Some 15 to 20 percent of all breast cancers are
triple-negative, meaning they lack receptors for estrogen, progesterone and
human epidermal growth factor type 2. They have the worst prognosis of all
breast cancers and very limited treatment options. Finding a treatment that distinguishes
between cancer cells and normal cells has been especially challenging.
A novel precision medicine strategy described today in Science Advancesoffers an intriguing ray of hope. Researchers at Boston Children’s Hospital, with bioengineers at the City College of New York (CCNY), showed that dually-targeted, antibody-guided nanoparticles, loaded with an existing chemotherapy drug, markedly improved tumor targeting, decreased tumor and metastatic growth and dramatically improved survival in a mouse model of triple-negative breast cancer. There were no observable side effects.
Most of us have somewhere around a trillion tiny platelets zooming around our bloodstreams. Joseph Italiano, PhD, of Boston Children’s Hospital’s Vascular Biology Program, calls them the “Swiss Army knives of the blood.” In addition to their key role in clotting, platelets are important in immunity, wound healing, chemical delivery, blood vessel development and more.
At healthcare facilities, platelets are in constant demand for patients with blood diseases, or those receiving radiation or chemotherapy for cancer. But unlike other blood products, platelets can’t be stored for more than a few days. If there’s a snowstorm or other emergency preventing donors from giving platelets, a hospital can easily run out. So researchers have been trying to make platelets in a lab setting.
Two teams at Boston Children’s Hospital are tackling the problem in slightly different ways. …
Endometriosis is a common
gynecological condition that may affect more than 1 in 10 reproductive-age
women. Yet, there’s very little research into the disease and limited options
for treatment. A team in the Vascular
Biology Program at Boston Children’s Hospital is trying to
Most of the time, cancer cells do a combination of two things: they overexpress genes that drive tumor growth and they lose normal genes that typically suppress tumors. No two tumors are exactly alike, but some combination of these two effects is usually what results in cancer. Now, for the first time, researchers have shown that it’s possible to treat cancer by delivering a gene that naturally suppresses tumors.
Researchers from Boston Children’s Hospital, Brigham and Women’s Hospital and Memorial Sloan Kettering Cancer Center combined their cancer biology and nanomaterials expertise and developed a therapeutic capable of delivering a tumor suppressor gene known as PTEN, the loss of which can allow tumors to grow unchecked.
In several preclinical models, their PTEN–boosting therapeutic was able to inhibit tumor growth. Their findings were published yesterday in Nature Biomedical Engineering. …
For the first time, scientists have shown that the elasticity of nanoparticles can affect how cells take them up in ways that can significantly improve drug delivery to tumors.
A team of Boston Children’s Hospital researchers led by Marsha A. Moses, PhD, who directs the Vascular Biology Program, created a novel nanolipogel-based drug delivery system that allowed the team to investigate the exclusive role of nanoparticle elasticity on the mechanisms of cell entry.
Sepsis, or blood poisoning, occurs when the body’s response to infection damages its own tissues, leading to organ failure. It is the most common cause of death in people who have been hospitalized, yet no new therapies have been developed in the last 30 years. Many treatments that have prevented death in animal experiments have failed in clinical trials, indicating that a more clinically-relevant sepsis model is needed for therapeutic development.
To bridge this gap, a team of scientists from the Wyss Institute at Harvard University and Boston Children’s Hospital think a better experimental model of sepsis in pigs could help weed out the therapies most likely to succeed in humans. Their method, a scoring criteria to evaluate sepsis in pigs that closely mirrors standard human clinical assessment, is reported in Advances in Critical Care Medicine.…
Three-dimensional modeling and CRISPR-Cas9 gene editing technology are giving scientists a new view into Sturge-Weber syndrome, a rare congenital disorder that causes small blood vessels, called capillaries, to be malformed. These capillary malformations can cause port wine birthmarks on the face and neck, and in some cases, abnormal vasculature in the brain that can spark seizures.
One of the biggest challenges facing cancer researchers — and lots of other medical researchers, in fact — is that experimental models cannot perfectly replicate human diseases in the laboratory.
That’s why human Organs-on-Chips, small devices that mimic human organ environments in an affordable and lifelike manner, have quickly been taken up into use by scientists in academic and industry labs and are being tested by the U.S. Food and Drug Administration.
Now, the chips have helped discover an important link between breathing mechanics and lung cancer behavior. …
On average, one in four people who have a heart attack sustain long-lasting damage to the mitral valve, which has the important job of making sure blood pumps through the heart’s ventricles in the right direction. If the valve is damaged, the heart’s pumping efficiency is reduced and blood can flow backward, which can lead to heart failure and death.
Now, a team of collaborators from Boston Children’s Hospital, Massachusetts General Hospital and Brigham and Women’s Hospital has shown, for the first time, that it’s possible to treat and even prevent mitral valve damage after heart attack with an FDA-approved, anti-hypertension drug called losartan. Their findings are published in the Journal of the American College of Cardiology. …
The average human has 60,000 miles of blood vessels coursing through their body. There are a number of mechanisms the body uses to keep that vast vascular network healthy, including a tiny fat molecule, a lipid called S1P, that plays a particularly important role.
S1P receptors dot the surface of the endothelium, a layer of cells that line the inside of all the body’s blood cells. Together, these so-called endothelial cells form a barrier between the body’s circulating blood and surrounding tissue. When S1P molecules activate their receptors, it suppresses endothelial inflammation and generally helps regulate cardiovascular health.
Now, researchers led by Timothy Hla, PhD, from the Boston Children’s Hospital Vascular Biology Program, report a novel therapeutic fusion that could trigger increased S1P receptor activity and recover blood vessel health following the onset of hypertension, atherosclerosis, stroke, heart attack and other cardiovascular diseases. …