"The interaction between the predominant cancer cell type and other types of surrounding cells is important in the development of disease."
The signals that go back and forth between cells contain selective pressures, not only on the cancer cell itself but also on the surrounding cell, she said.
"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."
Van Dyke's UNC collaborators in the new research were 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.
Their series of experiments involved a genetically engineered mouse model of prostate cancer developed in Van Dyke's UNC laboratory. The researchers manipulated epithelial cells ?the target cell type for prostate cancer ?causing them to divide at an accelerated rate.
First, they found that this accelerated division triggered a signal to fibroblasts, connective cells in the surrounding supporting tissue, to grow and proliferate. The signal then induced a tumor suppressor, p53, within the fibroblasts, which stopped this action.
Thus, a change made only in epithelial cells had an impact on surrounding tissue cells.
Next, the researchers showed that fibroblasts eventually lost p53 function. This resulted in cells continuing to divide and proliferate, thereby fueling the cancer's growth. "This occurred in 100 percent of the animals studied. It's a strong selective pressure," Van Dyke said. "Now the whole organ is evolving as a cancer, not just a single populati
Source:University of North Carolina School of Medicine