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In a new study, researchers found significant differences in the biological pathways leading to cancer of alcoholic fatty liver compared to non-alcoholic fatty liver disease.
The results of the study presented at the 2019 experimental biology meeting could benefit more than 3 million people diagnosed each year with hepatic steatosis.
The accumulation of fat in the liver known as fatty liver sometimes leads to liver cancer difficult to treat.
Scientists have not understood why the risk of cancer was higher for fatty liver conditions caused by excessive alcohol consumption than for non-alcoholic liver disorders, badociated with obesity and high blood pressure. Type 2 diabetes.
"We want to discover the key factors and pathways that lead to liver cancer in patients with fatty liver to slow down or even prevent liver cancer." It is estimated that this type of liver cancer is responsible for 250,000 to 1 million deaths a year, "said Yue Jia, who led the study.
In this study, researchers examined the levels of protein expression in liver biopsies from a group of patients with alcoholic fatty liver disease and a group of patients with non-fatty liver disease. alcoholic.
The proteins studied are involved in epigenetic regulation, which controls the expression of genes, and inflammation, which plays an important role in the disease.
The researchers observed that both groups of patients exhibited significant differences in the expression of proteins involved in epigenetic regulators and inflammation.
It is important to note that these differences correspond to the observed liver cancer development ratio for both groups. "If, thanks to additional studies, we can prove that the molecules and pathways we have identified modulate the development of liver cancer in alcoholic fatty liver patients, this could help identify new targets to prevent or reduce the risk of liver cancer arising from other liver diseases, "said Jia.
The researchers plan to carry out additional experiments on animal models of fatty liver to learn more about the epigenetic and inflammation-regulating mechanisms leading to liver cancer.
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