Researchers have identified a new potential weapon against Alzheimer’s: blocking a protein called PTP1B. In mice, this approach boosted memory and helped brain immune cells clear harmful plaque buildup. Since PTP1B is also linked to diabetes and obesity—both risk factors for Alzheimer’s—it could offer a broader treatment strategy.
Barrier organs that form boundaries between the body and the outside environment, such as the lungs, skin, and intestines, face a difficult balancing act. They must respond quickly to threats such as infection, but they also need to avoid triggering unnecessary inflammation that can damage the tissue. A new study led by Whitehead Institute member Pulin Li and graduate student in her lab Diep Nguyen reveals one way the lung manages that tradeoff.
Published in Cell Systems, the research found that immune sensitivity is not evenly distributed across the lung. Instead, it arranges in tiers: cells at the outer surface respond cautiously, while cells deeper in the tissue are more likely to sound the alarm when a threat breaks through.
“The central question was how tissues balance the benefits and harmful effects of immune activation when they face different degrees of danger or stress,” says Li, who is also a professor of biology at MIT. “Too little immune activation leaves the tissue unprotected, but too much can create inflammation and damage.”
A personalized vaccine to treat glioblastoma, a fast-growing and incurable brain cancer that affects four in 100,000 people in the U.S., is safe and elicits robust and broad immune responses that appears to increase recurrence-free survival in a subset of patients after surgery, according to an early-stage clinical trial co-led by researchers at Washington University School of Medicine in St. Louis.
In patients with an especially aggressive form of glioblastoma, the vaccine caused no serious side effects and prolonged patients’ overall survival compared to historical outcomes after standard-of-care surgery and chemo-radiotherapy. One long-term survivor remains recurrence-free nearly five years later.
The results of the phase 1 trial, conducted at Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine, were published May 12 in Nature Cancer. The study was led jointly by Mass General Brigham and Geneos Therapeutics, a Philadelphia-based biotechnology company.
“We are extremely encouraged by these results,” said Tanner M. Johanns, MD, PhD, lead author of the study and an assistant professor in the Division of Oncology in the John T. Milliken Department of Medicine at WashU Medicine. “This kind of vaccine is a first for glioblastoma, and it is exciting to think how we can leverage this individualized therapeutic DNA cancer vaccine platform to make a positive impact on the lives of patients who are fighting this disease. Additionally, combination therapies leveraging this personalized platform are currently being investigated at WashU to test if outcomes may be improved further.”
Abstract: Nature Cancer
Johanns and colleagues report the results (including safety, efficacy and immunogenicity) of a phase 1 clinical trial of a DNA-based personalized therapeutic cancer vaccine administered following surgical resection and radiation in patients with MGMT unmethylated glioblastoma.
Researchers at Tampere University, Finland, have developed a groundbreaking 3D-printed ceramic implant material that closely mimics real human bone. The findings advance the development of personalized bone regeneration and may lead to more effective and accessible treatments for bone defects.
The research article, titled “Biomimetic bone calcium phosphate-based scaffolds fabricated via ceramic vat photopolymerization: Effect of porosity, sintering temperature, mineralogical phases and trace elements on the osteogenic potential,” was published in Materials Today Bio.
Bone grafting is the second most common tissue transplantation procedure worldwide, with more than 2 million operations performed annually. Current treatments often rely on bone taken from the patient or a donor, approaches that are limited in availability and may involve additional surgery, lengthy recovery times and complications. As populations age, the need for safer and more effective alternatives is growing rapidly.
In this study, we identify an unexpected and previously unrecognized role for PI3Kδ in promoting stromal fibrosis in PDAC, expanding its known function beyond immune regulation. Through mechanistic and preclinical studies, we show that PI3Kδ controls the biosynthesis of LPA in cancer cells and stromal fibroblasts, establishing an immunometabolic axis that sustains both fibrosis and immune evasion in PDAC.
Strikingly, PI3Kδ inhibition alone was sufficient to suppress tumor growth, reduce fibrosis, restore antitumor immune responses, and prolong survival across multiple PDAC models. Dual inhibition of PI3Kδ and ATX produced additive effects on stromal remodeling and immune activation, significantly enhancing responsiveness to chemotherapy and PD-1 blockade. These findings position PI3Kδ as a central regulator of the PDAC tumor microenvironment and highlight its therapeutic targeting, alone or in combination, as a promising strategy to treat PDAC.