Cancer cells in the pancreas are capable of repressing the human immune system to facilitate tumor growth, the science journal Blood reported.
The study’s author, Hsieh Shie-liang (謝世良), an immunology professor at National Yang Ming University’s Institute of Microbiology and Immunology, told reporters that pancreatic cancer cells were found to release decoy receptor 3, or DcR3, to interfere with the immune system.
“The DcR3s can promote angiogenesis, induce dendritic cell apoptosis and disarrange macrophage differentiation,” Hsieh said, adding that dendritic cells and macrophages would block tumor growth if they were not “turned off” by the DcR3.
In the human immune system, dendritic cells serve as “identifiers” that can tell the system whether a target is friendly or not; macrophages are the “vanguards” that release alerts to T-cells destroying abnormal cells.
“By disabling these two cells, the cancer cells can earn themselves precious time for growth,” Hsieh said.
Angiogenesis is the development of a network of blood vessels that feed cancerous growths and is considered to be a key element in the spread of cancers.
In the May 15 issue of Blood, the team — composed of researchers from National Yang Ming University, Chang Gung Memorial Hospital and Academia Sinica — showed in transgenic rodents that the over-expression of DcR3 can inhibit macrophage’s activity and reduce the survival time of pancreatic cancer patients.
Earlier studies indicated that high levels of DcR3s could be observed in 50 percent of human patients with pancreatic cancer: The higher the level of DcR3, the less effective chemotherapy becomes and the shorter the life expectancy.
As for the possibility of developing new drugs based on the findings, Hsieh said that, in theory, a histone deacetylase inhibitor could repress DcR3’s expression, but real application requires further research.