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The team, led by CSHL Associate Professor Mikala Egeblad and researchers from the Dana Farber Cancer Institute and UC Davis, also demonstrates a way of blocking the signaling that awakened the dormant cancer cells, a concept that could prevent cancer recurrence or lessen its frequency.
Researchers showed that sustained lung inflammation, caused either by exposing mice to tobacco smoke or to a component of bacteria- endotoxin, induced common white blood cells-neutrophils to awaken nearby dormant cancer cells in an extraordinary way.
Neutrophils, which kill invaders like bacteria and yeast, have several ways of vanquishing their prey. One is to expel their DNA into the space beyond the cell membrane. Laced with toxic enzymes, this expelled DNA forms a gauzy, net-like trap (called neutrophil extracellular traps, or NETs) that can kill a pathogen.
Sustained lung inflammation causes the formation of NETs in the area around dormant cancer cells. Two enzymes in the NETs, called NE (neutrophil elastase) and MMP9 (matrix metalloproteinase 9), interact with a protein in tissue called laminin. In sequence, first NE then MMP9 make cuts in laminin proteins. This changes the protein’s shape, exposing a new surface, called an epitope.
This epitope, when recognized by dormant cancer cells nearby, spurs signaling that awakens the cancer cells. The dormant cancer cells recognize that new shape of the laminin and should start growing again. They created an antibody to block the epitope exposed on the laminin proteins. In mice, this prevented the reawakening of dormant cancer cells.