Duke-NUS scientists have discovered that ageing muscle may contribute to cancer growth by releasing fewer extracellular vesicles, tiny particles that cells use to communicate with one another. Their study also found that composition of these particles changes with age, weakening protective signals that help suppress tumour development. Encouragingly, exercise appears to restore this protective function.

Scientists at the State University of Campinas have identified a variable capable of predicting patients at higher risk of unfavorable disease progression by combining data on the radiodensity of visceral fat and muscle.

A new study led by researchers at The University of Texas MD Anderson Cancer Center has uncovered a previously unknown connection between nucleic acid structures called R-loops and age-related inflammation – or inflammaging – that could herald new intervention options for chronic inflammation and the subsequent health conditions.

A comprehensive multi-cancer study from researchers at The University of Texas MD Anderson Cancer Center has revealed that cancer cells within tumors are genetically diverse, yet all carry the same core genetic changes that can be traced back to a common ancestral cell, providing a single-cell view of how tumors adapt, survive and diversify. Understanding this helps explain why some cancer cells manage to survive treatments, paving the way for more tailored diagnostic and therapeutic strategies.

The Pew Charitable Trusts has selected Gladstone Institutes Investigator Magnus Hoffmann, PhD, to join its 2026 Pew Scholars Program in the Biomedical Sciences in order to advance his work developing cancer vaccines.

Christina Tringides is the recipient of the highly prestigious Pew Biomedical Scholar award.

BUFFALO, NY — June 16, 2026 — A new research paper was published in Volume 18 of Aging on May 22, 2026, titled “Systemic cancer risk profile in neovascular age-related macular degeneration: insights into shared aging-related mechanisms from a nationwide population-based study.”

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.