokines, during the liver injury also causes extra hepatic disorders such as artherosclerosis, glomerulonephritis, arthritis, cardio vascular and brain disease. In addition, these viral infections have been reported to contribute to non-Hodgkin lymphoma, cholangio carcinoma and pancreatic cancer. Host genetics also play an important role in the HBV/HCV mediated viral hepatitis and the accumulation of mutations in the host genes responsible for mounting antiviral effects (cytokines and interferon receptors) has been shown to produce differential immune responses among individuals and increase susceptibility to chronic infections. Viral proteins are known to modulate the host immune response by a variety of mechanisms such as by exerting direct or indirect effects on the cytokine pathways, oxidative stress, miRNAs and other cellular processes. However, the complete network of cytokines involved in the disease pathogenesis is yet not fully understood. This review analyzes the interplay of inflammatory molecules and viral proteins, the impact of local and systemic inflammation during HBV and HCV infection and the contribution of host genetics to such responses.

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Hepatitis B and C virus infections as possible risk factor for pancreatic adenocarcinoma

Cited by 18 publications

References 268 publications

The hepatitis B virus X protein promotes pancreatic cancer through modulation of the PI3K/AKT signaling pathway

The hepatitis B virus X protein promotes pancreatic cancer through modulation of the PI3K/AKT signaling pathway

The status of HBV infection influences metastatic pattern and survival in Chinese patients with pancreatic cancer

HBV/HCV Infection and Inflammation

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