Radically different
Nature Medicine, Published online: 12 May 2026; doi:10.1038/s41591-026-04385-8
A phylogenetic analysis examined the origins of the first mpox outbreak in Sierra Leone and found evidence of an emerging lineage (G.1) that has likely descended from the Nigerian epidemic and emerged in Sierra Leone months before first detection.
Capsida Biotherapeutics said Tuesday that it still had no answers in its investigation into the death of a child in a gene therapy trial last September.
Its scientists’ efforts, it said, have been stymied because the hospital where the study was conducted has declined to share tissue samples from an autopsy.
The therapy, known as CAP-002, was the first of a wave of new gene therapies designed to deliver genes deep into the brain. Scientists around the world engineered viruses that could slide through the blood-brain barrier that walls off our most vital organ from the rest of the body. Companies spun up promising treatments for devastating rare genetic diseases and common conditions like Alzheimer’s and Parkinson’s.
The accumulation of fluid in the belly, known as ascites, is something that women with advanced ovarian cancer may know all too well. The results of research by a team at Duke University School of Medicine now suggest that, more than causing discomfort, this fluid may protect cancer cells from a form of cell death known as ferroptosis, helping cancer cells survive and spread. The studies also indicated that a decades-old cholesterol-lowering drug, bezafibrate, may be able to disrupt that protection.
The findings, derived through lab experiments and an analysis of patient samples, do not show that bezafibrate treats ovarian cancer. But they do suggest that changing the environment that cancer depends on could make it more vulnerable to existing cancer treatment.
“Doctors have mostly viewed ascites as a symptom rather than an active driver of disease,” said Jen-Tsan Chi, PhD, a professor in the department of molecular genetics and microbiology and co-leader of the Cancer Biology Program at the Duke Cancer Institute. “We’ve learned it gives cancer a survival advantage, which fills a major gap in understanding how ovarian cancer spreads.”
Chi is senior and corresponding author of the team’s published paper in Nature Communications, titled “Ascites protects against ferroptosis and enables the peritoneal growth of ovarian cancer.” In their paper, the authors concluded, “Our findings identify ascites as a key determinant of ferroptosis resistance in metastatic OVCA and highlight its role in promoting tumor survival and dissemination within the peritoneal cavity.”
The peritoneum is a frequent site of metastasis in ovarian cancer (OVCA), the authors explained, and this is often accompanied by the accumulation of ascites in the peritoneal cavity. And while ascites is observed in other diseases such as liver cirrhosis, it’s most often associated with metastatic OVCA. The fluid occurs in 90% of those with advanced ovarian cancer. Doctors will drain ascites to ease pain, improve mobility, and make breathing easier, which offers patients relief even if it doesn’t stop the disease.
“Due to the enrichment of cellular and acellular factors, the ascitic fluid is reported to harbor a growth-promoting and immune-evading environment for cancer cells and is thought to serve as a medium for cancer cell dissemination and tumor progression and metastasis,” the team continued. However, they noted, “Despite its prevalence, ascites and its role in the peritoneal growth of OVCA remain poorly understood.”
According to the newly reported study findings, ascites also acts as a shield, helping cancer cells evade a specific form of cell death called ferroptosis. Ferroptosis is a kind of cellular rusting. It happens when iron inside a cell reacts with certain fats, causing the cell membrane to break apart. Many metastatic cancer cells—those that float freely through the abdomen looking for new places to grow—are naturally vulnerable to this kind of damage. “… we and other groups have reported that detached and metastasizing OVCA cells are especially vulnerable to ferroptosis, a form of cell death characterized by iron dependency and an irreversible accumulation of lipid hydroperoxides,” the authors wrote.
The study in Nature Communications shows how they survive anyway. For their research, the scientists bathed cancer cell lines and patient-derived tumor cells in ascites collected from patients, and observed how they responded to ferroptosis triggers. “Nothing is currently known about how ascites may influence OVCA cells’ ferroptosis,” they noted. “Given the common occurrence of ascites with peritoneal metastasis, ascites may be crucial for the peritoneal spread of OVCA.”
![From left, Duke University School of Medicine researchers Susan K. Murphy; Andrew Berchuck, MD; Yasaman Setayeshpour, PhD, and Jen-Tsan Ashley Chi, PhD, are studying how a common class of cholesterol drugs, called fibrates, can strip away a key defense used by ovarian cancer cells, making them more vulnerable to treatment. [Duke University School of Medicine/Mark Dolejs]](https://www.genengnews.com/wp-content/uploads/2026/05/Low-Res_20260311_Jen-Tsan-Ashley-Chi_MRD14-300x200.jpg)
The team found that the fluid protected cancer cells by changing how the cells store fats and control iron levels, effectively blocking cell death. The protection required only trace amounts. As little as 2% immersion shielded cancer cells from destruction, even though in patients these cells are entirely enveloped by the fluid.
“What surprised us was how selective this effect was,” said first author Yasaman Setayeshpour, a graduate student in molecular genetics and microbiology at Duke School of Medicine. “Ascites didn’t protect the cancer cells from other well-known types of cell death, like apoptosis or necrosis—it only blocked ferroptosis.
“To figure out why, we broke ascites down into major parts, like lipids, proteins, and small molecules, and tested what happened when each was removed. When we took the lipids out, the protective effect disappeared. That told us lipids are the key reason ascites helps these cancer cells survive,” Setayeshpour said.
The researchers also found an unexpected helper in the form of bezafibrate, an older type of cholesterol-lowering drug that is used to lower triglycerides by altering how the body processes fats. “The idea behind testing lipid-lowering drugs was to mimic what happens when lipids are removed from ascites,” Setayeshpour explained.
The studies showed that bezafibrate restored sensitivity to ferroptosis, but only when ascites was present. On its own, the drug did not trigger cell death, nor did it slow tumor growth in mice. The researchers found that the drug’s impact hinged on the cancer’s surroundings, in this case, the fat-rich fluid bathing the tumor. The studies showed that targeting this environment, using repurposed drugs like bezafibrate, could leave cancer cells more exposed to existing cancer treatments. “Given the intrinsic vulnerability of metastatic cancer cells to ferroptosis, these data suggest that ascites-mediated protection represents a critical mechanism supporting peritoneal survival,” the team noted. “Importantly, re-sensitization to ferroptosis by bezafibrate raises the possibility that therapeutic targeting of this pathway may limit peritoneal dissemination.”
Chi said the finding could have implications beyond ovarian cancer. Other cancers, including colorectal and pancreatic cancers, can also spread within the abdominal cavity. “These findings may also extend beyond ovarian cancer to other metastatic settings, including peritoneal colorectal cancer and pleural, brain, or spinal metastases,” the authors stated.
“This work shows how much the environment around a tumor matters,” Chi said. “Biological fluids like ascites don’t just give cancer cells a place to move. They actively help drive how cancer spreads.”
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A South American court upheld the steps taken by the Colombian government when it issued a compulsory license two years ago for an HIV medicine, a move that confirmed the legal framework for using such an approach in the future.
The Court of Justice of the Andean Community — a tribunal that settles trade, intellectual property, and labor disputes for Bolivia, Colombia, Ecuador, and Peru — also ruled that the Colombian government had properly justified the reasons for issuing a license and appropriately set an expiration date for its license.
“The court concluded that Colombia did not incur a breach of Andean regulations, since such measures are valid when there are reasons of public interest,” the health ministry said in a statement. “Colombia adequately complied with the obligation to determine the duration of the compulsory license” for the medicine, which is sold by ViiV Healthcare.
Researchers at Garvan Institute of Medical Research have identified a previously underappreciated mechanism that may explain why some breast cancers return many years, even decades, after apparently successful treatment.
The study, published in Nature Communications, reveals that certain estrogen receptor-positive (ER+) breast cancer cells survive therapy not by entering complete dormancy, but by continuing to divide at an extraordinarily slow pace. These stealth-like cells can gradually form microscopic secondary tumors that remain undetectable for years before eventually triggering metastatic relapse.
The findings offer new insight into one of the most persistent challenges in breast cancer care: why relapse can occur long after patients are considered cancer-free.
ER-positive breast cancer is the most common subtype of breast cancer and is typically treated with hormone therapies designed to block estrogen signaling. These treatments are often highly effective at eliminating actively dividing tumor cells.
However, ER-positive disease has a unique clinical problem: recurrence risk persists for decades.
Even after five to ten years of endocrine therapy, up to 30% of patients can eventually develop metastatic relapse. Once breast cancer spreads to distant organs such as bone, lung, or brain, the disease becomes largely incurable.
Traditionally, relapse has been attributed to dormant cancer cells—cells that enter a state of complete hibernation before later “waking up.” But the new study suggests this may not be the only pathway.
“We have become very good at treating primary breast cancer, but late relapses remain a major challenge,” said Liz Caldon, associate professor and senior author of the study.
The researchers discovered that some breast cancer cells never fully stop proliferating during therapy. Instead, they survive by drastically slowing their rate of division.
This subtle distinction may be clinically critical.
Rather than entering complete cellular arrest, these cells continue to grow at an almost imperceptible pace, allowing them to evade therapies that primarily target rapidly dividing cells.
“Instead, they survive by growing extremely slowly in the background, until a tiny speck becomes a pebble,” Caldon explained.
Over many years, these microscopic lesions, known as micrometastases, can gradually expand until they become clinically detectable or disrupt vital organs.
The work challenges a long-standing binary view of cancer persistence in which tumor cells are considered either actively proliferating or fully dormant. Instead, the findings support the existence of an intermediate “slow-cycling” state that may be particularly effective at evading treatment.
Studying these rare cells was technically difficult because of their exceptionally slow growth.
The research team spent years isolating and cultivating these populations in the laboratory. Once established, they introduced the cells into preclinical models to determine whether slow proliferation impaired metastatic potential.
It did not.
Despite dividing slowly, the cells retained the ability to migrate throughout the body and colonize distant organs such as bone and lung.
“It took years to isolate these specific cells because they were dividing so slowly, almost in defiance of how we typically expect cancer to behave,” said Kristine Fernandez, first author of the study.
“These cells were migrating to organs like the bone and lungs, proving that speed isn’t everything when it comes to metastasis.”
The findings reinforce a growing understanding in oncology that aggressive cancer behavior is not solely defined by rapid proliferation. Cellular adaptability and survival under therapeutic pressure may be equally important.
After identifying the slow-growing cells, the researchers investigated what allowed them to survive.
The study pinpointed a signaling pathway centered on Rac1, a protein involved in cell movement, structural organization, and survival. Using advanced biosensor imaging, the team directly visualized Rac1 pathway activation inside live slow-growing cancer cells.
Inhibiting this pathway appeared therapeutically promising.
Experimental Rac1 inhibitors significantly reduced tumor size and tumor number in patient-derived breast cancer models.
This suggests that targeting Rac1-dependent survival programs could potentially eliminate slow-growing residual cancer cells before they evolve into clinically significant metastases.
The findings contribute to a broader shift in cancer biology away from viewing residual disease as uniformly dormant.
Instead, tumors may contain multiple survival states, including cells that persist through continuous but ultra-slow proliferation. These populations may be especially dangerous because they remain biologically active while escaping conventional therapeutic detection.
The work also raises important clinical questions about long-term endocrine therapy. Current treatment durations are largely standardized, yet some patients may harbor persistent slow-cycling tumor cells despite years of therapy.
“If we can understand the specific biology of these slow-growing cells, we might eventually be able to offer better ways to track whether a decade of hormone therapy is actually working and ultimately prevent recurrence,” Caldon said.
The study’s implications extend beyond breast cancer alone. Slow-cycling drug-tolerant cancer cells have increasingly been identified across multiple tumor types, including melanoma, lung cancer, and leukemia.
By identifying a concrete signaling mechanism underlying this state in ER-positive breast cancer, the research provides a potential therapeutic entry point for preventing relapse before metastatic disease emerges.
The next challenge will be determining whether Rac1 inhibitors, or similar approaches targeting slow-cycling survival programs, can safely and effectively eliminate residual cancer cells in patients.
If successful, such strategies could fundamentally alter how clinicians approach long-term relapse prevention in breast cancer, shifting the focus from simply suppressing visible disease to actively eradicating the hidden cellular reservoirs that remain years after treatment ends.
The post Slow-Growing Breast Cancer Cells May Explain Why Relapse Happens Decades Later appeared first on Inside Precision Medicine.
Researchers at the Medical University of South Carolina (MUSC) have found evidence that the asthma medication formoterol may reverse metabolic dysfunction-associated steatohepatitis (MASH), a progressive fatty liver disease associated with obesity and type 2 diabetes that can lead to fibrosis, cirrhosis, liver failure, and liver transplantation. The research, published in npj Metabolic Health and Disease, arose unexpectedly as a result of findings on the use of formoterol in mouse models of diabetic kidney injury, which also showed that the mice had low levels of liver fat accumulation.
“Kind of unexpectedly, we found that the liver damage also reversed,” said senior author Joshua Lipschutz, MD, division director of nephrology and Arthur Williams Endowed Chair in nephrology at MUSC.
Based on this observation, the MUSC researchers initiated a study to find out whether the beta-2 adrenergic receptor pathway targeted by formoterol could influence metabolic disease in the liver as well as the kidney. According to the researchers, the connection between the diseases lies in shared metabolic dysfunction associated with type 2 diabetes relating to mitochondrial dysfunction and impaired energy metabolism.
To test the hypothesis, the team used a high-fat diet mouse model designed to mimic MASH. Mice fed the diet for 16 weeks developed liver steatosis and were subsequently treated with formoterol for four weeks. Testing of the mice after the four weeks of treatment found that steatosis was largely resolved as a result.
The evidence showed that formoterol increased mitochondrial biogenesis, a process that increases the number and function of mitochondria within cells.
“It looked like formoterol was rescuing the injury by increasing mitochondrial biogenesis,” Lischutz said. “It kind of revs up the mitochondria so they work better.”
The researcher noted that mice treated with formoterol had increased levels of PGC1α (a protein that helps control how cells produce and use energy) and electron transport chain proteins, along with an increase in mitochondrial proteins and lower lipid accumulation in liver tissue. Human HepaRG liver cells exposed to free fatty acids also showed reduced lipid accumulation and increased after formoterol treatment.
“The coordinated induction of oxidative phosphorylation and amino acid metabolism pathways suggests that formoterol may promote metabolic competence through non-lipid sources, including amino acids,” the researchers wrote.
While there were no approved drugs to treat MASH when the MUSC researchers initiated their study, current treatments still remain limited with resmetirom and semaglutide the only current approved therapies for this condition. Both medications have shown only limited efficacy in a subset of patients and have known side effects.
“All the current drugs for diabetic nephropathy only slow progression, but they don’t reverse the damage. This drug actually reversed the damage at the histologic, ultrastructural, and functional levels,” said Lipschutz.
Further, formoterol is already an approved and established medication that has been prescribed for year to treat both asthma and chronic obstructive pulmonary disease (COPD). Because its metabolic effects in humans and its safety profile has been detailed in its approval for these conditions, it could hasten approval for these other therapeutic uses.
“If you can repurpose something that’s approved and already being used safely, that’s kind of our dream as physician-scientists,” Lipschutz added.
Lipschutz and colleagues are currently conducting a clinical trial for the use of formoterol in chronic kidney disease (NCT07022418). Future research will focus on what dosing levels would be appropriate to use as treatment for CKD and MASH, whether inhaled delivery would be effective, and how durable the response to this potential treatment could be.
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Scientists at Columbia University have developed a brain-controlled hearing technology that allows users to amplify the conversation they are focusing on while reducing other voices. Published today in Nature Neuroscience, this study marks the first time this kind of technology has been tested in humans.
“We have developed a system that acts as a neural extension of the user, leveraging the brain’s natural ability to filter through all the sounds in a complex environment to dynamically isolate the specific conversation they wish to hear,” said Nima Mesgarani, PhD, principal investigator at Columbia’s Zuckerman Institute and associate professor of electrical engineering at Columbia’s Fu Foundation School of Engineering and Applied Science. “This science empowers us to think beyond traditional hearing aids, which simply amplify sound, toward a future where technology can restore the sophisticated, selective hearing of the human brain.”
While modern hearing aids can amplify human speech while suppressing background noise, they cannot separate and enhance specific voices when multiple people are speaking. This can make it difficult for users to concentrate on a specific conversation in everyday scenarios such as restaurants, classrooms, busy workplaces, and family gatherings.
The hearing device developed by Mesgarani’s team mimics the way the human brain can naturally identify and focus on a single speaker out of many within a crowd. Previously, the researchers had found a way of identifying which brain signals are linked to a specific conversation, by matching the timing of peaks and valleys of the brain waves to the sounds and silences of that conversation. They also identified distinct patterns of brain activity that indicate which conversation a person is focusing on and which one they are filtering out.
In the current study, the scientists developed a machine learning algorithm that could examine the user’s brainwaves and identify which conversation they are paying attention to in real time, making that voice louder and others quieter to make it easier to listen to. This system was tested on epilepsy patients who already had electrodes implanted in their brains. The electrodes were used to measure the user’s brain activity as they focused on two overlapping conversations played simultaneously, and the algorithm automatically detected which conversation they were trying to focus on.
“The results mark an important step toward a new generation of brain-controlled hearing technologies that align with the listener’s intent, potentially transforming how people navigate noisy, multi-talker environments,” said Vishal Choudhari, PhD, who led the development and evaluation of the system.
More research will be needed before minimally invasive wearable systems can integrate this kind of brain sensing technology with advanced audio processing capabilities, especially to ensure they can accurately decode conversations in real time and in real-world scenarios where multiple voices can be heard.
“The central unanswered question was whether brain-controlled hearing technology could move beyond incremental advances, towards a prototype that could help someone hear better in real time,” said Choudhari. “For the first time, we have shown that such a system that reads brain signals to selectively enhance conversations can provide a clear real-time benefit. This moves brain-controlled hearing from theory toward practical application.”
The post Brain-Controlled Hearing Aid Singles Out Voices in a Crowd appeared first on Inside Precision Medicine.