Cancer researchers just found a new way to take on tumors.

CAR T cell therapy revolutionized blood cancer treatment by supercharging a patient’s own immune cells to hunt down cancers. But the approach has struggled in solid cancers. These are some of our top killers—breast, lung, prostate. Roughly two million Americans are expected to be diagnosed with cancer in 2026, and over 600,000 will likely succumb to the disease.

Unlike blood cancers, solid tumors rarely share a single, universal target for CAR T cells. Even cells within the same tumor are a mishmash. Some have little or none of a target protein, allowing them to evade the engineered immune cells, survive treatment, and fuel relapse.

“Target discovery remains a considerable challenge in the development and translation of

CAR T cell therapies for solid tumors,” wrote Christopher Mount and Marcela Maus at the Massachusetts General Brigham Cancer Institute.

Now, two independent teams have converged on the same promising target: A cell-surface protein called GPNMB. In one study, CAR T cells engineered to recognize GPNMB rapidly destroyed glioblastoma—a lethal brain cancer—in tissues taken from patients and shrank tumors in mice.

A second team used a similar strategy against an aggressive soft tissue cancer to fight tumors in organoids and mice. In an early clinical trial involving a single participant, one infusion stabilized the disease for three months without serious side effects.

CAR T designers are often wary of broadly shared targets because they can trigger dangerous attacks on healthy tissue. But GPNMB is an odd duck. In addition to cancer cells, it also sits on immune cells that spur cancer growth or suppress the body’s innate ability to get rid of tumors.

“Our approach attacks both the tumor and the environment that allows it to thrive,” said Sheila Singh at McMaster, who led the glioblastoma study, in a press release. “We’re going beyond targeting the cancer alone and eliminating the immune cells that help shield it from treatment.”

Cancer Fortress

Solid cancers have plenty of tricks to outsmart CAR T cells.

Researchers make these supercharged immune cells  by extracting a patient’s own T cells and genetically engineering them to produce protein “claws” that latch onto a specific cancer target. After infusing the cells back into the body, they seek and destroy tumor cells. CAR T has transformed treatment for several blood cancers and is showing promise in autoimmune diseases and excessive heart and kidney scarring. To simplify the procedure, researchers are also exploring ways to directly transform T cells inside the body with gene therapy.

Solid cancers, however, are far tougher opponents. Unlike blood cancers, which are heavily coated with a shared target called an antigen, solid tumors are molecular patchworks. Cells within the same tumor can display different targets—or none at all—allowing some to evade a CAR T attack and trigger relapse. Many of these targets also appear on healthy tissues, raising the risk of dangerous side effects. And then there’s the tumor microenvironment: A toxic, glue-like “fortress” that hijacks immune cells and uses them to battle incoming CAR T cells.

These barriers aren’t impenetrable. Previous work enlisted  bacteria to help CAR T cells burrow into tumors. Other efforts engineered ultra-sensitive CAR T cells capable of detecting tiny amounts of a cancer target shared across multiple solid tumors.

“Recent reports of activity in several clinical trials reinforce optimism that these efforts may result in true clinical benefit,” wrote Mount and Maus, who were not involved in either study.

But these strategies require additional engineering steps, increasing complexity and cost. And most still leave one major roadblock intact: The tumor’s immune defenses.

One-Two Punch

In the glioblastoma study, the team at McMaster University scoured donated tumors for proteins that distinguished the most aggressive cancer cells. They found one standout: GPNMB. Another test of every protein dotting the cell surface confirmed it as a promising target. The protein is evident across a cancer cell’s membrane, making it readily accessible to CAR T cells.

In lab tests, CAR T cells engineered against GPNMB performed well, nearly eliminating tumors grown from patient samples and extending survival in mice.

The target turned out to be far more valuable than expected. The team soon realized that GPNMB also marked the immune cells that suppress anti-cancer drugs. CAR T cells attacked both fronts simultaneously, weakening the tumor’s immune shield and killing the cancer itself.

“Most approaches have focused on killing cancer cells alone,” said study author Shan Grewal. “Our work suggests we may also need to dismantle the immune support system that helps the tumor survive.”

The second team focused on alveolar soft-part sarcoma, a rare soft-tissue cancer that often spreads to the lungs, brain, and bones before it’s diagnosed. Treatment often comes too late.

The disease is driven by a type of “fusion” gene created when pieces of genetic material are accidentally stitched together. These genes are extremely tough to target directly. Instead, the team screened all surface proteins on the cancer cells and again landed on GPNMB as a top candidate for intervention. The protein’s levels closely tracked the activity of the fusion gene.

CAR T cells targeting GPNMB cleared tumors and prevented metastasis in mice. But because an earlier antibody drug against the protein caused severe skin toxicity in patients, the team also tested their CAR T cells in mice carrying small human skin grafts. Although inflammation initially flared, there were no signs of ongoing skin damage.

Encouraged, the team treated a patient with relapsed, metastasized alveolar soft-part sarcoma. After a single infusion, the engineered cells rapidly divided in the bloodstream and remained detectable for roughly a month. The treatment didn’t trigger skin rashes or more dangerous side effects, like cytokine release syndrome where the body mounts a hyperactive immune defense that harms healthy organs.

The treatment’s benefits outlasted the engineered cells themselves. For roughly three months, imaging tests found fewer of the small, round spots on the patient’s lungs that often signal metastatic cancer, suggesting the disease had stabilized.

A final analysis identified another roadblock: Clusters of cells that suppress the immune system and could blunt the benefits. Adding drugs to block these immune molecules boosted tumor killing in mice. Because the same kind of gene fusion drives other cancers, including kidney, the CAR T cells could have reach beyond this specific type of sarcoma.

Together, the studies underscore that the best CAR T targets might extend beyond cancer cells to expose and attack cancer’s immune cell supporters too. Finding a viable target is a delicate balancing act. Chosen well, and CAR T cells could tackle multiple drivers for cancer growth. Choose poorly, and healthy tissues could get hurt in the crossfire.

Even so, “these two studies indicate that GPNMB represents an actionable target for CAR T cell therapies in several solid tumors,” wrote Mount and Maus.

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Synthetic biologists have long dreamed of constructing artificial cells from the bottom up. Researchers have now taken a major step in this direction by demonstrating that non-living components can be assembled into a system that grows, copies its DNA, and divides.

The genomic revolution transformed our ability to understand and manipulate cellular machinery, allowing scientists to rewire cells’ genetic circuitry to fight disease, produce valuable chemicals, and make crops more resilient. The holy grail for the field, however, has been to use these tools to create entirely synthetic cells—a milestone that would signal humanity’s mastery of life’s key ingredients.

How best to do this has long been an open question. Genomics pioneer Craig Venter made significant progress by stripping living bacteria back to their bare essentials, culminating in the 2016 unveiling of a minimal cell with just 473 genes. The Synthetic Yeast Genome Project has taken the opposite approach, building artificial versions of all 16 yeast chromosomes from scratch, though they’ve yet to get them working together in a single cell.

Now, researchers from the University of Minnesota, have assembled a synthetic cell out of engineered, non-living components housed inside an artificial, cell-like membrane. Their creation was capable of the four hallmarks of a living entity—the ability to feed, grow, copy genetic material, and produce offspring.

“We’ve replicated in chemistry what only used to be possible in biology: the complete set of behaviors of a cell,” Kate Adamala, who led the project, said in a press release. “It proves that the most fundamental functions of life, like growth and replication, do not need a mysterious magical spark.”

The researchers outline the design for their synthetic organism—nicknamed SpudCell for its potato-like shape under the microscope—in a non-peer reviewed paper uploaded to bioRxiv. SpudCell features a genome 90,000 base pairs long, which is considerably smaller than the 113,000 base pairs researchers had previously predicted would be the bare minimum needed to support a viable cell.

Rather than housing all the genes in a single chromosome, the team split them across several small, circular DNA molecules called plasmids, each specialized to fulfill specific functions. The researchers say this makes it possible to modify different aspects of the organism more easily.

To read the genome and build proteins, SpudCell uses a pre-defined kit of 36 purified enzymes drawn largely from E. coli. The whole assembly sits inside a liposome, a hollow bubble of the same fatty molecules that form natural cell membranes.

The artificial cell feeds in two distinct ways. Small molecules pass directly into the cell through protein pores implanted across the membrane. Molecules too large to squeeze through—like ribosomes and enzymes—are packaged inside tiny lipid bubbles that fuse with the membrane and empty their contents inside.

While the cell can feed, it’s entirely reliant on the researchers providing it with specially prepared meals. This means it’s a long way from surviving in the wild, which is both a major limitation and a key safety mechanism. “It’s a bed-ridden Frankenstein’s monster that has to be spoon-fed,” Adamala told New Scientist. “There’s no danger of it running amok.”

After ingesting “food,” SpudCell’s genes use the material to churn out proteins, while folding the incoming lipids into its membrane. This causes the whole cell structure to swell. Within a few hours, it’s bulked up enough to reproduce by dividing into two smaller cells.

Replicating cell division has been a longstanding challenge in the field. Natural cells split using an intricate protein scaffold called a cytoskeleton that’s fiendishly difficult to recreate. Adamala’s team sidestepped this problem by using a completely different mechanism, in which proteins bunch up on the membrane’s surface, putting it under mechanical strain. Eventually this squeezes two parts of the membrane together to pinch off a new cell.

The cells even manage a crude form of evolution. When the researchers introduced a genetic tweak boosting the cells’ ability to feed, those with the variant outcompeted the original lineage within five generations, and their edge widened when the researchers exposed the population to nutrient scarcity.

However, no one is claiming SpudCell is alive. Crucially, the cells cannot make their own ribosomes—the machines that build proteins from genetic instructions—and the ribosomes provided by the researchers degrade over time, limiting the cells to five to ten divisions.

The University of Chicago’s Jack Szostak told Quanta the work is an “impressive step” but the inability to produce ribosomes seriously limits potential for sustained growth. “If their system was able to generate its own ribosomes and other proteins and RNAs, it would be much closer to existing biological cells such as bacteria,” he said.

Nonetheless, the researchers think these artificial cells are a promising way to manufacture drugs, fuels, and materials without the toxic, energy-hungry industrial chemistry we rely on today. And they’ve created a new nonprofit called Biotic to share the tools they’ve developed with researchers.

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Researchers at the University of Cambridge have developed what they describe as a fundamentally new type of vaccine using artificial intelligence. The vaccine’s key component was designed entirely by AI and has now been tested in people for the first time.

The goal is ambitious: a single vaccine that works not just against all known human coronavirus variants, but against related bat viruses that could jump from animals to humans and cause future pandemics.

Traditional vaccines train our immune system to recognize one specific virus. The problem is that viruses mutate. When they change enough, the vaccine stops working, which is why we need a new flu shot every year and why Covid vaccines have been updated repeatedly since 2021.

AI offers a way around this. By analyzing genetic data from thousands of related viruses, it can identify the parts that stay the same across different strains and that are unlikely to change over time. Target those stable features, and you have a vaccine that should work against the whole family, not just the strain you started with.

This is exactly what the Cambridge team did. They used AI to scan viruses from the sarbecovirus family, which includes the viruses that cause both SARS and Covid, as well as a range of animal coronaviruses—looking for shared features that evolution has left largely untouched. Those features became the basis of the vaccine.

DNA Vaccines

While many people are familiar with the mRNA shots used during the pandemic, this new vaccine uses DNA. DNA vaccines are generally more stable than mRNA vaccines, making them easier to store and transport. This is a significant advantage in lower-income countries where “cold-chain” infrastructure is limited.

They can also be administered without needles. A high-pressure stream of liquid delivers the vaccine through the skin, making administration less painful and easier to scale up during an outbreak.

Could It Protect Against Future Pandemics?

These practical advantages matter most if the vaccine itself can do something no existing jab can: protect against viruses we haven’t encountered yet.

Broad-spectrum vaccines could change the way the world responds to emerging infectious diseases. By offering much wider protection than traditional vaccines, they could provide rapid immunity against new and emerging viral threats. This would equip public health officials with tools to stop future outbreaks in their tracks before they have a chance to turn into global pandemics.

They could also transform our approach to more familiar diseases. Influenza is a prime target because it exists in many different strains and evolves so rapidly. Scientists have to predict which strains will dominate each flu season, and if they guess wrong, vaccine effectiveness can suffer. A universal flu vaccine that targets features shared across multiple strains could eventually end the annual race to keep up with the virus.

The Ebola virus shows why this matters right now. The recent outbreak in the Democratic Republic of the Congo and Uganda is driven by the Bundibugyo strain, which bypasses existing vaccines. While researchers rush to create a new vaccine specifically for this strain, local communities remain at high risk. A broad-spectrum vaccine designed to cover an entire virus family could transform that picture.

What the Trial Found

This is the first human trial of an AI-designed vaccine. The results showed that this DNA vaccine was able to stimulate the immune system to produce antibodies that can recognize different types of sarbecoviruses. The technology was found to be safe and well tolerated.

This is an exciting advance because it demonstrates how AI has the potential to design variant-proof vaccines against future pandemic threats. The needle-free delivery system could also make the vaccine easier to administer and distribute worldwide.

However, there is more work to do. Although the results in this study are encouraging, the immune responses following vaccination were modest. It was also uncertain how long the protection lasts and whether further boosters will be required. Larger trials are also needed to determine whether the vaccine can prevent or reduce viral infections in the real world.

A universal vaccine remains a few years away. And any new vaccine must still pass larger trials to prove it is safe, effective, and provides lasting protection. But this study shows the goal is getting closer—and AI may help us get there faster.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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A handful of healthy senior citizens are about to trip on psilocybin—to see if the psychedelic protects aging brains.

Psilocybin, the active ingredient in magic mushrooms, is best known for its ties to 1960s counterculture. But now it may also herald a new genre of mental health treatment. From severe depression to post-traumatic stress disorder, studies have highlighted psychedelic drugs’ ability to reshape brain networks and relieve debilitating symptoms.

Most of these studies have focused on younger people with mental health conditions that don’t respond to standard treatment. The field’s success is prompting scientists to ask if psychedelics could also help healthy brains age better.

A team from the UC Berkeley Center for the Science of Psychedelics is about to find out. In a first-of-its-kind study focused on adults between the ages of 60 and 85, they’ll investigate how psilocybin affects perception, emotion, and memory using a battery of psychological tests.

Multiple scans before and after dosing will track changes in the brain. And detailed surveys will gauge broader shifts in well-being: Do participants feel more “in tune” with their emotions, feel less isolated, or experience a renewed sense of wonder about the world?

“What really excites me is that we’re focused on healthy older adults,”  said Tyler Toueg, who co-led the study’s design, in a press release. “Most clinical trials with older adults are focused on people who already have a diagnosis. We’re asking whether we can actually promote positive outcomes in older adults who are healthy.”

Called PLASTICITY, the trial could also open a rare window into how a psychedelic experience reshapes healthy brain networks. And because the drug alters our sense of self, psilocybin could help researchers probe the ways in which the brain constructs reality.

“I’m very interested in psilocybin as a potential mental health treatment, but I’m also interested in it as a way to shed light on these central mysteries in neuroscience and psychology,” said study designer Michael Silver.

Chasing the White Rabbit

Psychedelic research was highly restricted for decades. But advocates, including the non-profit Multidisciplinary Association for Psychedelic Studies, have steadily pushed to reopen the field, arguing that these drugs might keep mental health symptoms at bay.

Early results helped usher psychedelics into the mainstream. In 2023, a randomized, placebo-controlled trial found that a single dose of psilocybin, paired with therapy, eased depression. Oregon later approved supervised psilocybin therapy—though the drug remains federally illegal in the US—and Australia became the first country to greenlight it for depression and post-traumatic stress disorder. More recently, two late-stage studies reported strong effects in severe depression, potentially paving the way for FDA approval.

Scientists still don’t fully understand how psilocybin works in the brain. But there are hints. The drug appears to rapidly reorganize the connections between brain cells, particularly in the hippocampus, a region of the brain central to learning, memory, and navigation.

Neurons constantly change their connections in a process called plasticity that encodes experiences into neural networks, allowing the brain to process information, learn, and lock in memories. In youth, these connections are flexible and expansive. But with age and in conditions like depression, the brain’s flexibility wanes.

The birth of new neurons, or neurogenesis, also contributes to plasticity. Neurogenesis only occurs in two brain regions, one of which is the hippocampus. Although whether it actually takes place in humans is controversial, it is strongly linked to learning, memory, and emotion, and it declines in both psychiatric disorders and aging.

Psilocybin may reset brain plasticity to a more youthful state.

In rats modeling depression, for example, a study showed the drug shifted dark moods into behavior that was more exploratory and engaging. Where traditional antidepressants, like Prozac, tend to blunt symptoms, psilocybin seems to overwrite entrenched negative patterns. This suggests deeper circuit-level changes.

In another study, the drug reopened a critical window for learning in mice. During adolescence, the brain is highly plastic, but it begins to stiffen in adulthood. Psilocybin temporarily restored malleability and changed the mice’s social behavior. In some brain regions, the drug increased sensitivity to oxytocin, the so-called “love hormone.” The authors suggested the drug induced a state called metaplasticity, in which neurons are more likely to respond to oxytocin and other regulators to rewire, form new connections, and grow their branches.

Psilocybin’s effects may extend beyond the brain. Depression, chronic stress, and the immune system are tightly linked. In a third study, researchers identified a brain-spleen connection that drives fear and anxiety. Psilocybin suppressed inflammatory immune cells associated with brain inflammation and dampened anxiety-like behavior in stressed mice, even under threat.

Both effects—dialing up plasticity and lowering inflammation—make psilocybin an intriguing way to potentially counter changes in the aging brain.

“We know that with age, we lose synaptic connections, especially in certain brain regions like the hippocampus and prefrontal cortex,” said Toueg. “There’s a lot of overlap between the mental states that psychedelics influence and those associated with successful aging.”

Tomorrow Never Knows

The PLASTICITY trial is designed to test whether psilocybin can produce lasting changes in neuroplasticity in healthy adults aged 60 to 85. Participants will first undergo assessments of cognition, visual perception, and brain structure using advanced MRI techniques.

Diffusion MRI scans will focus on the hippocampus to capture microscopic changes in its structure. Functional MRI will focus on brain activity as participants perform learning and memory tasks, offering a dynamic view of how activity shifts after dosing.

The study will also see if psilocybin increases vagus nerve activity, which has been linked to better stress recovery. Participants will complete detailed surveys about the experience ranging from emotional responses, like wonder, to potential shifts in outlook and social cognition.

“Things like depression, anxiety, stress and rumination are all associated with worse aging outcomes,” said Toueg. “Things like having purpose in life, emotional regulation, and awe are all associated with more successful aging.”

The trial began enrolling participants in November last year. Two volunteers have already completed the tests, and the team aims to dose 20 people by the end of 2026.

Although psilocybin trials are now widespread, older adults remain underrepresented. One estimate suggests just 1.4 percent of participants are 65 or older, despite potentially being among those most likely to benefit from interventions that enhance plasticity.

“This study allows us to directly test whether the promising findings from animal models translate to older humans and to generate data that will inform future research on aging, cognition, and mental health,” said Silver.

Toueg agrees. “I think that no matter what we find, this study will have implications for how we think about intervening in the aging brain,” he said.

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