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The hidden role of a cell-cycle regulator in senescent cells that don’t divide

In a tale of identities as divergent as “The Prince and the Pauper,” a well-known cancer-causing gene also influences cells in a zombie-like state meant to prevent cancer.

Scientists at Sanford Burnham Prebys Medical Discovery Institute and an international team of collaborators published findings Aug. 20, 2026, in Nature Aging that unpack this biological paradox, showing that this cell proliferation gene played a distinct role in cells that no longer proliferate. It served as a driver of chronic inflammation linked to age-related disease, making it a promising target for future therapies to reduce sustained inflammation and promote healthier aging.

The code for producing the protein cyclin D1 is carried by the gene CCND1. This gene made waves in the field of oncology in the early-to mid-1990s when overexpressing it was shown to cause cancer. Normally, cyclin D1 governs the activity of signaling molecules needed to push cells along the cell cycle toward replicating their DNA and dividing to make new cells. This process goes haywire and becomes hyperactive in cancer, but it is nonexistent in zombie-like senescent cells.

Time’s great mystery

From the starting gun to the final whistle, time is central to our lives. We shape our days with diaries and timetables, even if the trains do not always take note. Yet the nature of time itself is elusive and unknown. A new year begins, and we get older, but however closely we look we cannot observe time, only its passing. Time is equally puzzling to science. Central to its laws from Newton to Einstein, science is unable to describe time itself. Strangely, in the so-called

Cancer is quantum: Studies show cancer cells may occupy limited, shared states like quantized energy levels

Andrea Califano began his career as a physicist. But that’s not why he’s now calling cancer a quantum disease. “We’re really just following the data,” says Califano, the Clyde ‘56 and Helen Wu Professor of Chemical Biology at Columbia University Vagelos College of Physicians and Surgeons and head of Biohub, New York.

“What we’ve seen over and over again is that each type of cancer has a limited number of cellular states. Just as electrons are restricted to a limited number of quantized energy states in an atom, cancer cells can only occupy one of these stable states or be in rapid transit between them. More critically, these states are conserved across virtually all patients with a specific type of cancer.”

The newest findings from the Califano lab—published recently in two papers in Nature Genetics —add critical evidence in support of the concept, which has enormous potential to transform and simplify the treatment of almost all cancers.

Unlocking 2e Potential: Helping TwiceExceptional learners Thrive, with Dr. Matt Zakreski

About our guest: Matthew “Dr. Matt” Zakreski, PsyD is a high energy, creative clinical psychologist and professional speaker who utilizes an eclectic approach to meet the specific needs of his neurodivergent clients. He is proud to serve the Gifted community as a consultant, a professor, an author, and a researcher. He has spoken nearly a thousand times all over the world about supporting neurodivergent clients, organizational wellness, and mental health. Dr. Zakreski graduated from Widener University’s Institute for Graduate Clinical Psychology (IGCP) in 2016. He is the co-founder of The Neurodiversity Collective, LLC, co-host of the podcast “Nerding out on Neurodiversity,” and the author of the Neurodiversity Playbook: How Neurodivergent People Can Crack the Code of Living in a Neurotypical World.

Largest ever molecular map of autism opens new paths to precision therapies

For more than two decades, researchers have identified hundreds of genes that increase the risk of autism spectrum disorder (ASD). Yet multiple fundamental questions have remained unanswered: Among them, how do mutations in these genes lead directly to changes in brain development, and how can that knowledge be translated into more effective therapies?

In a new study published in Science, scientists at the Quantitative Biosciences Institute (QBI) and the Department of Psychiatry and Behavioral Sciences at the University of California, San Francisco (UCSF) have taken a major step toward answering both questions. The findings are the result of more than a decade of work. By building the largest molecular interaction map of autism, the team revealed how hundreds of genes and dozens of mutations converge within a surprisingly small number of shared protein networks, overcoming a major roadblock to the development of new precision medicines.

Rather than focusing only on the genes linked to autism, the researchers mapped the proteins encoded by those genes and discovered how individual disease-causing mutations can rewire the molecular machinery of the developing brain. The work uncovers an entirely new layer of disease biology, offering therapeutic targets and providing a framework for designing medicines that directly address a wide range of underlying molecular causes of autism.

Cell therapy substantially reduces severe rheumatoid arthritis in first clinical trial

Immunotherapies such as CAR T-cell therapy are used primarily to treat cancer. In the future, these patient-specific therapies, manufactured from patients’ own immune cells, could also help cure autoimmune diseases. Six patients with particularly severe rheumatoid arthritis have now received this treatment at Charité—Universitätsmedizin Berlin. In the journal Nature Medicine, the researchers report the results from the world’s first clinical trial of its kind: Disease activity decreased substantially in all participants. By the end of the observation period, three of the patients no longer required any medication for rheumatoid arthritis.

Rheumatoid arthritis is a chronic disease in which the immune system mistakenly attacks the body’s own joints. This causes recurrent inflammation and joint swelling and, as the disease progresses, can lead to joint damage. Currently available treatments can usually keep the inflammation under control but do not cure the disease. Patients therefore require lifelong medication, including anti-inflammatory drugs and medications that suppress the immune system, with all the associated side effects.

In some patients, even several of the newer treatments fail to produce an adequate response. Doctors then call the disease treatment-refractory. For those affected, this means persistent pain, restricted mobility and a substantial impact on quality of life.

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