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Proteins can be selectively controlled with radio waves

In a significant advance in biological quantum sensing, a research team led by the Technical University of Munich (TUM) has discovered and tested a new mechanism of action in which proteins can be controlled with radio waves. In doing so, they influence a sensitive quantum state known as spin and make it visible via light. In the future, such findings could help detect and even direct biochemical processes in cells simply from the outside using radio waves.

Until now, quantum sensing has primarily been known from solid-state materials such as diamonds with deliberately introduced tiny defects. The researchers are now transferring this principle to proteins —biological molecules that can be genetically produced and specifically tailored. In the future, this could allow quantum sensors to be built directly into cells or tissue.

These protein-based sensors are potentially particularly well suited for biosensing—that is, for imaging living cells, tissues, or organs. In theory, they sit directly where measurement is needed, making them suitable for studies in organisms—unlike bulky solid-state sensors.

A new origin story for multicellular life points to physics, not genes alone

How did life make the leap from single cells to coordinated, multicellular organisms? And how do genetically identical cells still perform a version of that feat every time an embryo begins to take shape?

In a new Perspective paper appearing in the journal Nature Biotechnology, Bren Professor of Biology and Biological Engineering Magdalena Zernicka-Goetz and collaborator Qi Chen of the University of Utah ask one of biology’s oldest questions in a new way. The paper is titled “Decoding the origins of cellular self-organization for engineered biology.”

Tiny brain probe reveals how deep-brain neurons can be measured and manipulated

A new breakthrough technology, co-developed by UCL scientists, that simultaneously records and manipulates neuron activity deep within the brain could transform our understanding of neural circuits and neurological conditions, such as Alzheimer’s disease and schizophrenia.

The device, known as Neuropixels Opto and researched in mice, integrates two powerful but traditionally separate techniques—electrophysiology (the study of the electrical activity of living cells) and optogenetics (combining genetics and optics to control cells). They form a single probe, enabling unprecedented insight into how individual neurons in the brain function and interact.

Published in Nature Methods, the system allows researchers to monitor the electrical activity of hundreds of neurons while also selectively activating or silencing specific cells using light.

Targeted therapy reduces risk of lung cancer recurrence by 83% in rare genetic subtype

A new study co-led by investigators at the UCLA Health Jonsson Comprehensive Cancer Center shows that the targeted cancer drug selpercatinib can significantly reduce the risk of lung cancer returning in patients with a rare genetic subtype of early-stage non-small cell lung cancer (NSCLC), potentially offering a new treatment option to help keep the disease from coming back after standard therapy.

The international phase 3 clinical trial, called LIBRETTO-432, found that after two years, 92% of patients with stage II–IIIA RET fusion-positive NSCLC who received selpercatinib after standard treatment were alive without their cancer returning—a measure known as event-free survival—compared with 61% of patients who received a placebo. Overall, the treatment reduced the risk of cancer recurrence or death by 83%.

The results were shared during the Plenary Session on May 31 at the American Society of Clinical Oncology Annual Meeting by Dr. Jonathan Goldman, Health Sciences Clinical Professor in the Department of Medicine at the David Geffen School of Medicine at UCLA. The paper was also published in the New England Journal of Medicine.

Scientists discover inherited traits that break Mendel’s Laws of genetics

A major mouse study found that some inherited traits are passed down through epigenetic changes that break the classic rules of genetics. Researchers discovered hundreds of cases where these chemical DNA marks behaved unexpectedly, including some that seemed to emerge out of nowhere. They also identified the first known naturally occurring paramutation in a mammal, hinting that environmental influences may play a larger role in inheritance than scientists realized.

Longevity-linked APOE2 gene variant helps neurons repair DNA and resist aging

People who carry the APOE2 version of the apolipoprotein E gene are more likely to live to advanced age and are partly protected against Alzheimer’s disease, but scientists have struggled to explain why. A new study from the Buck Institute for Research on Aging, now published in Aging Cell, offers a mechanistic answer: APOE2 helps human neurons keep their DNA intact and resist becoming senescent, a damaged, dysfunctional state that accumulates with age and contributes to neurodegeneration.

The findings shift attention away from APOE’s well-known role in cholesterol transport and toward a previously underappreciated function of the gene: shaping how brain cells maintain the integrity of their genome as they age.

“We’ve known for years that APOE2 carriers tend to live longer and have a lower risk of Alzheimer’s, but the protective mechanism has been a black box,” says senior author Lisa M. Ellerby, Ph.D., professor at the Buck Institute. “Our work shows that APOE2 neurons are better at preventing and repairing DNA damage, and they resist the cellular aging program that drives so much of late-life decline. Our findings point to entirely new therapeutic directions.”

Inside Alzheimer’s neurons, tau may set off a genetic chain reaction that ends in cell death

Alzheimer’s disease is a neurodegenerative disease characterized by a progressive decline in mental functions and memory loss. Along with frontotemporal dementia and some other neurodegenerative disorders, Alzheimer’s disease has been associated with an accumulation inside neurons of abnormal clumps of a protein called “tau.”

The tau protein is important for brain health, stabilizing structures called microtubules inside neurons. In Alzheimer’s disease and other tauopathies (i.e., diseases linked with the abnormal accumulation of tau), tau proteins aggregate into toxic and insoluble clumps that are harmful to brain cells, gradually leading to their death.

Researchers at Zhejiang University, Xiamen University and other institutes in China recently carried out a study aimed at better understanding the processes via which tau aggregation contributes to the death of neurons in patients with Alzheimer’s disease. Their findings, published in Nature Neuroscience, suggest that these tau clumps prompt the reactivation of transposable DNA elements in neurons, which can in turn lead to their death.

Legend scientific founder returns to ASCO with new ambition for high-yield, non-gene-editing CAR-T platform

Nine years after wowing the audience at the American Society of Clinical Oncology annual meeting with a CAR-T candidate that would become Carvykti—now the world’s most successful cell therapy—Legend Biotech’s scientific founder, Frank Fan, M.D., Ph.D., is returning to the spotlight with an entirely new playbook.

This time, Fan isn’t showcasing an autologous product engineered with each individual patient’s cells. Instead, with his new venture, Wondercel Therapeutics, Fan hopes an off-the-shelf universal CAR-T platform can tackle two bottlenecks of the cell therapy industry: massive production scalability and the pitfalls associated with gene editing.

“If this approach proves successful, the critical thing is that we can achieve linear scalability in CAR-T production capacity that can match traditional biologics,” Fan said in an interview with Fierce.

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