Researchers from the University of Pittsburgh School of Medicine report a significant new advance in the search for an effective treatment for human liver cancer in the July issue of Molecular Cancer Therapeutics.
Using a newly available monoclonal antibody, they demonstrated significant reductions in tumor cell proliferation and survival in human and mouse hepatocellular cancer (HCC) cell lines.
According to the researchers, this finding has significant implications not only for the treatment of liver cancer but for a number of different types of cancer.
Most cases of HCC are secondary to either a viral hepatitis infection or cirrhosis of the liver. Despite recent advances, it remains a disease of grim prognosis due to the poorly understood mechanism of how the disease originates and spreads. Most patients live only a short time after diagnosis.
Based on previous studies showing that some pathways that were previously thought to be active only during fetal liver development, particularly the class III receptor tyrosine kinase (RTK) family pathway, became highly active again in the liver of HCC patients, Satdarshan P. Singh Monga, M.D., associate professor, division of cellular and molecular pathology and colleagues at the University of Pittsburgh School of Medicine, obtained rat and human liver cancer cell lines and analyzed them for level of expression of an RTK protein known as platelet-derived growth factor receptor-alpha.
The investigators also analyzed the cells for their level of activation of the PDGFR gene.
At an early fetal stage of liver development in the mouse, the investigators found that the level of expression of PDGFR was 37 times higher compared to later stages of development in the adult mouse liver.
They also found significantly higher levels of PDGFR in rat and human liver cancer cell lines as compared to normal cells in culture.
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