The main causes of liver cancer (also known as hepatocellular carcinoma [HCC]), which is the fifth most common cancer in the world, are well defined. However, the molecular pathways activated by the triggers of liver cancer are not well characterized.
In a new study, Snorri Thorgeirsson and colleagues from the National Institutes of Health, Bethesda, shed some light on this, showing that the extent to which the genome of a person's liver cancer cells is modified by a process known as methylation correlates with clinical outcome. They therefore suggest that preventing aberrant methylation or targeting the genes whose expression is altered by the aberrant methylation might provide new targets for the treatment of liver cancer.
Detailed analysis of the methylation status of the genome of human liver cells revealed that tumor cells could be identified from healthy cells by genome-wide hypomethylation and CpG hypermethylation.
Furthermore, greater genome-wide hypomethylation and CpG hypermethylation correlated with shorter survival. In addition, these changes in methylation were associated with selective inactivation of a number of genes, including inhibitors of Ras and some inhibitors of angiogenesis.
The authors therefore suggest that in individuals with liver cancer, analyzing the methylation status of the genome of their tumor cells might have prognostic value and that either modifying genome methylation or targeting the Ras pathway might have therapeutic value.
Article: Mechanistic and prognostic significance of aberrant methylation in the molecular pathogenesis of human hepatocellular carcinma
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