The key to regeneration has been inside you all along, new research suggests.
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Copper-induced cell death stimulates antitumor immune cell responses
A preclinical study from researchers at The University of Texas MD Anderson Cancer Center, published today in Cell, details a connection between the immune system and cuproptosis, a type of copper-induced cell death. The findings suggest a new approach to help overcome resistance to immunotherapy.
The study, led by Boyi Gan, Ph.D., professor of Experimental Radiation Oncology, demonstrates that cancer cells undergoing cuproptosis release signals that activate the immune system. Significantly, this study is among the first to demonstrate that cuproptosis can actively engage the immune system and enhance responses to immunotherapy. In preclinical models, a combination approach of cuproptosis-inducing treatment along with anti-PD-L1 immunotherapy significantly slowed tumor growth.
“This study reveals a previously unrecognized partnership between the immune system and cuproptosis,” Gan said. “Importantly, because the cuproptosis-inducing agents used in our studies already have clinical experience and favorable safety profiles, these findings may offer a practical path toward developing new combination treatments for patients whose cancers no longer respond to immunotherapy.”
An open competition for biomarkers of aging
Ying, K., Paulson, S., Reinhard, J. et al. An open competition for biomarkers of aging. Nat Aging 6, 1193–1195 (2026). https://doi.org/10.1038/s43587-026-01139-6
The Revolving Door of Adenovirus Cell Entry: Not All Pathways Are Equal
An interesting review on adenoviral cell entry and trafficking. Its discussion of how species B adenoviruses tolerate lower endosomal pH and accumulate in later-endosomal compartments before escaping were particularly intriguing. Link.
Adenoviruses represent exceptional candidates for wide-ranging therapeutic applications, from vectors for gene therapy to oncolytics for cancer treatments. The first ever commercial gene therapy medicine was based on a recombinant adenovirus vector, while most recently, adenoviral vectors have proven critical as vaccine platforms in effectively controlling the global coronavirus pandemic. Here, we discuss factors involved in adenovirus cell binding, entry, and trafficking; how they influence efficiency of adenovirus-based vectors; and how they can be manipulated to enhance efficacy of genetically modified adenoviral variants. We focus particularly on endocytosis and how different adenovirus serotypes employ different endocytic pathways to gain cell entry, and thus, have different intracellular trafficking pathways that subsequently trigger different host antiviral responses.
Opposing protein pathways steer skin stem cells toward renewal or repair
Two proteins with opposing functions orchestrate the development and maintenance of healthy skin, Stanford Medicine researchers have found. Modulating their activity with topical drugs could reduce inflammation, aid wound healing and slow or halt the growth of skin cancer, the researchers believe. The findings are published in the journal Science.
The proteins are part of a family called ubiquitin-like proteins. Ubiquitination controls the targeted destruction and disposal of unneeded proteins in a cell. But in the skin, certain ubiquitin-like proteins instead switch on or off wide swaths of genes involved in cellular growth and development, the study found. In particular, they trigger progenitor (stem) cells in the lower layer of the skin to either mature and migrate to the skin surface or to self-renew.
“These two ubiquitin-like protein systems are remarkably dedicated and opposite in their functions,” said Paul Khavari, MD, Ph.D., chair of dermatology at the Stanford School of Medicine and senior author of the study. “One promotes the stem-cell state while the other drives differentiation. It’s like having two opposing forces that determine a cell’s fate.”
Ancient stellar flyby may still be steering long-period comets today
The Gaia mission has allowed researchers to understand the motions of stars like never before, even revealing possible interactions between our solar system and nearby stars. Planetary Science Institute Senior Scientist Nathan Kaib and collaborator Sean Raymond (Universite de Bordeaux) have found that a recent stellar passage likely triggered a huge increase in comet formation as the star’s gravity altered Oort cloud objects’ orbits, sending them cascading into the inner solar system. We may even still be feeling the effects of this passage today. This work is being presented at the American Astronomical Society Division on Dynamical Astronomy.
HD 7,977 is a nearby sun-like star in the constellation Cassiopeia whose close passage was discovered by the Gaia mission. Approximately 2.5 million years ago, the orbits of the sun and HD 7,977 brought the two stars close together, but exactly how close is still an open question. Gaia data suggest they passed within 4,000–25,000 astronomical units of one another. Now, Kaib and Raymond have shown that the orbits of long-period comets suggest HD 7,977 came within 6,000–10,000 AU of our sun, setting off a major shower of new comets into the inner solar system.
Scientists measure hidden quantum forces that could power a new generation of pharmaceutical drugs
It’s one thing to design a pharmaceutical drug. It’s another to know if and why it actually works; not on paper or in a computer model, but inside the chaotic world of living systems, where proteins twist into shape, atoms constantly pull and push each other apart, and molecular interactions are the difference between health and disease.
For decades, scientists have known that these interactions are driven by hidden quantum forces. The problem is that, like working blindfolded, they’ve never been able to measure them directly in biological systems.
Now, that era of blindfolded work may be ending.
Iron accumulation in the brain may contribute to neurodegeneration
Neurodegenerative diseases affect tens of millions of people worldwide. Among these, Alzheimer’s and Parkinson’s diseases are the most common; in the United States alone, the Alzheimer’s Disease Association and Parkinson’s Foundation report roughly 7 million people with Alzheimer’s and another million with Parkinson’s. An intriguing clue lies in the tangled mystery of neurodegeneration that scientists are working to solve: iron accumulation.
Scientists have noticed that iron can slowly build up inside neurons. Early in life, this iron accumulation appears to have little effect on neuronal function. However, later in life, it can contribute to a slow neuronal demise. Salk Institute researchers studied nerve cells to figure out whether and how this iron accumulation relates to neurodegenerative diseases. They found that the excess iron stuck in neurons lowers the cells’ defenses, making them more vulnerable to stressors and other cellular insults through a process they named chronoferroptosis.
The study, published in Cell Death Discovery on June 18, 2026, points to iron accumulation as a key target in the effort to predict, prevent and treat neurodegenerative diseases.