Our own contribution and what I have just presented is the accumulation of p62 and the activation of Nrf2 is a key event in the pathogenesis of HCC. I think, you either allow cells to accumulate reactive oxygen species and eventually accumulate mutations that can lead to cancer, or you allow these cells to die and never progress to cancer
We have described a population of hepatocytes that are much more effective in liver regeneration. We call them hybrid hepatocytes, and we hope that when we learn how to culture and isolate these cells from the human liver it will be a good treatment for degenerative liver diseases.
We need to improve on various techniques other than liver transplantation for the repair of liver damage and to better understand how to culture cells that have high regenerative capacity and do not lead to the development of cancer. This is going to be very important for the future.
The major differences are usually conceptual at least, to convince people who work on human HCC that the mouse studies are relevant to humans.
Unfortunately, I don’t think there have been any advances in HCC chemotherapy. When the patient has minimal liver function left, chemotherapy is really not applicable. The important thing is to detect HCC very early and to treat it aggressively when the liver can still tolerate a more aggressive approach to treatment.