AMHERST, Mass. – Researchers at the University of Massachusetts Amherst are developing microenvironments that allow them to study how cancer cells that move around in the human body change from dormant to active and what causes or prevents that change. Understanding this process, the researchers say, could lead to new treatments that prevent cancer from metastasizing throughout the body.
The research team is headed by Jungwoo Lee, assistant professor of chemical engineering. It includes Shelly R. Peyton, associate professor of chemical engineering, Ryan A. Carpenter, a graduate student, and Jun-Goo Kwak, an undergraduate, both in chemical engineering. Their latest findings are published in the journal Nature Biomedical Engineering.
The team, working in UMass Amherst’s Institute for Applied Life Sciences, is studying disseminated tumor cells (DTCs), cancer cells that have left the original tumor site and moved to other parts of the body. These cells are known to spread to distant organs in the body, but metastasis, transplanting active cancer cells to create new tumors, generally happens in a subset of organ tissues including lung, bone, liver and brain.
Understanding how the local microenvironment regulates the transition of DTCs from a quiescent state to active proliferation could suggest new therapeutic strategies to prevent or delay the formation of metastases, the researchers say.
As expected human life-span has significantly extended in the last few decades, cancer becomes the leading cause of death. The most limited aspect in treating cancer is the metastatic relapse after years and decades of asymptomatic dormancy. Standard clinical care for more than 11 million cancer survivors in the U.S. focuses on early detection. It is imperative to develop better therapies to prevent or delay metastasis.
In the recent Nature Biomedical Engineering paper, they report a new class of experimental metastasis model that can recapitulate and dissect the complex and dynamic processes of dormancy and recurrence of disseminated human tumor cells in the presence of human stromal and immune cells, the team says.
The result is that the tissue-engineered metastasis model captured three distinct stages of metastasis; early dormant, intermediate, and late advanced stages. “We believe our tissue-engineered metastasis model system can be used for quantitative testing the efficacy of anti-metastasis (metastasis prevention) drug screening as currently there exists no good experimental model for long-term suppression of metastasis,” Lee says.
Human immune cells can be replaced with chemotherapy drugs. In doing so, we can also study the positive and negative effect of chemotherapy that kills systemic spread active tumor cells but may awake dormant tumor cells via acute inflammation and microenvironment remodeling, he says. This capability can help find drugs that can mitigate and counter the negative impact of chemotherapy.