With the fight against cancer focusing at the molecular and genetic levels, the role played by the surrounding non-cancerous cells is coming under increasing scrutiny. Now scientists at the University of North Carolina at Chapel Hill have demonstrated that these supporting cells are indeed key players in the ultimate development and aggressiveness of cancer.
These findings were arrived at after studying a genetically engineered mouse model of prostate cancer. The researchers also accelerated the development of the cancer in the tumor cells. This rapid rate caused a change in the fibroblasts in the surrounding cells. These fibroblasts, which are connective tissue cells, began to proliferate rapidly. Eventually these fibroblasts lost the protective action of the tumor suppressor, p53. This meant that the cells continued to merrily divide thereby evolving as cancer cells. "This occurred in 100 percent of the animals studied. It's a strong selective pressure," said Dr. Terry Van Dyke, professor of genetics and biochemistry and biophysics in the School of Medicine, member of the UNC Lineberger Comprehensive Cancer Center and lead author of the study. "Now the whole organ is evolving as a cancer, not just a single population of cells." Van Dyke added that the interaction between the predominant cancer cell and the surrounding cells played a key role in the development of the cancer. "Think of it as a microcosm of evolution, such that every change that goes on in the cancer cell can impact cells around it. It's a back-and-forth cross-talk via which the whole entity evolves, not just a subset of cells within the cancer. It's an environment where changes in the surrounding cells are selected that will help tumor growth."
Although the study has no immediate implication in the fight against cancer, it does provide valuable insights into what goes on in the supporting cells. Future anti-cancer therapies can be evolved after taking these interactions into consideration. The findings of the UNC team are published in the December 16 issue of the journal Cell. Graduate student Reginald Hill and postdoctoral researcher Dr. Yurong Song. Dr. Robert D. Cardiff, professor of pathology at the University of California at Davis, also collaborated in the study.
Contact: L.H. Lang
University of North Carolina School of Medicine