- David Q. H. Wang, MD, PhD
- Professor of Medicine and Genetics, Director, Molecular Biology and Next Generation Technology Core, Department of Medicine and Genetics, Division of Gastroenterology and Liver Diseases, Marion Bessin Liver Research Center, Einstein-Mount Sinai Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York, USA.
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Special Issue Introduction
In the USA, liver cancer is the most rapidly increasing cancer, with incidence rates more than tripling since 1980. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer, which occurs most often in people with chronic liver diseases such as chronic liver inflammation (i.e., chronic viral hepatitis B or C infection) or exposure to toxins such as alcohol, aflatoxin, or pyrrolizidine alkaloids. Some metabolic factors such as obesity and diabetes have been implicated as risk factors for HCC, most likely through the development of nonalcoholic steatohepatitis (NASH), hepatocyte necrosis and fibrosis, and liver cirrhosis. By racial and ethnic group, the rates of incidence are highest in Hispanics, followed by Asians/Pacific Islanders, then American Indians/Alaska Natives, blacks, and whites, suggesting that genetic factors may contribute to racial and ethnic differences in HCC incidence rates.
In the USA, approximately 50% of HCC patients have histories of alcohol abuse, with ~30% of HCC cases being associated with excessive alcohol use (i.e., >80 g/day or > 6-7 drinks per day for more than 10 years). Moreover, as many as 50% of alcoholics may have subclinical HCC at autopsy. The risk of HCC in patients with decompensated alcoholic cirrhosis is approximately 1% per year. Obviously, alcohol abusers are at increased risk of HCC.
Although the pathophysiology of HCC has not been elucidated definitively, it is clearly a multifactorial event for the pathogenesis of HCC. Epidemiological and clinical studies, as well as pathophysiological and pathological analyses have clearly demonstrated that chronic inflammation, necrosis, fibrosis, and ongoing regeneration greatly contribute to the development of cirrhotic liver, eventually leading to a high risk of HCC. In addition to alcohol‐related liver disease, some metabolic factors such as dysfunctional lipid and glucose metabolism can cause chronic liver diseases, which are also involved in cirrhotic liver and its progression to HCC.
In this special issue, the topics will be focused on genetic variants in development of HCC in individuals with alcohol-related liver disease. In addition, other special emphasis will be given to the abnormal genetic, cellular, and molecular mechanisms, as well as the dysfunctional lipid and glucose metabolisms as risk factors for the development of HCC and alcohol-related liver disease. Taken together, basic, translational, and clinical studies on these topics are strongly recommended for publication in this special issue.
We cordially invite all investigators, scientists, and clinicians who work in these fields to submit their articles (i.e., original research papers, review articles, commentaries, and editorials) for publication in this special issue of Hepatoma Research.
1.Genetic and epigenetic analyses of HCC and alcohol-related liver disease;
2.Cellular and molecular mechanisms on the pathogenesis of HCC and alcohol‐related liver disease;
3.Molecular links between HCC and alcohol-related liver disease;
4.Role of Reactive oxygen species in epigenetic alterations at the sites of DNA repair in the development of HCC and alcohol-related liver disease;
5.Pathophysiology and pathology of HCC and alcohol‐related liver disease;
6.Systemic and hepatic molecular mechanisms involved in hepatic carcinogenesis;
7.Biomarkers of early HCC;
8.Sex differences in HCC and alcohol-related liver disease;
9.Genetic and clinical analyses of racial and ethnic differences in the incidence rates of HCC and alcohol-related liver disease;
10.Epidemiology and natural course of HCC and alcohol-related liver disease;
11.Personalized diagnosis and management of HCC and alcohol-related liver disease;
12.Dysfunctional lipid and glucose metabolisms of enhancing susceptibility to HCC and alcohol-related liver disease;
13.Metabolic disorders such as insulin resistance, diabetes, obesity, nonalcoholic fatty liver disease, NASH, and the metabolic syndrome as risk factors for being involved in the pathogenesis of HCC and for amplifying the role of alcohol‐related liver disease in the development of HCC;
14.Dysregulation of autophagy in the development of HCC and alcohol-related liver disease;
15.Basic, translational, or clinical studies of HCC and alcohol-related liver disease.
Submission Deadline30 Jun 2021