Beasley’s 1981 paper: The power of a well-designed cohort study to drive liver cancer research and prevention

Koshiol, Jill; Liu, Zhiwei; O’Brien, Thomas R.; Hildesheim, Allan

doi:10.1016/j.canep.2018.01.007

Cited by 5 publications

(7 citation statements)

References 45 publications

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“…Almost all HBV-associated HCCs harbor chromosomally integrated DNA [319,320]. Due to the circular structure of the HBV genome, no formation of infectious viral particles can occur based on the integrated DNA, but the expression of regulatory proteins occurs.…”

Section: Ros Nrf2 and The Virus-associated Pathogenesismentioning

confidence: 99%

Effect of Hepatitis Viruses on the Nrf2/Keap1-Signaling Pathway and Its Impact on Viral Replication and Pathogenesis

Bender

Hildt

2019

IJMS

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With respect to their genome and their structure, the human hepatitis B virus (HBV) and hepatitis C virus (HCV) are complete different viruses. However, both viruses can cause an acute and chronic infection of the liver that is associated with liver inflammation (hepatitis). For both viruses chronic infection can lead to fibrosis, cirrhosis and hepatocellular carcinoma (HCC). Reactive oxygen species (ROS) play a central role in a variety of chronic inflammatory diseases. In light of this, this review summarizes the impact of both viruses on ROS-generating and ROS-inactivating mechanisms. The focus is on the effect of both viruses on the transcription factor Nrf2 (nuclear factor erythroid 2 (NF-E2)-related factor 2). By binding to its target sequence, the antioxidant response element (ARE), Nrf2 triggers the expression of a variety of cytoprotective genes including ROS-detoxifying enzymes. The review summarizes the literature about the pathways for the modulation of Nrf2 that are deregulated by HBV and HCV and describes the impact of Nrf2 deregulation on the viral life cycle of the respective viruses and the virus-associated pathogenesis.

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Section: Ros Nrf2 and The Virus-associated Pathogenesismentioning

confidence: 99%

Effect of Hepatitis Viruses on the Nrf2/Keap1-Signaling Pathway and Its Impact on Viral Replication and Pathogenesis

Bender

Hildt

2019

IJMS

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“…Aflatoxin, however, did not remain the only answer to the question of liver cancer causation. In the early 1970s, scientists hypothesized that the recently discovered hepatitis B virus could cause liver cancer (Koshiol et al 2018). A series of Sino-US collaborative epidemiological studies sought to confirm this hypothesis (Jiang 2018).…”

Section: Molecularized Environments: Practices Of Studying Liver Cancer In Kenyamentioning

confidence: 99%

Cancer in the tropics: geographical pathology and the formation of cancer epidemiology

Mueller

2019

BioSocieties

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Researchers have long been concerned with cancer in what has been called the tropics, developing world, and low-and middle-income countries. Global health advocates' recent calls to attend to an emergent cancer epidemic in these regions were only the latest effort in this long history. Researchers, known as geographical pathologists, sought to determine the etiologies of cancer and other non-infectious diseases between the 1920s and the 1960s by comparing their occurrence across different environments. The geographical pathologists used the concept of the environment to analyze the influences that natural and artificial surroundings had on health. While the international network of geographical pathology fostered medical thinking about environmental health in the early and mid-twentieth century, the very meaning of environment, alongside the scientific methods for studying the environment, changed in this period. In the 1960s, epidemiology, previously used for the study of infectious diseases, displaced geographical pathology as the cohesive framework of cancer research. This signaled a shift in research focus, from one dedicated to diagnostics and the environment to one centered on population and statistical studies. This article shows that it was not the lack of knowledge about cancer in the developing world but rather specific configurations of knowledge that shaped which cancer interventions in the developing world researchers and public health officials conceived. I confirm that the manuscript is comprised of original material that is not under review elsewhere, and that the studies on which the research is based has been subject to review by the Committee on the Use of Humans as Experimental Subjects (COUHES) of the Massachusetts Institute of Technology.

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“…[ 2 , 15 ] However, these studies have investigated the general population rather than focusing on patients with schizophrenia. Long-term hepatic outcomes, such as liver cancer, [ 16 , 17 ] liver failure, [ 18 , 19 ] and liver decompensation, [ 20 ] in patients with schizophrenia and viral hepatitis remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Hepatitis C virus and hepatitis B virus in patients with schizophrenia

et al. 2021

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This study evaluated the severe hepatic outcome (SHO) in patients with schizophrenia and viral hepatitis who received antipsychotics. Using the nationwide Taiwan National Health Insurance Research Database, patients first diagnosed with schizophrenia between 2002 and 2013 were identified. Patients diagnosed with schizophrenia who had viral hepatitis, including hepatitis B virus (HBV) or hepatitis C virus (HCV), were designated as the viral hepatitis group. A control group without viral hepatitis was matched for age, sex, and index year in a 2:1 ratio. Patients with severe hepatic outcomes before enrollment were excluded. The 2 cohorts were observed until December 31, 2013. The primary endpoint was occurrence of a SHO, including liver cancer, liver failure, liver decompensation, or transplantation. Among the 16,365 patients newly diagnosed with schizophrenia between January 2002 and December 2013, we identified 614 patients with viral hepatitis and 1228 matched patients without viral hepatitis. Of these 1842 patients, 41 (2.22%) developed SHOs, including 26 (4.23%) in the viral hepatitis group and 15 (1.22%) in the control group, during the mean follow-up period of 3.71 ± 2.49 years. Cox proportional hazard analysis indicated that the SHO risk increased by 3.58 (95% confidence interval [CI]: 1.859–6.754; P < .001) in patients with schizophrenia and viral hepatitis. Moreover, patients with schizophrenia having HCV had a higher SHO risk than those without viral hepatitis (hazard ratio: 5.07, 95% CI: 1.612–15.956; P < .0001). Patients having both schizophrenia and viral hepatitis, especially HCV, had a higher risk of SHOs.

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Beasley’s 1981 paper: The power of a well-designed cohort study to drive liver cancer research and prevention

Cited by 5 publications

References 45 publications

Effect of Hepatitis Viruses on the Nrf2/Keap1-Signaling Pathway and Its Impact on Viral Replication and Pathogenesis

Effect of Hepatitis Viruses on the Nrf2/Keap1-Signaling Pathway and Its Impact on Viral Replication and Pathogenesis

Cancer in the tropics: geographical pathology and the formation of cancer epidemiology

Hepatitis C virus and hepatitis B virus in patients with schizophrenia

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