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Alcohol and hepatocellular carcinoma

BACKGROUND: Alcohol is classified as a Group 1 carcinogen by the International Agency for Research on Cancer because it induces hepatocellular carcinoma (among other cancers) in humans. An excessive alcohol intake may result in fatty liver, acute/chronic hepatitis, and cirrhosis and eventually lead...

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Autores principales: Matsushita, Hiroshi, Takaki, Akinobu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BMJ Publishing Group 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6505979/
https://www.ncbi.nlm.nih.gov/pubmed/31139422
http://dx.doi.org/10.1136/bmjgast-2018-000260
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author Matsushita, Hiroshi
Takaki, Akinobu
author_facet Matsushita, Hiroshi
Takaki, Akinobu
author_sort Matsushita, Hiroshi
collection PubMed
description BACKGROUND: Alcohol is classified as a Group 1 carcinogen by the International Agency for Research on Cancer because it induces hepatocellular carcinoma (among other cancers) in humans. An excessive alcohol intake may result in fatty liver, acute/chronic hepatitis, and cirrhosis and eventually lead to hepatocellular carcinoma. It has been reported that alcohol abuse increases the relative risk of hepatocellular carcinoma by 3- to 10-fold. AIM AND METHODS: To clarify the known mechanisms of alcohol-related carcinogenesis, we searched Pubmed using the terms alcohol and immune mechanism, alcohol and cancer, and immune mechanism and cancer and summarized the articles as a qualitative review. RESULTS: From a clinical perspective, it is well known that alcohol interacts with other factors, such as smoking, viral hepatitis, and diabetes, leading to an increased risk of hepatocellular carcinoma. There are several possible mechanisms through which alcohol may induce liver carcinogenicity, including the mutagenic effects of acetaldehyde and the production of ROS due to the excessive hepatic deposition of iron. Furthermore, it has been reported that alcohol accelerates hepatitis C virus-induced liver tumorigenesis through TLR4 signaling. Despite intense investigations to elucidate the mechanisms, they remain poorly understood. CONCLUSION: This review summarizes the recent findings of clinical and pathological studies that have investigated the carcinogenic effects of alcohol in the liver.
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spelling pubmed-65059792019-05-28 Alcohol and hepatocellular carcinoma Matsushita, Hiroshi Takaki, Akinobu BMJ Open Gastroenterol Review BACKGROUND: Alcohol is classified as a Group 1 carcinogen by the International Agency for Research on Cancer because it induces hepatocellular carcinoma (among other cancers) in humans. An excessive alcohol intake may result in fatty liver, acute/chronic hepatitis, and cirrhosis and eventually lead to hepatocellular carcinoma. It has been reported that alcohol abuse increases the relative risk of hepatocellular carcinoma by 3- to 10-fold. AIM AND METHODS: To clarify the known mechanisms of alcohol-related carcinogenesis, we searched Pubmed using the terms alcohol and immune mechanism, alcohol and cancer, and immune mechanism and cancer and summarized the articles as a qualitative review. RESULTS: From a clinical perspective, it is well known that alcohol interacts with other factors, such as smoking, viral hepatitis, and diabetes, leading to an increased risk of hepatocellular carcinoma. There are several possible mechanisms through which alcohol may induce liver carcinogenicity, including the mutagenic effects of acetaldehyde and the production of ROS due to the excessive hepatic deposition of iron. Furthermore, it has been reported that alcohol accelerates hepatitis C virus-induced liver tumorigenesis through TLR4 signaling. Despite intense investigations to elucidate the mechanisms, they remain poorly understood. CONCLUSION: This review summarizes the recent findings of clinical and pathological studies that have investigated the carcinogenic effects of alcohol in the liver. BMJ Publishing Group 2019-04-03 /pmc/articles/PMC6505979/ /pubmed/31139422 http://dx.doi.org/10.1136/bmjgast-2018-000260 Text en © Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.
spellingShingle Review
Matsushita, Hiroshi
Takaki, Akinobu
Alcohol and hepatocellular carcinoma
title Alcohol and hepatocellular carcinoma
title_full Alcohol and hepatocellular carcinoma
title_fullStr Alcohol and hepatocellular carcinoma
title_full_unstemmed Alcohol and hepatocellular carcinoma
title_short Alcohol and hepatocellular carcinoma
title_sort alcohol and hepatocellular carcinoma
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6505979/
https://www.ncbi.nlm.nih.gov/pubmed/31139422
http://dx.doi.org/10.1136/bmjgast-2018-000260
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