Three children Alejandro Gutierrez, MD, treated for leukemia during his fellowship at Boston Children’s Hospital still haunt him more than a decade later. One 15-year-old boy died from the toxicity of the drugs he was given; the other two patients went through the whole treatment only to die when their leukemia came back. “That really prompted a deep frustration with the status quo,” Gutierrez recalls. “It’s motivated everything I’ve done in the lab since then.”
Gutierrez, now a researcher in the Division of Hematology/Oncology, has made it his mission to figure out why leukemia treatments cure some patients but not others. And in today’s issue of Cancer Cell, he and 15 colleagues report progress on two important fronts: They shed light on how leukemia cells become resistant to drugs, and they describe how two drugs used in combination may overcome that resistance, offering new hope to thousands of children and adults with leukemia.
The human immune system includes about a dozen major cell
types with specialized roles in the body’s defenses. They serve as sentries,
identify threats, mobilize troops, capture and transport invaders, interrogate
and kill those deemed dangerous and clear the battlefield of casualties. This intricate
command-and-control system is what enables us to fend off most of the dangerous
bacteria and viruses that come our way.
But in patients who suffer from inflammatory bowel disease (IBD), the immune system itself becomes the enemy. Even when the body faces no threat, immune cells called “helper T cells” take up arms, resulting in a kind of perpetual warfare that — far from being helpful — causes collateral damage to the gut.
“The system goes into overdrive,” says Yu Hui Kang, an
immunology graduate student at Harvard Medical School and a researcher at
Boston Children’s Hospital.
“These cells have gone too far, and they can’t stop.”
Now Kang and colleagues in the lab of Scott Snapper, MD, PhD, director of Boston Children’s Inflammatory Bowel Disease Center, may have found a way to turn the tables on the immune system by recruiting its own “natural killer” cells to wipe out the harmful T cells. Though clinical applications are years away, the work suggests new avenues for developing treatments for the debilitating disease.
Schwarz, PhD, is a cell biologist who conducts his research in a cluttered laboratory
overlooking Boston Children’s Hospital. But he likens his scientific approach
to that of the great explorers of the past. “It’s like
marching off into the jungle,” he says, “because you really don’t know what
you’re going to find.”
Schwarz and colleagues at the F.M. Kirby Neurobiology Center have just returned from an “expedition” that could profoundly change our understanding of how the nervous system forms — and give an unexpected new role to an old standby in cell biology: the kinetochore.