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From blood to solid tumors: A new way to power up CAR T cell therapy

Chimeric Antigen Receptor (CAR) T cell therapies have revolutionized cancer treatment—but so far, their success has been largely limited to blood cancers. Solid tumors, which account for around 90% of all adult cancers, remain a major challenge because they are difficult for CAR T cells to infiltrate and are often highly heterogeneous, making them harder to target with a single therapy.

Researchers at Monash University, in collaboration with scientists from the Peter MacCallum Cancer Center, used CRISPR-based gene editing or a PTPN2 inhibitor to enhance the function of human CAR T cells engineered to recognize an antigen expressed on many .

The study, led by Professor Tony Tiganis and Dr. Florian Wiede, was published in Science Translational Medicine.

Decoding how cells choose to become muscles or neurons

Every cell in the body has the same DNA, but different cell types—such as muscle or brain cells—use different parts of it. Transcription factors help cells activate specific genes by reading certain DNA sequences, but since these sequences are common across the genome, scientists have long wondered how the factors know exactly where to bind.

Researchers in the Schübeler lab set out to address this question by looking at two closely related transcription factors—NGN2 and MyoD1—that steer cells toward becoming neurons and , respectively. Using stem cells, they switched these transcription factors on one at a time and watched where they attached to the DNA and how they influenced gene expression. Their research is published in the journal Molecular Cell.

They found that the binding of transcription factors to the DNA molecule depends not only on the DNA sequence but also on how open the DNA is and which partner proteins are present. Sometimes, transcription factors act as “pioneer factors” and are able to open tightly packed DNA at specific sites to turn on genes. Small DNA changes—sometimes just one letter—and the proteins these factors partner with can affect whether genes are activated.

Breakthrough brain discovery reveals a natural way to relieve pain

Using powerful 7-Tesla brain imaging, researchers mapped how the brainstem manages pain differently across the body. They discovered that distinct regions activate for facial versus limb pain, showing the brain’s built-in precision pain control system. The findings could lead to targeted, non-opioid treatments that use cannabinoid mechanisms instead of opioids, offering safer pain relief options.

We doubled human lifespans in the last 200 years. Can we do it again? | Andrew Steele

“Over the last 10 or 15 years, scientists have really started to understand the fundamental underlying biology of the aging process. And they broke this down into 12 hallmarks of aging.”

Up next, Why 2025 is the single most pivotal year in our lifetime | Peter Leyden ► • Why 2025 is the single most pivotal year i…

We track age by the number of birthdays we’ve had, but scientists are arguing that our cells tell a different, more truthful story. Our biological age reveals how our bodies are actually aging, from our muscle strength to the condition of our DNA.

The gap between these two numbers may hold the key to treating aging – which could help save 100,000 lives per day and win us $38 trillion dollars.

00:00 Rethinking longevity.
01:27 Understanding aging.
02:58 Biological age and epigenetics.
04:29 New frontiers in longevity science.
08:04 Future possibilities and ethical questions.
10:24 The moral debate around living longer.

AI tool uncovers genetic blueprint of the brain’s largest communication bridge

For the first time, a research team led by the Mark and Mary Stevens Neuroimaging and Informatics Institute (Stevens INI) at the Keck School of Medicine of USC has mapped the genetic architecture of a crucial part of the human brain known as the corpus callosum—the thick band of nerve fibers that connects the brain’s left and right hemispheres. The findings open new pathways for discoveries about mental illness, neurological disorders and other diseases related to defects in this part of the brain.

The corpus callosum is critical for nearly everything the brain does, from coordinating the movement of our limbs in sync to integrating sights and sounds, to higher-order thinking and decision-making. Abnormalities in its shape and size have long been linked to disorders such as ADHD, bipolar disorder, and Parkinson’s disease. Until now, the genetic underpinnings of this vital structure had remained largely unknown.

In the new study, published in Nature Communications, the team analyzed and from over 50,000 people, ranging from childhood to late adulthood, with the help of a new tool the team created that leverages artificial intelligence.

Hair-thin fiber can control thousands of brain neurons simultaneously

Fiber-optic technology revolutionized the telecommunications industry and may soon do the same for brain research.

A group of researchers from Washington University in St. Louis in both the McKelvey School of Engineering and WashU Medicine have created a new kind of fiber-optic device to manipulate neural activity deep in the brain. The device, called PRIME (Panoramically Reconfigurable IlluMinativE) fiber, delivers multi-site, reconfigurable optical stimulation through a single, hair-thin implant.

“By combining fiber-based techniques with optogenetics, we can achieve deep-brain stimulation at unprecedented scale,” said Song Hu, a professor of biomedical engineering at McKelvey Engineering, who collaborated with the laboratory of Adam Kepecs, a professor of neuroscience and of psychiatry at WashU Medicine.

Brain-inspired chips are helping electronic noses better mimic human sense of smell

After years of trying, the electronic nose is finally making major progress in sensing smells, almost as well as its human counterpart. That is the conclusion of a scientific review into the development of neuromorphic olfactory perception chips (NOPCs), published in the journal Nature Reviews Electrical Engineering.

Evolution has perfected the human nose over millions of years. This powerful sense organ, while not the best in the animal kingdom, can still detect around a trillion smells. The quest to develop electronic noses with human nose-like abilities for applications like security, robotics, and medical diagnostics has proved notoriously difficult. So scientists have increasingly been turning to neuromorphic computing, which involves designing software and hardware that mimics the structure and function of the human nose.

In this review, a team of scientists from China highlights some of the key advances in developing olfactory sensing chips. The paper focuses heavily on because they are key components of the system. They must physically detect and convert them into electrical signals.

Scientist Solves 100-Year-Old Physics Puzzle To Track Airborne Killers

Researchers at the University of Warwick have created a straightforward new way to predict how irregularly shaped nanoparticles, a harmful type of airborne pollutant, move through the air.

Each day, people inhale countless microscopic particles such as soot, dust, pollen, microplastics, viruses, and engineered nanoparticles. Many of these particles are so small that they can reach deep into the lungs and even pass into the bloodstream, where they may contribute to serious health problems including heart disease, stroke, and cancer.

While most airborne particles have uneven shapes, existing mathematical models often treat them as perfect spheres because that makes the equations easier to handle. This simplification limits scientists’ ability to accurately describe or track how real, non-spherical particles move, especially those that are more dangerous.

Viral Appropriation of Specificity Protein 1 (Sp1): The Role of Sp1 in Human Retro- and DNA Viruses in Promoter Activation and Beyond

Specificity protein 1 (Sp1) is a highly ubiquitous transcription factor and one employed by numerous viruses to complete their life cycles. In this review, we start by summarizing the relationships between Sp1 function, DNA binding, and structural motifs. We then describe the role Sp1 plays in transcriptional activation of seven viral families, composed of human retro- and DNA viruses, with a focus on key promoter regions. Additionally, we discuss pathways in common across multiple viruses, highlighting the importance of the cell regulatory role of Sp1. We also describe Sp1-related epigenetic and protein post-translational modifications during viral infection and how they relate to Sp1 binding. Finally, with these insights in mind, we comment on the potential for Sp1-targeting therapies, such as repurposing drugs currently in use in the anti-cancer realm, and what limitations such agents would have as antivirals.

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