Any given tumor is composed of a multitude of cell types that can each look or behave differently from its neighbors. An emerging body of research suggests that these differences can influence disease progression or the way a tumor responds to drugs.
Now, a new study by Harvard Medical School scientists shows that such cell diversity can also play a critical role in a cancer’s ability to invade distant sites throughout the body, a process known as metastasis.
The research, conducted in mice and published in Nature Communications, identifies a transient, cooperative interaction between ovarian cancer cells that allows otherwise nonmetastatic tumor cells to metastasize.
The team isolated subpopulations of cells from human ovarian tumors and found that none had the ability to form metastatic tumors on its own. But when certain subpopulations commingled, a cooperative biochemical interaction between the cells acted as a switch that triggered metastasis.
The findings shed light on a novel mechanism that drives tumor spread and opens new paths of study to prevent or design targeted treatments against one of cancer’s deadliest features.
“Crosstalk between otherwise innocuous cells within a tumor can play a key role in determining the metastatic capacity of a cancer,” said senior study author Joan Brugge, the Louise Foote Pfeiffer Professor of Cell Biology in the Blavatnik Institute at HMS.
“This mechanism needs to be considered in efforts to identify relevant therapeutic targets for the extremely difficult challenge of blocking metastasis,” said Brugge, who is also co-director of the Ludwig Center at Harvard.
HMS Labcast spoke with Joan Brugge on her path to cancer biology