Atypical intraductal proliferation is a prostate biopsy finding with morphological features intermediate between high-grade prostatic intraepithelial neoplasia and intraductal carcinoma. This Review discusses histopathological features, molecular characteristics and clinical outcomes associated with AIP, and highlights the clinical implications of AIP, primarily due to the frequent association of AIP with clinically significant prostate cancer.
Glioblastoma (GBM) is one of the most common and aggressive primary brain tumors in adults, carrying an extremely poor prognosis and a median overall survival typically less than two years. Temozolomide (TMZ) is currently the only chemotherapeutic agent widely used in clinical practice. However, around 90% of cases experience tumor recurrence due to acquired resistance. How to overcome TMZ resistance remains a challenge.
In a study published in Nature Chemical Biology, Dr. Dong Peng’s team from the Shenzhen Institute of Advanced Technology of the Chinese Academy of Sciences and collaborators from Sun Yat-sen University have discovered that TMZ treatment induces the formation of HDAC1-CTCF condensates in GBM cells. The team identified the small-molecule compound resminostat as a therapeutic agent capable of targeting these condensates.
Through three-dimensional (3D) super-resolution imaging independently developed by Dr. Dong’s team, the researchers observed a significant reduction in chromatin accessibility in TMZ-resistant GBM cells. The team characterized their 3D genomic structural features, and revealed that the decreased chromatin accessibility in resistant cells is primarily attributed to TMZ-induced formation of HDAC1-CTCF condensates, which accumulate on chromatin and restrict local accessibility.
Severe blood loss remains the primary cause of death from combat injuries. To address this challenge, a research team at KAIST that included an active duty Army Major set out to develop a faster and more reliable way to stop bleeding.
Their work led to a next-generation powder-type hemostatic agent that can halt bleeding within one second when sprayed directly onto a wound, offering a potential breakthrough for saving lives on the battlefield.
Here, Marco L. Davila & team recapitulate these high-grade toxicities in mice, revealing Th1-Th17 imbalance drives the co-occurrence of CRS and neutropenia; effects that could be prevented with IFNg blockade.
4Department of Medicine, Roswell Park Comprehensive Cancer Center, Buffalo, New York, USA.
5University of Florida College of Medicine, Division of Hematology-Oncology, Gainesville, Florida, USA.
6Department of Blood and Marrow Transplant and Cellular Immunotherapy, H. Lee Moffitt Cancer Center & Research Institute, Tampa, Florida, USA.
Jun Inamo & team profiles nearly 400,000 cells across 9 patients with juvenile idiopathic arthritis (JIA), revealing disease-specific immune–stromal interactions within the synovium.
1Department of Biomedical Informatics, Center for Health Artificial Intelligence, and.
2Division of Rheumatology, University of Colorado School of Medicine, Aurora, Colorado, USA.
3Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Sarcoidosis is a systemic, granulomatous disorder commonly affecting the lungs that has the potential to cause numerous thoracic complications. We present a novel case of a 44-year-old woman with pulmonary sarcoidosis who demonstrated a large pulmonary infarction. The disease presentation ultimately was attributed to arterial stenosis resulting from sarcoidosis-associated fibrosing mediastinitis and compressive mediastinal adenopathy. The patient was treated with an extended course of prednisone and subsequently was transitioned to azathioprine with eventual resolution of symptoms, but persistence of imaging findings.
Enzymes are the molecular machines that power life; they build and break down molecules, copy DNA, digest food, and drive virtually every chemical reaction in our cells. For decades, scientists have designed drugs to slow down or block enzymes, stopping infections or the growth of cancer by jamming these tiny machines. But what if tackling some diseases requires the opposite approach?
Speeding enzymes up, it turns out, is much harder than stopping them. Tarun Kapoor is the Pels Family Professor in Rockefeller’s Selma and Lawrence Ruben Laboratory of Chemistry and Cell Biology. Recently, he has shifted the focus of this lab to tackle the tricky question of how to make enzymes work faster.
Already, his lab has developed a chemical compound to speed up an enzyme that works too slowly in people with a rare form of neurodegeneration. The same approach could open new treatment possibilities for many other diseases where other enzymes have lost function, including some cancers and neurodegenerative disorders such as Alzheimer’s.