Scientists Discover New Way to Combat Hepatocellular Carcinoma

Inhibiting growth receptor presents promising treatment option.

A recent study revealed that the growth factor receptor FGFR3 increases the rate of growth and aggressiveness of hepatocellular carcinomas (liver cell cancer), meaning that the inhibition of this receptor could be a viable treatment option for patients.

Hepatocellular carcinoma (HCC) is the most common form of liver cancer and is one of the most aggressive tumors in the world. HCC accounts for 6% of all cancers in men and 3% of all cancers in women.

It is one of the most frequent causes of death from cancer and until now treatment options have been limited. Fibroblast Growth Factor Receptors (FGFR) are proteins found on the surface of cells, which control growth in organs and tissue.

A cell receives the command to divide if a growth factor binds to one of these receptors. There currently exist 4 members of the growth factor receptor family (FGFR1 to FGFR4) and 23 growth factors.

Some of the receptors are misregulated in certain types of cancers. However, its role in the development and progression of the disease is insufficiently researched. A recent study led by Bettina Grasl-Kraupp at the Institute for Cancer Research (Director Maria Sibilia) of MedUni Vienna has shown that both isoforms of FGFR3 play a role in the growth and progression of hepatocellular carcinoma.

The study involved analyzing cell lines and tumor tissue from HCC patients and conducting mouse model studies.

“The results showed that, in 50% of the HCC cases, there were noticeably raised levels of at least one of the two FGFR3 isoforms on the surface of the tumor cells,” said study lead author Jakob Paur, member of the Comprehensive Cancer Center (CCC) of MedUni Vienna and Vienna Genereal Hospital. “The greater the concentration of the receptor in the tumor tissue, the larger the primary tumor and the greater the probability of finding recurrences. When both FGFR3 isoforms in tumor cell lines were downregulated, tumor growth declined dramatically and the cells became much less aggressive. This was very clearly observed, not only in the cell culture but also in a mouse model.”