Researchers at MUSC Hollings Cancer Center and the University of Arizona have uncovered a previously unknown way that prostate cancer cells can survive treatment, helping explain why some therapies eventually lose effectiveness. The study, led by Noel Warfel, associate professor of Biochemistry and Molecular Biology at MUSC, focused on PIM1, a protein that is active in many prostate cancers and has long been considered a promising drug target.

The team found that while existing PIM1 inhibitors successfully block the protein’s signaling activity, they also cause cancer cells to accumulate larger amounts of the PIM1 protein itself. The excess protein activates a separate survival pathway that helps cancer cells to withstand treatment. Specifically, PIM1 promotes a process called mitophagy, which allows cancer cells to remove damaged mitochondria, reduce oxidative stress and continue surviving despite therapy.

The findings suggest that simply inhibiting PIM1 may not be enough. Instead, researchers showed that completely degrading the protein could be a more effective strategy. Using an experimental drug known as PIMTAC, Warfel’s team removed PIM proteins from cancer cells rather than blocking their activity. In laboratory studies and mouse models, this approach increased oxidative stress in tumor cells and led to greater cancer cell death.

The discovery provides new insight into how prostate cancer develops treatment resistance and highlights a potential path toward more effective therapies. Beyond prostate cancer, the findings could have implications for other cancer types where PIM proteins play a role in tumor survival and drug resistance.

A research team from the Institute of Aging and Regenerative Medicine at Jinan University, China, has examined how aging and disease are connected by exploring the aging-related remodeling of chromatin architecture. This study of chromatin architecture, the three-dimensional organization of DNA, gives scientists a better understanding of aging and its underlying mechanisms. Their review is published in Aging Research on May 8, 2026.

A new study investigates autologous rib cartilage resorption in microtia reconstruction, identifies fixation material-induced inflammation, gene dysregulation and mitochondrial dysfunction as key mechanisms, and provides insights for clinical intervention.

This review addresses the growing global burden of hereditary hearing loss, summarizes key advances in gene therapy, and aims to accelerate its clinical translation.

Type 2 diabetes (T2D) is marked by insulin resistance together with the progressive failure of pancreatic β-cells. Increasing evidence suggests that this failure is shaped not only by β-cells themselves, but also by the local islet immune microenvironment, where resident and recruited macrophages can influence inflammation, islet architecture, and insulin secretion. Exercise is a cornerstone of diabetes management, yet how it acts within this islet microenvironment has remained unclear.

A new fluorescent reporter capable of visualizing biologically active iron and oxygen inside living cells at single-cell resolution has been developed, as reported by researchers from Science Tokyo. Using this new tool, they revealed striking differences in the distribution of iron and oxygen across organs and even between neighboring cells of the same type. This innovation could serve as a platform for studying cancer, liver diseases, neurodegeneration, and aging.