The Glue of Life

(3 of 4)

Another antiadhesion drug is being developed for the treatment of traumatic shock. Here too the goal is to prevent the body's own healing process from going awry. Traumatic shock can occur when accident victims lose large quantities of blood, causing cells in vital organs to starve for oxygen. The starving tissues trigger a distress signal that summons leukocytes and other members of the body's damage-control team, which begin to destroy distressed cells. Alas, if the signal stays on too long, cells are killed at a phenomenal rate and major organs begin to die even while hospital trauma teams are rushing to the rescue. Each year 25% of the shock victims who make it to the emergency room are revived only to die later. "It seems evolution never intended for someone to be resuscitated after shock," says John Harlan, head of hematology at the University of Washington in Seattle. Harlan and his colleagues hope to outfox evolution with a CAM-blocking drug that keeps white cells from sticking after shock. In a series of animal studies, the drug saved 75% from certain death.

Furthest along of the new adhesion drugs is an "artificial matrix" designed to promote wound healing. Normally, a wound site looks like the Grand Canyon to arriving rescue cells. But this biodegradable gel, produced by Telios Pharmaceuticals, is peppered with synthesized CAM molecules so that cells arriving at a wound site will have plenty of places to get a grip. With the new gel filling in the gap, repairing wounds, including severe burns or skin ulcers, takes 30% less time and leaves less of a scar, claims company scientific director Michael Pierschbacher.

All this is coming from a science that nearly became extinct. Following some excitement during the war on cancer in the early 1970s, many scientists abandoned the field in frustration for the more glamorous search for the genes of disease. Yet a handful pressed on, captives of their own curiosity. Many, like Harvard's Martin Hemler, had their research proposals regularly sent back from the U.S. National Institutes of Health stamped IRRELEVANT. Without a group to call their own, with no papers circulating, with no annual meetings, sticky cellsters worked in isolation, unaware that anyone else was keeping the faith.

Two events saved the field. The first, in 1976, was the discovery of hybridoma technology. This allowed scientists to build exquisitely precise probes to explore cell surfaces and search for CAMs. The second boost came in the mid-1980s, when M.I.T.'s Hynes noticed a resemblance between research coming from obscure labs working on cancer, immunology, developmental biology and hematology. Hynes began to see that these researchers were all exploring aspects of cell adhesion. In 1987 he drew together these separate lines of research and published a landmark paper in the journal Cell that finally connected the dots. "All of a sudden, these fields fused; they were one," says Hynes.