You are what you eat, the saying goes. For some conditions (think cardiovascular disease or type 2 diabetes), there are clear connections between diet, health and illness.
For breast cancer, the picture is less clear. Many epidemiologic and laboratory studies have examined the Western diet (in particular, cholesterol) and its relation to breast cancer, with conflicting results.
“There’s been a raging debate in the field,” says Christine Coticchia, PhD, who works in the laboratory of Boston Children’s Hospital’s Vascular Biology Program director, Marsha Moses, PhD. “The biology of cancer and of cholesterol are so complex, and there are many subsets of breast cancer. In order to find any connections, you have to ask very specific questions.”
Banding together with Keith Solomon, PhD, in Boston Children’s Urology Department, Coticchia and Moses asked whether dietary cholesterol might encourage progression of the most aggressive, so-called “triple-negative” breast tumors. As they report in the American Journal of Pathology, they found a big impact, at least in mice. But it’s too early to say just yet that cutting back on cholesterol will help women avoid breast cancer. …
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. …
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. …
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. …