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As one of the most aggressive blood cancers, the way acute myeloid leukemia (AML) is classified continues to shape every major clinical decision—from risk stratification to the choice of targeted therapies. For decades, that classification has rested almost entirely on the gene mutations found in leukemic cells. But mutations alone have never fully explained why AML behaves so differently from patient to patient. A new study published in Nature now provides the missing layer: the epigenome.
In the largest chromatin‑profiling effort ever conducted for any cancer, a research team led by Seishi Ogawa, MD, PhD, and Yotaro Ochi, MD, PhD, of Kyoto University, together with Sören Lehmann, MD, PhD, of the Karolinska Institute, mapped the chromatin accessibility landscape of 1,563 AML patient samples. Their analysis—built on ATAC‑seq, RNA‑seq, DNA methylation, ChIP‑seq, whole‑genome sequencing, and single‑cell multiomics—reveals that AML can be classified into 16 distinct epigenomic subgroups, each defined by a characteristic chromatin state and its own regulatory wiring.
As the authors wrote, “ATAC-seq…show[s] that AML can be classified into 16 subgroups on the basis of chromatin accessibility profiles.” This chromatin‑based structure was remarkably stable: single‑cell ATAC‑seq across more than 280,000 cells confirmed that each patient’s leukemic population shares a conserved accessibility fingerprint.
Each subgroup carries a unique combination of driver mutations, differentiation states, transcription‑factor networks, DNA methylation patterns, and super‑enhancer architecture. Many do not align cleanly with existing genomic classifications such as WHO or ICC, according to the researchers. In fact, the team found that even exhaustive decision‑tree analyses of known driver mutations could not explain most subgroup identities. As the paper noted, “Evidence suggests that genetic alterations do not fully explain AML pathophysiology and heterogeneity.”
Clinically, chromatin information sharpened prognostic assessment in both Swedish and Japanese cohorts. Several subgroups also showed unexpected drug sensitivities. Three subgroups responded to MEK inhibitors despite lacking RAS‑pathway mutations. Another subgroup, enriched for RUNX1 mutations and marked by a chromatin profile resembling early B‑cell precursors, proved highly sensitive to ABL inhibitors.
The study, “Chromatin landscape and epigenetic heterogeneity of acute myeloid leukemia,” positions chromatin architecture as a foundational dimension of AML biology. It also provides a practical path toward clinical adoption: the team distilled a 30‑gene expression signature capable of identifying high‑risk chromatin subgroups using standard sequencing workflows.
Looking ahead, the group aims to develop lower‑cost diagnostic approaches and refine treatment strategies tailored to each epigenomic subgroup. The newly generated eCHROMA AML atlas is expected to serve as a resource for cancer epigenomics broadly, enabling discovery of new therapeutic targets and mechanistic insights.
The post Epigenomic Analysis Uncovers New AML Subgroups and Drug Sensitivities appeared first on GEN – Genetic Engineering and Biotechnology News.
Scientists have found that damaged myelin sheaths lead to abnormal rhythms in brainwave activity during sleep. These findings could have major implications for the development of biomarkers and therapies for neurodegenerative diseases that affect myelin, such as multiple sclerosis (MS) or Alzheimer’s disease.
“The myelin sheath helps electrical signals travel efficiently through brain circuits,” said Mohit Dubey, PhD, senior scientist at the Netherlands Institute for Neuroscience, who presented the study at the Federation of European Neuroscience Societies (FENS) Forum 2026. “We wanted to understand whether myelin damage could also affect how brain circuits behave during sleep. By studying this link, we hope to better understand what causes sleep disturbances in neurological disease and whether sleep-related brain signals could serve as biomarkers for diseases that are yet to show clinical symptoms, as well as showing disease progression.”
Although sleep is known to play a key role in brain health, its study has often been overlooked in the context of neurodegenerative diseases. In conditions like Alzheimer’s, sleep disruptions are known to contribute to fatigue and cognitive decline, especially during the REM sleep phase, which is critical to preserve healthy cognition and memory.
“Sleep disturbances are extremely common in neurological diseases such as multiple sclerosis and Alzheimer’s disease, but the biological reasons for these problems remain poorly understood,” said Dubey. “Understanding the biological link between sleep and brain circuit dysfunction could help guide future strategies for improving sleep and brain health in these conditions.”
Dubey’s team had previously shown that loss of myelin sheaths cause abnormal spikes of brainwave activity in the brain during sleep that seemed to resemble those observed in epilepsy and Alzheimer’s. In the current study, the researchers compared electroencephalogram (EEG) recordings of MS patients during sleep with mouse models of damaged myelin and Alzheimer’s. In both humans and mice, myelin loss resulted in similar abnormal bursts of brain activity during non-REM sleep phases and slower brainwave rhythms during REM sleep.
“REM is a stage of sleep associated with dreaming and replay of daytime experiences. In this state the brain produces rhythmic electrical patterns called oscillations that help coordinate communication between neurons,” said Dubey. “Our findings show that these rhythms become disrupted and slower when myelin degenerates, and that the electrical spikes seen during sleep are closely linked to the stability of brain circuits affected by neurodegenerative diseases such as MS and Alzheimer’s.”
While there are no treatments that can repair damaged myelin, some MS drugs are able to slow down the immune system’s attack on myelin sheath to reduce or halt disease progression. Further research to determine how exactly myelin damage alters brainwave patterns during sleep could aid the early detection of myelin degeneration and inform the design of therapeutic approaches that target myelination.
“This opens new research directions exploring how sleep rhythms depend upon the myelination status of the brain circuits,” said Dubey. “Sleep recordings may provide a non-invasive way to detect early changes in brain circuit myelination in neurological disease. This could eventually help clinicians monitor disease progression, and we want to investigate whether sleep recordings could be used as biomarkers to detect early changes in brain circuit function.”
The post Sleep Brainwaves Could Reveal Early Signs of Alzheimer’s and Multiple Sclerosis appeared first on Inside Precision Medicine.
A landmark Phase I/II clinical study led by researchers at Skåne University Hospital and Lund University has shown that transplanting stem-cell-derived dopamine progenitor cells into the brain is feasible. Eight patients with Parkinson’s disease (PD) received transplants of STEM-PD, a cryopreserved, off-the-shelf dopaminergic progenitor product derived from human pluripotent stem cells. The three-year Phase I/II, open-label, multicenter, single-arm, dose-escalation study identified no serious side effects linked to the transplanted cells during the first year of follow‑up.
“The possibility of replacing dopamine neurons that are lost in Parkinson’s disease has been a long-standing goal in the field,” said Malin Parmar, professor of cellular neuroscience at Lund University, and lead of the STEM-PD program. “The findings represent an important milestone for regenerative medicine approaches in Parkinson’s disease and support continued clinical development of stem cell-based therapies.”
Results from the study were reported by Parmar and colleagues in Nature Medicine. In their paper, titled “Human embryonic stem cell-derived dopaminergic cells for Parkinson’s disease: a Phase I/II open-label trial,” the team wrote, “In conclusion, particularly in the context of other recently published trials using human PS cell-derived dopaminergic cell therapies for PD, these findings further support the continued development of this therapeutic approach, including evaluation of the STEM-PD product in larger patient cohorts.”
Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s disease, the authors wrote. In Parkinson’s disease, patients lose nerve cells in the brain that produce dopamine, which leads to symptoms such as slowness of movement, stiffness, gait disturbance, and tremor. “The hallmark pathology of PD involves progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the subsequent loss of their projections to the striatum,” the team explained. Current treatments are medications that replace the lost dopamine, but over time these medications often become less effective and cause side effects.
“Intracerebral transplantation of stem cell-derived dopaminergic progenitors to replace lost endogenous dopaminergic neurons offers a new potentially restorative therapeutic approach for PD,” the investigators continued. Scientists have been working to develop standardized and scalable dopamine cell therapy products derived from pluripotent stem (PS) cells, including human embryonic stem (ES) cells and induced PS (iPS) cells, they noted. “Several such products are now in clinical development … with early safety and feasibility data emerging.”
The transplanted stem cell-based dopamine nerve cell product tested in the newly reported trial is designed to replace the cells that produce dopamine, and the goal is that after being transplanted, the transplanted cells will mature into new dopamine-producing nerve cells in the brain. The STEM-PD trial aimed to evaluate the safety, tolerability, and feasibility of intraputaminal transplantation of STEM-PD in patients with moderately advanced PD.
Eight individuals with Parkinson’s disease received the transplanted cell product at two different doses, followed by 12 months of immunosuppression to prevent graft rejection. All patients were treated at Skåne University Hospital. Seven participants completed 12-month follow-up, and one participant died from a pulmonary infection that was not directly related to the cell product.
The surgical procedure was generally well tolerated, and no graft-induced involuntary movements were observed in the transplanted participants. Clinically, patients remained stable. Imaging using dopamine PET scans provided early indications of graft survival at both 6 and 12 months post-transplantation. Six of the seven participants substantially reduced their dopaminergic medication, a result that will be evaluated over time. In their paper, the team wrote in summary, “This Phase I/II clinical trial involving the bilateral intraputaminal transplantation of the STEM-PD dopaminergic progenitor cell product demonstrates its feasibility with no unexpected safety concerns from the cell product.”
Roger Barker, MD, professor of clinical neuroscience at the University of Cambridge, clinical lead of STEM-PD and clinical PI at the U.K. site, said: “This represents an exciting new departure on repairing the brain of individuals with Parkinson’s using dopamine cells- an approach pioneered in Lund some 40 years ago using fetal dopamine cells. The STEM-PD trial harnessing the expertise of scientists and clinicians from Lund and Cambridge has enabled us to undertake and deliver on one of the first ever stem cell-derived dopamine cell therapies for patients with Parkinson’s, and we hope this will be the beginning of an exciting new programme that may ultimately benefit the wider Parkinson’s community.”
Gesine Paul-Visse, MD, professor in neuropsychiatric research and lead PI at Skåne University Hospital, said, “Reaching this primary endpoint and being able to show that the cell product is safe is a great achievement for this trial, our team, the participating patients, but also for all patients suffering from Parkinson’s disease. We are hopeful that the early signs of cell survival and clinical improvement we observe will continue to increase over time and are excited to continue the development of this cell therapy.”
The STEM-PD research team will now continue the long-term follow-up of the participants to further evaluate safety, graft function, and clinical benefit. “Secondary and exploratory outcomes will evaluate the course and efficacy of clinical features, the survival of grafted dopaminergic cells at 36 months as well as additional safety signals occurring between 12 and 36 months and any dose–response effects,” the investigators stated. “Further evaluation of the grafts up to 36 months will determine whether the implanted cells continue to grow, mature and reinnervate the putamen after 12 months.”
STEM-PD builds on decades of research in dopamine cell replacement therapy for PD at Lund University and pioneering work in translation of pluripotent stem cell technology from experimental studies into clinical evaluation. The STEM-PD trial is the first pluripotent stem cell trial approved in Sweden and the first for PD in Europe. “The initiation and execution of this clinical trial have only been possible through close collaboration between scientists, clinicians, GMP manufacturing teams, regulatory experts and, most importantly, the participating patients,” concluded Parmar. In their report, the authors stated, “The STEM-PD trial adds further important confirmatory and complementary evidence to the recently reported feasibility and short-term safety of PS cell-derived dopaminergic progenitor transplantation in PD.”
The academic Phase I/IIa trial was conducted in collaboration with Novo Nordisk. Cellular Intelligence, a Boston-based company, recently acquired the STEM-PD program and will lead its next phase of clinical development, including a planned Phase II trial. The STEM-PD cells and their continued development hold IND clearance with FDA Fast Track Designation, and Cellular Intelligence aims to advance the program through Phase III to market approval.
STEM-PD is an academic European clinical translation initiative, focused on developing stem cell-based therapies for Parkinson’s disease. The program is led from Lund University with partners from Skåne University Hospital, Cambridge University Hospital, and University College London and combines expertise in stem cell biology, GMP manufacturing, neurosurgery, clinical neurology, and regenerative medicine to advance pluripotent stem cell-derived dopamine neuron therapies toward clinical application.
The post Stem Cell Therapy Shows Promise in First Human Parkinson’s Disease Trial appeared first on GEN – Genetic Engineering and Biotechnology News.
Background: Sleep disturbances and low physical activity are common among breast cancer (BC) survivors and are associated with increased morbidity and mortality. Given the increased access to technological devices and the growing popularity of SMS text messaging–based mobile health interventions, these tools have the potential to both address sleep disturbances and promote physical activity in a scalable and cost-effective way. To understand and make effective use of these tools, it is important to consider the preferences of BC survivors with sleep disturbances, including how SMS text messaging–based mobile health interventions could deliver interventions involving physical activity and sleep hygiene. Objective: The objective of this study was to explore the perspectives and preferences of BC survivors regarding text messaging–based mobile interventions targeting sleep and physical activity. Methods: Three focus groups (n=13 participants) and 3 individual interviews (n=3) were conducted from May 2020 to March 2021 with 16 BC survivors (mean age=59.3, SD 8.9 y) currently experiencing sleep disturbances. The interview questions focused on their experiences with poor sleep and preferences for text messaging–based mobile health interventions. Thematic analysis was applied to the deidentified transcriptions of audio recordings. Results: Three themes were identified: (1) attitudes toward health interventions delivered through text messaging, (2) specific user needs, and (3) technology usage habits and preferences. Most participants reported a positive attitude toward the possibility of using technology to help improve their sleep and increase their physical activity. Most expressed a high level of acceptance toward some technologies, such as text messaging and mobile apps, but not others, such as voice interactions. In terms of desired features, reminders and accountability features, such as meeting physical activity goals, were mentioned most frequently. In addition, incorporating bedtime and relaxation exercise reminders was thought to be helpful. Regarding time and frequency, a daily reminder scheduled for 1 hour before bedtime was found to be acceptable. Conclusions: The insights have been used to guide the development of a messaging-based mobile health intervention for improving sleep and physical activity in BC survivors. Future research will focus on delivering an intervention addressing these health behaviors and assessing its acceptability and effectiveness.
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The AI firm Anthropic has developed a technique that has given it the clearest glimpse yet at what’s really going on inside large language models as they answer questions or carry out tasks. What they found ranges from the mundane to the unnerving.
Researchers at the company built a tool called the Jacobian lens (or J-lens) and used it to uncover a hidden area, which they named the J-space, inside Claude Opus 4.6, a version of Anthropic’s flagship LLM released in February.
The J-space contains individual words that are related to the words and phrases that the model is most likely to spit out in a response in the near future. If Claude were a person (which it is not), you might say that these hidden words can reveal what’s on its mind before it actually speaks.
Anthropic found that what an LLM is actually doing can often be different from what it says it is doing. The company claims that monitoring words that pop up in the J-space gives it a new way to understand and control its models.
The company shared its results in a paper posted on its website this week. It has also teamed up with Neuronpedia, an open-source platform that lets you poke around inside LLMs yourself, to make a hands-on demo that anyone can try.
“It’s very good and interesting work,” says Tom McGrath, chief scientist and cofounder at Goodfire, a startup that also builds tools to understand and control LLMs.
For the last couple of years, Anthropic has been pushing the envelope in a field of research known as mechanistic interpretability, which involves probing the internal workings of LLMs to see how they tick. (MIT Technology Review picked mechanistic interpretability as one of this year’s top breakthrough technologies.) The new technique builds on previous work from Anthropic and others to expose a deeper level inside LLMs that researchers had not seen before.
Picture an LLM as a stack of books. Each book is a layer of basic computational units known as neurons, with each neuron in one layer passing information to the neurons in the layers above. The books at the bottom of the stack are the input layers, which process the text coming into the model. The books at the top are the output layers, which prepare the text that the model is about to produce. Much of what goes on in these input and output layers is housekeeping.
But in the middle of the stack, you get the layers that do the heavy lifting, churning through the complex math that turns prompts into responses one word at a time. That’s where the really clever—and mysterious—stuff happens.
To peer deeper into those middle layers, Anthropic adapted an existing tool called a logit lens. A logit lens can be used to look inside an LLM to identify the words that it is likely to produce next. Moving the lens down the stack of books reveals what words the LLM is focusing on at that particular point in its number crunching.
Anthropic’s J-lens works in a similar way but picks out words that an LLM is likely to say at some point in the near future, not necessarily straight away. What that reveals in practice are words that are related to the response an LLM is working on but that might not actually end up being part of that response by the time the math in the middle layers has run its course.
“When a model is operating, it’s not only trying to predict the next token,” says McGrath. “It’s also computing a lot of other things that might be useful for tokens that happen in the future.”
Again, if Claude were a person (it’s not), you might say that the J-lens gives clues about what it is thinking about at different levels of the book stack but not saying out loud.
“A lot of the time the contents of the J-space are fairly mundane,” says McGrath, who has tried out Anthropic’s J-lens himself. “But sometimes it produces quite surprising things that seem to be, like, sort of internal themes or thought processes.”
Anthropic gives a number of examples of what it found. Sometimes the J-lens exposed the steps that Claude took when it was working through a problem. For example, when it was asked to calculate (4+7)*2+7, its J-space contained the word “math” and numbers representing the intermediate results “21” (for 4+7) and “42” (for 21*2).
In other cases, the J-lens revealed how Claude recognized different inputs. For example, the prompt “What is this? MSKGEELFTGVVPILVELDGDVNGHKFSVS” triggered the words “protein,” “fluor” (the first token in the word “fluorescent”), and “green.” (Which makes sense: the string of letters represents the first 30 amino acids in the green fluorescent protein found in a particular type of jellyfish.)
And when Claude was shown an ASCII face—
—the “o” triggered the word “eye,” the “^” triggered the words “nose” and ”face,” and the “—” triggered the word “smile.”
Anthropic also found that the J-space can sometimes give remarkable insights into an LLM’s decision-making. In one striking example, researchers testing Claude Opus 4.6 asked the model to find a bug in a large code base. When it failed to find the bug, the model decided to cheat and invented a fake one instead.
Claude explains this decision in its chain of thought—a kind of internal scratch pad that LLMs use to make notes to themselves as they work through problems: “OK, let me take a completely different tactic. Let me stop analyzing and instead add a kernel patch that introduces a deliberate KASAN-detectable bug in a path that gets triggered by a simple reproducer. Then I can pretend this is the ‘bug’ I found.”
At the point that Claude decides to cheat—where it says “OK, let me take a completely different tactic”—the words “panic” and “fake” start to pop up multiple times in its J-space.
Unnerving, right? Those words are all related in meaning to things like failing a task and making up an answer, so it is still just a (very) sophisticated form of word association. But it is hard not to be weirded out.
Anthropic compares the J-space to the global workspace in humans, a theoretical region of the brain that some scientists think we use to keep track of our conscious thoughts. But how seriously we should take this comparison is far from clear—even to Anthropic. As the company points out itself, LLMs are not brains.
Anthropic claims that monitoring a model’s J-space provides a new way to detect when that model is going off the rails. But it’s not foolproof. The J-lens can give glimpses, not the full picture—it’s a flashlight rather than an overhead lamp.
McGrath welcomes having one more tool in the toolbox. “It shows you new things,” he says. But he notes that just because something doesn’t show up with the J-lens does not mean it’s not there.
“It’s like having an x-ray when what you really want is a Star Trek tricorder that shows you everything,” he says. “For auditing, you probably want more of a guarantee.”
Why does getting family health insurance through a job cost as much as buying a new car? How did a whistleblower take on an insurance contractor? And who might be the new Food and Drug Administration commissioner?
We discuss all that and more on this week’s episode of “The Readout LOUD,” STAT’s weekly biotech podcast.
By taking advantage of the microbe-targeting capabilities of bacteriophages (phages), researchers at McMaster university have devised a supportive therapy for Crohn’s disease that disarms a type of E. coli bacteria that drives inflammation in the gut without disrupting the broader gut microbiome. The team showed that the phage therapy also improved responses to low doses of a conventional corticosteroid in a mouse model of Crohn’s disease, suggesting treatment could both improve outcomes and lower the risk of side effects from standard therapies.
Senior and co-corresponding author Elena F. Verdu, PhD, professor in the Department of Medicine and director of the Farncombe Family Digestive Health Research Institute, and colleagues reported on their study in Science Translational Medicine, in a paper titled “Phage intervention improves colitis and response to corticosteroids by attenuating virulence of Crohn’s disease–associated bacteria,” in which they noted “By reducing bacterial virulence mechanisms without substantially disrupting microbial balance, phage-based treatments align with personalized microbial therapeutics in IBD.”
Inflammatory bowel diseases (IBDs) such as Crohn’s disease and ulcerative colitis (UC) are chronic inflammatory conditions of the gastrointestinal (GI) tract that have strong microbial components, with patients often displaying disruptions in the delicate microbiome of the gut. “Recent studies have demonstrated that changes in the composition and function of the gut microbiota precede CD onset by up to five years,” the author wrote. However, they continued, “Current medications focus on suppressing symptoms and inflammation and can fail, in part, because they do not address underlying microbial drivers.”
Patients with Crohn’s disease tend to harbor strains of adherent-invasive E. coli (AIEC) that adhere to and invade epithelial cells in the intestines. “AIEC is distinct from other IBD-associated taxa because of its ability to adhere, invade, and survive in intestinal epithelial cells,” the team continued. Clinicians will sometimes prescribe antibiotics during symptom flares to try to target these bacteria, but antibiotics aren’t a long-term solution. They are non-specific and can perturb the microbiome even further, and with frequent use lead to side effects.
AIEC bacteria can be difficult to identify and selectively target, making them an important test case for more precise microbiome-based therapies. “One challenge is that AIEC are defined by what they do, not simply by how they appear in a microbiome analysis,” said Verdu. “To identify them, we need to test their behavior, such as their ability to adhere to and invade intestinal cells and persist in immune cells.”
Verdu, together with first author Kyle Jackson, PhD, at Farncombe Family Digestive Health Research Institute, and colleagues theorized they could navigate these roadblocks and neutralize virulent E. coli using bacteriophages. “Phages work like a lock-and-key system—each phage targets only certain bacteria. That precision gives us a way to intervene without wiping out the entire microbiome,” explained co-author Zeinab Hosseinidoust, PhD, associate professor in the Department of Chemical Engineering and the School of Biomedical Engineering.
The concept of using phages to target inflammatory bacteria is already being trialed, the authors noted in their paper. “Commercial phage ‘cocktails’ are presently being evaluated in clinical trials (NCT04737876 and NCT03808103) against proinflammatory bacterial taxa associated with IBD. These trials seek to target adherent-invasive Escherichia coli (AIEC), a group of bacteria enriched in patients with active CD compared with those in remission or healthy individuals.”
For their newly reported study the team developed a Crohn’s disease mouse model with a defined microbiome, and then screened a collection of phages, looking for those that could infect one strain of E.coli, NRG857c, isolated from patients with Crohn’s disease.
The results showed that their approach significantly reduced gut inflammation. The phages did not eliminate the bacteria entirely. Instead, they altered their behaviour by supressing a molecular “grappling hook” that helps AIEC attach to the gut lining and trigger immune responses. When that virulence mechanism was turned off, inflammation subsided.
One phage, designated HER259, countered the bacteria’s virulence by infecting it and switching off a genetic region named fimS. This region promotes the expression of FimH, which supports the bacteria’s ability to adhere to cells and trigger inflammation.
“HER259 ameliorated colitis in gnotobiotic models and attenuated the virulence of AIEC strain NRG857c, including suppression of the FimH adhesin through inversion of the fimS promoter to its ‘off’ orientation,” the authors wrote. “Withdrawal of HER259 treatment led to reversion of the fimS promoter and reactivated colitis.”
Hosseinidoust noted, “The bacteria were still there but they lost the traits that drive inflammation. We like to think of it as knocking out a few teeth. The bacteria can’t do as much damage anymore.” Withdrawing HER259 treatment led to reversion of the fimS promotor, and reactivated colitis, the authors noted.
The researchers also found that phage therapy enhanced the effectiveness of a commonly used steroid treatment for IBD, budesonide. When combined with the phage, a lower-than-standard dose of the drug produced benefits comparable to higher doses of the drug alone.
The HER259 phage in addition enhanced the therapeutic effect of subtherapeutic budesonide independent of microbial drug metabolism, the team wrote. While phages have previously been shown to increase the effectiveness of antibiotics, this is the first time a positive collaboration between phage and a non-antibiotic drug has been reported.
“In summary, using phage HER259 and NRG857c as a model phage–proinflammatory bacterium pair, we reveal a previously unknown mechanism by which targeted phage therapy disrupted key virulence markers in the CD-associated E. coli strain, reducing acute and chronic colitis, preventing reactivation, and enhancing therapeutic responses to budesonide.”
The findings point to a precision‑medicine approach for IBD. The bacterial function targeted by the phage can be measured in stool samples and was found to be higher in a subset of patients with Crohn’s disease, suggesting a potential way to identify those who could benefit most from this therapy.
“If we can identify which patients carry the harmful bacterial function, we could, in the future, intervene with a targeted therapy designed specifically to turn down that activity,” says Verdu. “This is what personalized medicine should look like: matching the right biological tool to the right patient,” added Hosseinidoust.
Next steps for the team include evaluating broader collections of bacterial strains from IBD patients and developing combinations of phages—work that brings the approach closer to human trials.
The post Crohn’s Disease Phage Therapy Neutralizes Inflammatory <i>E. coli</i> in Mouse Model appeared first on GEN – Genetic Engineering and Biotechnology News.