The main cause of hepatocellular carcinogenesis today is chronic liver disease following HCV and HBV infection.

By virtue of recent advances in treatment methods, the number of patients with HCC caused by these infections is expected to decrease in the future.

 

On the other hand, the number of patients with NAFLD and NASH is increasing due to lifestyle changes, and there is growing concern that the number of HCC patients derived from these metabolic diseases will increase ^[1].

 

Various molecular biological pathways have been implicated in the carcinogenic mechanism of HCC.

Today, we would like to share the gene expression data of one of the major pathways, “the Wnt/β-catenin pathway”, in our STAM™ model.

 

In human HCC patients, mutations in the β-catenin gene and its downstream signal activation have been reported ^[2].

We have analyzed the gene expression of β-catenin and its downstream signals in the STAM™ model using RNAseq data.

 

In the HCC phase, an increasing trend in expression of these genes was confirmed, and mutations in the β-catenin gene were found in around half of individuals. Since this model shows a similar expression pattern in the Wnt/β-catenin pathway as seen in the human disease, we believe that this model could be useful to validate drug efficacy against HCC.

 

 

In HCC research, it is considered essential to use not only a single model but combine multiple models.

If you are currently considering research in the field of oncology, why not consider using this model for your research?