University of Cambridge

The finding could pave the way for a new type of treatment for glioblastoma, the most aggressive form of brain cancer, although extensive testing will be required before it can be trialled in patients. Glioblastoma is the most common type of brain cancer, with a five-year survival rate of just 15%. The researchers, from the University of Cambridge, found that cancer cells rely on the flexibility of hyaluronic acid (HA) — a sugar-like polymer that makes up much of the brain’s supporting structure — to latch onto receptors on the surface of cancer cells to trigger their spread throughout the brain. By locking HA molecules in place so that they lose this flexibility, the researchers were able to ‘reprogramme’ glioblastoma cells so they stopped moving and were unable to invade surrounding tissue. Their results are reported in the journal Royal Society Open Science. “Fundamentally, hyaluronic acid molecules need to be flexible to bind to cancer cell receptors,” said Professor Melinda Duer from Cambridge’s Yusuf Hamied Department of Chemistry, who led the research. “If you can stop hyaluronic acid being flexible, you can stop cancer cells from spreading. The remarkable thing is that we didn’t have to kill the cells — we simply changed their environment, and they gave up trying to escape and invade neighbouring tissue.” Glioblastoma, like all brain cancers, is difficult to treat. Even when tumours are surgically removed, cancer cells that have already infiltrated the brain often cause regrowth within months. Current drug treatments struggle to penetrate the tumour mass, and radiotherapy can only delay, not prevent, recurrence of the cancer. However, the approach developed by the Cambridge team does not target tumour cells directly, but instead attempts to change the tumour’s surrounding environment – the extracellular matrix – to stop its spread. “Nobody has ever tried to change cancer outcomes by changing the matrix around the tumour,” said Duer. “This is the first example where a matrix-based therapy could be used to reprogramme cancer cells.” Using nuclear magnetic resonance (NMR) spectroscopy, the team showed that HA molecules twist into shapes that allow them to bind strongly to CD44 — a receptor on cancer cells that drives invasion. When HA was cross-linked and ‘frozen’ into place, those signals were shut down. The effect was seen even at low concentrations of HA, suggesting the cells were not being physically trapped but instead reprogrammed into a dormant state. The study may also explain why glioblastoma often returns at the site of surgery. A build-up of fluid, or oedema, at the surgical site dilutes HA, making it more flexible and potentially encouraging cell invasion. By freezing HA in place, it could be possible to prevent recurrence. “This could be a real opportunity to slow glioblastoma progression,” said Duer. “And because our approach doesn’t require drugs to enter every single cancer cell, it could in principle work for many solid tumours where the surrounding matrix drives invasion. “Cancer cells behave the way they do in part because of their environment. If you change their environment, you can change the cells.” The researchers are hoping to conduct further testing in animal models, which could lead to clinical trials in patients. The research was supported in part by the European Research Council and the Engineering and Physical Sciences Research Council (EPSRC), part of UK Research and Innovation (UKRI). Melinda Duer is a Fellow of Robinson College, Cambridge. Melinda Duer will be discussing her research on Saturday, 27 September, as part of the Cambridge Alumni Festival 2025.  Reference: Uliana Bashtanova, Agne Kuraite, Rakesh Rajan, Melinda J Duer. ‘Molecular flexibility of hyaluronic acid has a profound effect on invasion of cancer cells.’ Royal Society Open Science (2025). DOI: 10.1098/rsos.251036 Scientists have found a way to stop brain cancer cells spreading by essentially ‘freezing’ a key molecule in the brain. This could be a real opportunity to slow glioblastoma progressionMelinda DuerKATERYNA KON/SCIENCE PHOTO LIBRARY via Getty ImagesComputer illustration of a brain tumour The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms. Yes

The visit brought together fundamental plant science research with crop and Agri-Tech researchers from across the University for a series of research demonstrations and a roundtable discussion.  Mr Zeichner toured the award-winning facility, meeting researchers in the open-plan office and lab spaces, which foster collaboration and advances in multi-disciplinary research.  The Minister saw exciting examples of foundational research, which have the potential to transform agriculture and ensure long term sustainability.   The first demonstration was led by Dr Sebastian Schornack and PhD student Nicolas Hernandez, who are investigating the plant developmental processes. The Minister saw through the microscope how they are using beetroot pigments to enable us to see how fungi is colonising living plant roots. This research allows us to track and measure in real time how chemicals, soil tillage and environmental conditions impact this beneficial plant-microbe relationship.   Mr Zeichner then visited the Lab’s microscopy room, and met with Dr Madelaine Bartlett and her colleague Terice Kelly. Dr Madelaine Bartlett's team researches the development of maize flowers (among other grass and cereal species) with a particular focus on the genetics behind these specialised flowers and future crop improvement. The team demonstrated how they image a maize flower on the Lab’s desktop scanning electron microscope.  The Sainsbury Laboratory boasts its own Bee Room, where Dr Edwige Moyroud demonstrated how bumble bees are helping to reveal the characteristics of petal patterns that are most important for attracting pollinators. Dr Moyroud and her team are identifying the genes that plants use to produce patterns that attract pollinators by combining various research techniques, including experiments, modelling, microscopy and bee behaviour.  Finally, overlooking Cambridge’ Botanic Gardens, academics from the Department of Plant Sciences and the Crop Science Centre presented on research into regenerative agriculture and using AI to measure and prevent crop disease.   Professor Lynn Dicks presented on the latest findings of the H3 research on regenerative agriculture. Professor Dicks and colleagues, during this ongoing five-year project, have worked collaboratively with farming clusters in the UK to study the impacts of a transition to regenerative agriculture, which has so far has been shown to improve soil health and reduce the use of chemicals.  Professor Eves-van Den Akker and his team, based at the University’s Crop Science Centre, have combined low-cost 3D printing of custom imaging machines with state-of-the-art deep-learning algorithms to make millions of measurements, of tens of thousands of parasites across hundreds of genotypes. They are now working with companies to translate this fundamental research, with the aim of accelerating their breeding programs for crop resistance to pests and disease.  The visit concluded with a discussion of the UK’s leading strengths in Agri-Tech and crop science, and how the UK and Cambridge are an attractive place for researchers from around the world to work, and make exciting advances, with global impact.  The University of Cambridge hosted a visit from local MP, and Farming Minister Daniel Zeichner MP, at the Sainsbury Laboratory. The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms. Yes

The visit brought together fundamental plant science research with crop and Agri-Tech researchers from across the University for a series of research demonstrations and a roundtable discussion.  Mr Zeichner toured the award-winning facility, meeting researchers in the open-plan office and lab spaces, which foster collaboration and advances in multi-disciplinary research.  The Minister saw exciting examples of foundational research, which have the potential to transform agriculture and ensure long term sustainability.   The first demonstration was led by Dr Sebastian Schornack and PhD student Nicolas Garcia Hernandez, who are investigating the plant developmental processes. The Minister saw through the microscope how they are using beetroot pigments to enable us to see how fungi is colonising living plant roots. This research allows us to track and measure in real time how chemicals, soil tillage and environmental conditions impact this beneficial plant-microbe relationship.   Mr Zeichner then visited the Lab’s microscopy room, and met with Dr Madelaine Bartlett and her colleague Terice Kelly. Dr Madelaine Bartlett's team researches the development of maize flowers (among other grass and cereal species) with a particular focus on the genetics behind these specialised flowers and future crop improvement. The team demonstrated how they image a maize flower on the Lab’s desktop scanning electron microscope.  The Sainsbury Laboratory boasts its own Bee Room, where Dr Edwige Moyroud demonstrated how bumble bees are helping to reveal the characteristics of petal patterns that are most important for attracting pollinators. Dr Moyroud and her team are identifying the genes that plants use to produce patterns that attract pollinators by combining various research techniques, including experiments, modelling, microscopy and bee behaviour.  Finally, overlooking Cambridge’ Botanic Gardens, academics from the Department of Plant Sciences and the Crop Science Centre presented on research into regenerative agriculture and using AI to measure and prevent crop disease.   Professor Lynn Dicks presented on the latest findings of the H3 research on regenerative agriculture. Professor Dicks and colleagues, during this ongoing five-year project, have worked collaboratively with farming clusters in the UK to study the impacts of a transition to regenerative agriculture, which has so far has been shown to improve soil health and reduce the use of chemicals.  Professor Eves-van Den Akker and his team, based at the University’s Crop Science Centre, have combined low-cost 3D printing of custom imaging machines with state-of-the-art deep-learning algorithms to make millions of measurements, of tens of thousands of parasites across hundreds of genotypes. They are now working with companies to translate this fundamental research, with the aim of accelerating their breeding programs for crop resistance to pests and disease.  The visit concluded with a discussion of the UK’s leading strengths in Agri-Tech and crop science, and how the UK and Cambridge are an attractive place for researchers from around the world to work, and make exciting advances, with global impact.  The University of Cambridge hosted a visit from local MP, and Farming Minister Daniel Zeichner MP, at the Sainsbury Laboratory. The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms. Yes

The discovery – found in a study in mice – sheds light on the role that inflammation can play in mood disorders and could help in the search for new treatments, in particular for those individuals for whom current treatments are ineffective. Around 1 billion people will be diagnosed with a mood disorder such as depression or anxiety at some point in their life. While there may be many underlying causes, chronic inflammation – when the body’s immune system stays active for a long time, even when there is no infection or injury to fight – has been linked to depression. This suggests that the immune system may play an important role in the development of mood disorders. Previous studies have highlighted how high levels of an immune cell known as a neutrophil, a type of white blood cell, are linked to the severity of depression. But how neutrophils contribute to symptoms of depression is currently unclear. In research published today in Nature Communications, a team led by scientists at the University of Cambridge, UK, and the National Institute of Mental Health, USA, tested a hypothesis that chronic stress can lead to the release of neutrophils from bone marrow in the skull. These cells then collect in the meninges – membranes that cover and protect your brain and spinal cord – and contribute to symptoms of depression. As it is not possible to test this hypothesis in humans, the team used mice exposed to chronic social stress. In this experiment, an ‘intruder’ mouse is introduced into the home cage of an aggressive resident mouse. The two have brief daily physical interactions and can otherwise see, smell, and hear each other. The researchers found that prolonged exposure to this stressful environment led to a noticeable increase in levels of neutrophils in the meninges, and that this was linked to signs of depressive behaviour in the mice. Even after the stress ended, the neutrophils lasted longer in the meninges than they did in the blood. Analysis confirmed the researchers’ hypothesis that the meningeal neutrophils – which appeared subtly different from those found in the blood – originated in the skull. Further analysis suggested that long-term stress triggered a type of immune system ‘alarm warning’ known as type I interferon signalling in the neutrophils. Blocking this pathway – in effect, switching off the alarm – reduced the number of neutrophils in the meninges and improved behaviour in the depressed mice. This pathway has previously been linked to depression – type 1 interferons are used to treat patients with hepatitis C, for example, but a known side effect of the medication is that it can cause severe depression during treatment. Dr Stacey Kigar from the Department of Medicine at the University of Cambridge said: “Our work helps explain how chronic stress can lead to lasting changes in the brain’s immune environment, potentially contributing to depression. It also opens the door to possible new treatments that target the immune system rather than just brain chemistry. “There’s a significant proportion of people for whom antidepressants don’t work, possibly as many as one in three patients. If we can figure out what's happening with the immune system, we may be able to alleviate or reduce depressive symptoms.” The reason why there are high levels of neutrophils in the meninges is unclear. One explanation could be that they are recruited by microglia, a type of immune cell unique to the brain. Another possible explanation is that chronic stress may cause microhaemorrhages, tiny leaks in brain blood vessels, and that neutrophils – the body’s ‘first responders’ – arrive to fix the damage and prevent any further damage. These neutrophils then become more rigid, possibly getting stuck in brain capillaries and causing further inflammation in the brain. Dr Mary-Ellen Lynall from the Department of Psychiatry at the University of Cambridge said: “We’ve long known that something is different about how neutrophils behave after stressful events, or during depression, but we didn’t know what these neutrophils were doing, where they were going, or how they might be affecting the brain and mind. Our findings show that these ‘first responder’ immune cells leave the skull bone marrow and travel to the brain, where they can influence mood and behaviour. “Most people will have experienced how our immune systems can drive short-lived depression-like symptoms. When we are sick, for example with a cold or flu, we often lack energy and appetite, sleep more and withdraw from social contact. If the immune system is always in a heightened, pro-inflammatory state, it shouldn’t be too surprising if we experience longer-term problems with our mood.” The findings could provide a useful signature, or ‘biomarker’, to help identify those patients whose mood disorders are related to inflammation. This could help in the search for better treatments. For example, a clinical trial of a potential new drug that targets inflammation of the brain in depression might appear to fail if trialled on a general cohort of people with depression, whereas using the biomarker to identify individuals whose depression is linked to inflammation could increase the likelihood of the trial succeeding. The findings may also help explain why depression is a symptom common in other neurological disorders such as stroke and Alzheimer’s disease, as it may be the case that neutrophils are being released in response to the damage to the brain seen in these conditions. But it may also explain why depression is itself a risk factor for dementia in later life, if neutrophils can themselves trigger damage to brain cells. The research was funded by the National Institute of Mental Health, Medical Research Council and National Institute for Health and Care Research Cambridge Biomedical Research Centre. Reference Kigar, SL et al. Chronic social defeat stress induces meningeal neutrophilia via type I interferon signaling in male mice. Nat Comms; 1 Sept 2025; DOI: 10.1038/s41467-025-62840-5 Immune cells released from bone marrow in the skull in response to chronic stress and adversity could play a key role in symptoms of depression and anxiety, say researchers. There’s a significant proportion of people for whom antidepressants don’t work. If we can figure out what's happening with the immune system, we may be able to alleviate or reduce depressive symptomsStacey KigarGift Habeshaw (Unsplash)Silhouette photography of man The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms. YesLicence type: Public Domain