Stories about: Vascular Biology Program

Capturing complexity: Modeling bone marrow on a chip

Bone marrow on a chip organs on chips Wyss Institute Donald Ingber
Microscopic view of the engineered bone with an opening exposing the internal trabecular bony network, overlaid with colored images of blood cells and a supportive vascular network that fill the open spaces in the bone marrow-on-a-chip. (James Weaver, Harvard's Wyss Institute)

We’ve had a lung on a chip, and a gut on a chip. Now researchers at the Wyss Institute for Biologically Inspired Engineering have added another tissue to their list of “organs-on-chips”— devices that mimic in vitro tissues’ in vivo structure and function for pharmaceutical discovery and testing. In a paper published in Nature Methods, a team led by Donald Ingber, MD, PhD, (a member of Boston Children’s Hospital’s Vascular Biology Program and founding director of the Wyss), announced that they have developed “bone marrow-on-a-chip.”

The sheer complexity of the new device sets it apart from the Wyss’s previous organs, reflecting the greater natural complexity of bone marrow.

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The platelet whisperers

Finding the switch that gets megakaryocytes to produce platelets
To manufacture platelets in the laboratory, we need to find the switch that starts their production.
Looking down at my bandaged finger—a souvenir of a kitchen accident a few nights prior—Joseph Italiano, PhD, smiles and says to me, “You should have come by, we could’ve given you some platelets for that.”

The problem is that Italiano really couldn’t; he needs every platelet his lab can put its hands on. A platelet biologist in Boston Children’s Hospital’s Vascular Biology Program, Italiano is trying to find ways to manufacture platelets at a clinically useful scale.

To do that, he needs to develop a deep understanding of the science of how the body produces platelets, something that no one has at the moment.

The path by which blood stem cells develop into megakaryocytes—the bone marrow cells that produce and release platelets into the bloodstream—is already known, Italiano says. We also know that platelets are essentially fragments of megakaryocytes that break off in response to some signal.

But that’s where our knowledge of platelet production largely ends. “Megakaryocytes themselves are something of a black box,” Italiano explains. “If you microinject the cytoplasm of an active megakaryocyte into a resting megakaryocyte, it will start to produce platelets as well. But we don’t know what factor or factors cause them to start platelet production.”

As Italiano and his laboratory peer into that black box, they know the stakes are big. Because in the end, they want to greatly reduce doctors’ and patients’ dependence on donated platelets.

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A day in the life: A pediatric neurosurgeon’s vision

Ed Smith explains the moyamoya operation during a live webcast.

Lindsay Hoshaw contributed to this post.

It’s 7 a.m. and neurosurgeon
Ed Smith, MD
, is downing a Diet Coke as he reviews the MRIs of today’s patients. He sprints up a stairwell to greet his first patient in the pre-operating wing.

Thirteen-year-old Maribel Ramos, about to have brain surgery at Boston Children’s Hospital, sits in her bed fidgeting. Smith reassures her about the operation, promises they’ll shave off as little hair as possible, and gets Maribel to crack a smile by telling her he moonlights as a hairdresser.

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Rousing dormant tumors: Where’s the “on” switch?

Like a seed, a tumor can remain dormant for years. But what's the trigger that causes a tumor to switch from dormancy to aggressive growth? (OpenCage/Flickr)

Believe it or not, you—and I, and everyone around us—quite likely has cancer right now.

While just a third of us will be diagnosed with cancer in our lifetimes, more than 90 percent of us harbor dormant, microscopically small tumors—maybe just a few cells in size—that will never be cause for alarm.

“Most people will live their lives without these tumors growing any larger,” says Randy Watnick, PhD, a researcher in the Vascular Biology Program at Boston Children’s Hospital. “But why? What is the difference between tumors that remain dormant and those destined to grow?”

It’s no small question: As screening and diagnostic technologies improve (allowing us to detect tumors smaller and earlier), the risks of overtreatment rise. That’s fueling a need for better ways to sift potentially dangerous tumors out from ones that will stay quiet.

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