New York, NY, July 15, 2025—Researchers at the Icahn School of Medicine at Mount Sinai and collaborators have identified a previously overlooked protein, Epac1, as a key driver of idiopathic pulmonary fibrosis (IPF), a chronic and progressive lung-scarring disease. Their findings, demonstrated across cell cultures, preclinical models, and samples of human lung tissue, show that blocking Epac1 can slow the progression of the disease.

Published in the July 7 online issue of European Respiratory Journal [https://doi.org/10.1183/13993003.02250-2024], the work could pave the way for a new class of treatments to help patients with this currently incurable condition. Published in the July 7 online issue of European Respiratory Journal [https://doi.org/10.1183/13993003.02250-2024], the work could pave the way for a new class of treatments to help patients with this currently incurable condition.

Conventional handheld photoacoustic and ultrasound Imaging (PAUS), while offering flexibility, offers only a narrow view of the target region, providing limited information on its structure. Alternative methods require external sensors and bulky equipment, which can also make measurements inaccurate. In a new study, researchers developed a MoGLo-Net, a deep-learning model for 3D reconstruction of 2D PAUS images. This method does not require any external sensors and can make treatments more accessible, safer, and effective.

Immune checkpoint blockade (ICB) therapies have revolutionized cancer treatment, yet many tumors remain resistant. Now, researchers at Korea University identifies the protein kinase WEE1 as a key driver of this resistance. They discovered that, outside its traditional role in the cell nucleus as tumor suppressor, cytoplasmic WEE1 fosters tumor growth and immune evasion by  enhancing AKT hyperactivation. Targeting WEE1 with clinically available inhibitors may re-sensitize tumors to immunotherapy, offering new hope for treatment-resistant cancer patients.