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Decades-old Puzzle Solved as Scientists Uncover Cause of IBD

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Scientists have identified the missing link between a long-known genetic signal in inflammatory bowel disease and a damaging immune response that switches off the body’s natural control of inflammation – opening the door to faster diagnosis and targeted treatment.

Interleukin-10.

Researchers at the Nuffield Department of Medicine, University of Oxford, together with Newcastle University’s Translational and Clinical Research Institute and the Department of Immunology at Cambridge University Hospitals NHS Foundation Trust, have identified an important driver of inflammatory bowel disease (IBD). This discovery reshapes understanding of IBD and opens the way to targeted approaches to diagnosis and treatment in a subset of patients. The findings suggest that inflammatory bowel disease is not a single condition, but a group of biologically distinct diseases driven by different underlying mechanisms.

In a study published in the New England Journal of Medicine, researchers analysed over 4900 patients with IBD and made two major discoveries: first, that a substantial subset of patients show autoimmune responses to one of the guardians of the immune system, interleukin-10 (IL-10), which leads to uncontrolled inflammation; and second, that this damaging immune response is the mechanism for one of the strongest known genetic risk factors for IBD.

Antibodies that block interleukin-10 (IL-10), a cell-to-cell messenger that normally acts as one of the body’s key controls on inflammation, effectively remove the immune system’s natural ‘brake’ on inflammation, allowing inflammatory responses to continue unchecked.

IBD, which includes Crohn’s disease and ulcerative colitis, affects around 500 000 people in the UK and millions worldwide. It is a lifelong condition that commonly begins in adolescence or early adulthood and can require repeated hospital treatment, long-term immunosuppressive medication and, in some cases, surgery. Despite advances in treatment, many patients cycle through multiple therapies without achieving lasting disease control – impacting their lives and costing the health care system millions.

The researchers found high levels of anti-IL10 neutralising autoantibodies in the blood of around 3.5% of IBD patients, both Crohn’s disease and ulcerative colitis, but not in healthy individuals. This could equate to 15 000-20 000 people with IBD in the UK carrying these autoantibodies.

The researchers also found that the presence of these antibodies was strongly linked to carriage of a particular genetic variant known as HLA-DRB1*01:03.

The link between HLA-DRB1*01:03 and a severe form of inflammatory bowel disease was first identified by Oxford researchers 30 years ago. The new findings show that people carrying this variant are far more likely to develop antibodies that block IL-10, helping explain how the gene contributes to disease.

The Oxford IL-10 Research GroupProfessor Holm Uhlig, a Paediatric Gastroenterologist and Director of the Centre for Human Genetics, Nuffield Department of Medicine, University of Oxford, and a senior author of the study, said: ‘We’ve suspected an important role of interleukin 10 in patients with inflammatory bowel disease for decades. The study now provides clear evidence and contributes the missing link between a well-known genetic variant that had been linked to severe inflammatory bowel disease in the past and the very recently discovered autoimmunity to interleukin 10. 

‘Understanding what drives the inflammation, provides a clear explanation for disease in this group of people and opens the door to new treatments that target the autoantibodies themselves or cells that produce those autoantibodies.’

The paper, ‘IL-10 Autoantibodies and HLA-DRB101:03 in Inflammatory Bowel Disease’, is published in the New England Journal of Medicine.

Source: University of Oxford

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Chimeric RNA Unique to Women Is an Important Controller of Health

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Strange “chimeric” RNA once thought to be the product of cancer is actually an important controller of women’s health, including influencing their susceptibility to infectious disease and autoimmune disorders, new University of Virginia School of Medicine research suggests.

UVA’s Hui Li, PhD, and colleagues have identified a chimeric RNA called UBA1-CDK16 that is found only in women. This RNA plays important roles in their blood cell development and in determining the severity of diseases such as COVID-19, the scientists found. The findings, published in Science Advances, could open the door to blood tests to help diagnose diseases or identify women at greatest risk for bad outcomes.

“Chimeric RNAs are RNA molecules composed of parts from different genes,” said Li, of UVA’s Department of Pathology and the UVA Comprehensive Cancer Center. “They were once believed to be cancer-specific. However, our research shows that they can also be part of normal physiology and play important roles in human health.”

Powerful Chimeras

RNA provides instructions for our cells, telling them what to do based on the genetic material, called DNA, that we inherit from our parents. Chimeric RNAs were long thought to be mistakes, as they are made up of instructions mashed together from different genes. This is why they were believed to be a byproduct of cancer; cancer itself is the result of cellular copying mistakes.

Li’s discovery, however, suggests that UBA1-CDK16  plays important roles in maintaining women’s health and in controlling their immune systems. This chimeric RNA is found only in women because women have two X chromosomes, while men have an X and Y. Normally, one of the two X chromosomes found in women’s cells are inactive. But Li found that the inactive X chromosome produces this peculiar chimeric RNA that he could identify in women’s blood.

Based on his findings, Li believes UBA1-CDK16 plays an important role in regulating blood cell formation. But his work also suggests the chimera may play an important role in the immune system’s response to infection. He found that the chimeric RNA was lost in 50% women who developed severe COVID-19 infections, while it was present in women who were asymptomatic. Further, the decrease in chimeric RNA correlated with the increasing severity of the infection.

Li suspects that the chimeric RNA may play an important role in governing the development of immune cells called neutrophils that act as the body’s first responders to infection. (Neutrophil count has already been identified as a way to predict how patients will fare against COVID-19.) 

“As humans share similar number of genes with fruit flies and worms, gene number does not explain why we are much more sophisticated than these lower organisms” Li said. “We believe chimeric RNAs are another means to expand the functional genome, without an actual increase in gene number.”

Li’s findings suggest that the chimeric RNA also may serve as a natural brake to protect women from excessive autoimmune activity. Women are far more likely to suffer autoimmune disorders than men, and Li is urging additional research to better understand the role chimeric RNA could be playing – and how it could be targeted to improve patient outcomes.

“This finding highlights there is another layer of control for gene expression,” Li said. “These chimeric RNAs may represent a hidden repertoire for biomarkers and therapy targets as well.”

Source: University of Virginia

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South African Scientists Make Breakthrough in Decoding Cancer’s Most Effective Survival Strategy

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Scanning electron micrograph of just-divided HeLa cells. Zeiss Merlin HR-SEM. Credit: National Center for Microscopy and Imaging Research

Kevin Naidoo, University of Cape Town

In the intricate biology of the human body, organs such as the breast, the colon and the lungs are lined with a defensive barrier known as the epithelium. At the heart of this barrier sits a remarkable protein called Mucin-1 (MUC1). In a healthy body, MUC1 is like a sentinel.

It stands on the cell wall, draped in a complex “armour” of long chains of sugar molecules (carbohydrates), where it serves as a physical shield against bacteria, viruses and toxins. Crucially, it communicates with the immune system, telling our natural defences when the body is under threat.

But in the case of cancer, this guardian exchanges its sugar coat armour for shorter sugar chains and so turns into a traitor. It stops sending danger signals to the immune system and instead binds to the immune cells, creating an anti-inflammatory microenvironment that promotes tumours.

The team I lead at the Scientific Computing Research Unit at the University of Cape Town is home to computer modelling experts and experimental chemical biology research scientists. The molecular details of this MUC1 alteration, which contributes to the transformation of normal cells into tumour cells, were recently published in Nature Communications, and provide a new look at exactly how this process happens.

By developing a novel “test-tube” synthetic biology approach, we modelled and decoded the molecular assembly line reorganisation that allows cancer to “redecorate” MUC1, turning it from a protective shield into a cloak of invisibility. We used our own computational chemistry algorithms to map the exact sugar coating positions that create a tumour-promoting environment.

Understanding the location and nature of the MUC1 sugars that prevent the immune system from detecting tumours provides the foundation for our laboratory and others in the field to develop cancer vaccines, biomarkers and therapeutics.

This South African-led discovery represents a major leap forward in our ability to decode one of cancer’s most effective survival strategies.

The problem: a malignant makeover

In a normal cell, the sugar molecules attached to MUC1 are long and complex. The process of attaching sugars is called glycosylation. In cancer cells, however, this process goes haywire. The sugar molecules are often cut short or altered, creating “aberrant” structures like the Tn and sialyl-Tn (sTn) antigens. These are specific types of sugar-protein combinations that are tags for tumour cells.

These altered sugars do two dangerous things: they allow the tumour to evade detection by the immune system, and they actively trigger the process of turning a normal cell into a cancerous one.

Because MUC1 is found in so many different types of cancer, the US National Cancer Institute has ranked it as the most accesible target.

To stop the cascading effect of the MUC1 changes from normal to tumour cells, scientists first had to understand exactly how the “assembly line” breaks down.

The discovery: relocating the factory

Our research team set out to do something ambitious: recreate the transition from a healthy sugar coating to a cancerous one in a laboratory setting.

In normal cells, the enzymes that build these sugar chains (long molecules) live in a part of the cell called the Golgi apparatus, the cell’s “packaging and delivery centre”. We built an in vitro (test-tube) model to simulate what happens when these conditions change. We discovered that in tumour cells, the enzymes responsible for starting the sugar chains are relocated to another part of the cell, the endoplasmic reticulum, essentially the cell’s “factory floor”.

This relocation changes everything. Here, the enzymes are no longer inhibited by the usual cellular checks and balances. They take over the sugar sites on the MUC1 protein, creating the foundation for the cancerous Tn antigen.

To take the study even further, we used quantum chemistry. We simulated the behaviour of atoms and molecules at the most fundamental level to find out where these changes are most likely to happen. We identified a specific location on the MUC1 protein, known as the T13 site, which cancer enzymes prefer. This specific interaction is what drives the massive increase in the sTn antigen seen in malignant tumours.

Why this matters: from lab to patient

Understanding the “how” and the “where” of these sugar changes is the first step towards stopping them. The research didn’t stop at the test tube; the team is already looking at what this means for patients.

The next phase of the research, as detailed in a recent paper in Glycobiology, involves building a sophisticated “systems biology” computational model. A model can connect the changes in the MUC1 sugar coating to the behaviour of immune cells. For example, scientists found that when these cancerous sugars interact with macrophages (a type of white blood cell), they trigger the release of specific signals that tell the tumour to grow and spread.

We are refining these details for various types of cancer. We are comparing common forms of breast cancer with more aggressive, currently untreatable types to see if the “sugar code” differs between them.

By using this accurate, atomic-level data to build computer models of the entire biological system, we hope to identify new drugs that can block these signals. The goal is to move towards precision medicine: treatments that can strip away cancer’s sugar shield, allowing the patient’s own immune system to finally see and destroy the tumour.

Kevin Naidoo, Professor of Scientific Computing and Physical Chemistry, University of Cape Town

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

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Gene Therapy Shows Promise for an Inherited Form of Cardiomyopathy

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Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014“. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436.

A new gene therapy appears to be safe in patients diagnosed with Friedreich ataxia cardiomyopathy, a progressive and fatal inherited cardiac disease, according to a phase 1 clinical trial led by Weill Cornell Medicine researchers. The treatment may also reduce heart damage, although further investigation is needed. 

The results, published June 17 in JAMA Cardiology, indicated that an intravenous infusion of a healthy frataxin (FXN) gene was generally well tolerated and shows early signs of efficacy. These include a decrease in heart wall thickness – enlarged walls are a sign of cardiomyopathy – and reduced levels of troponin I, a marker of heart damage.

“This is a fatal disease, but this is a potential therapy, and our goal is FDA-approval,” said Dr Ronald G. Crystal, the study’s lead author, professor and chair of the Department of Genetic Medicine at Weill Cornell Medicine and a pulmonologist at NewYork-Presbyterian/Weill Cornell Medical Center.

What is Friedreich Ataxia?

Friedreich ataxia is caused by variants in the FXN gene, leading to decreased levels of the FXN protein, which is essential for energy production in cells. “The two most energy consuming organs in the body are your brain and the heart, so the disease is primarily a brain and heart disease,” Dr Crystal said.

It is an autosomal recessive hereditary disorder, meaning a person must inherit a faulty copy of the FXN gene from both parents. As many as one in 50 000 people in the United States are diagnosed with the disease, according to some reports.

Nervous system symptoms typically begin in childhood and include problems with balance, walking and speaking. While neurologic disease is devastating for maintaining quality of life, most people with Friedreich ataxia develop heart disease, which is the cause of death in up to 65 percent of patients, according to reported estimates. Decreased FXN protein levels in the heart mean the heart cells don’t have the energy to beat normally. The muscle cells grow and the heart walls thicken, a condition known as hypertrophic cardiomyopathy, which can cause dangerous irregular heartbeats and heart failure.  

The US Food and Drug Administration has approved only one other drug, omaveloxolone, to treat Friedreich ataxia. It slows the neurological symptom progression but does not address the direct genetic cause of the disease.

A New Gene Therapy

Based on promising preclinical research, Dr Crystal and his colleagues studied the safety and efficacy of the FXN gene therapy in 17 patients with Friedreich ataxia cardiomyopathy.

“We put the healthy FXN gene in a virus, called adeno-associated virus, which is given intravenously and likes to travel to the heart,” he said.

The researchers pooled data from two independent studies: nine patients were from a Weill Cornell Medicine study, funded by National Heart Lung Blood Institute, and eight were treated in a study by Lexeo Therapeutics, a clinical stage genetic medicine company founded by Dr Crystal. Weill Cornell Medicine Enterprise Innovation, which aims to accelerate the translation of scientific discoveries into patient impact, played a crucial role in launching Lexeo in 2020 and later licensed to it additional technology to further support the clinical trial.

In both studies, the patients received a one-hour infusion of the gene therapy and were evaluated from six to 36 months. Three different doses were tested among three groups of patients.

Overall, the drug was safe, causing four serious adverse events, which were all resolved. Three of these were possibly related to prednisone, an immunosuppression drug that patients took so their bodies did not attack the gene therapy.

In the Lexeo study, researchers took biopsies of the heart before therapy and three months after therapy and found that frataxin protein levels increased in cardiac tissue in all eight patients. Researchers also found that the left ventricular mass index, which is an MRI measurement of heart wall thickness, decreased, demonstrating that the treatment was therapeutic for cardiomyopathy. 

Levels of troponin I, a structural protein of the heart that is released into the circulation when the heart is damaged, also decreased. Troponin I levels are typically high in patients with Friedreich ataxia cardiomyopathy. 

Using the modified Friedreich Ataxia Rating Scale (mFARS), which assesses balance, coordination, speech, and limb function in patients, the researchers found that some neurological components of the disease stabilised. “But we’re unsure whether this was related to the gene therapy reaching the skeletal muscle or the brain,” Dr. Crystal said. “That remains to be seen.”

Because most of the patients evaluated in this study had early cardiomyopathy, the researchers also hope to study the gene therapy in people who have a wider range of heart disease severity.

Source: Weill Cornell Medicine

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Trade Marks, Trust and the GLP-1 Surge

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The surge in demand for GLP-1 and GIP medicines—particularly those containing semaglutide and tirzepatide—has created significant commercial opportunity. It has also exposed a growing problem: the manufacture and sale of unregistered and potentially unlawful alternatives.

Recent enforcement action by the South African Health Products Regulatory Authority (SAHPRA) highlights the scale of the issue, particularly in relation to products marketed for weight loss (see SAHPRA and the SAPC Crack Down on Unlawful Manufacturing of Unregistered GLP-1/ GIP Medicines). While this is often viewed as a regulatory concern, it raises equally important questions for trade mark law.

Trade marks are traditionally seen as tools for distinguishing one trader’s goods from another’s. In the pharmaceutical sector, however, they do far more. They signal quality, safety, efficacy and regulatory legitimacy.

When those signals are misused, the consequences extend beyond commercial harm—they can directly affect public health.

More Than Molecules: Reputation as the Real Asset

The success of products such as OZEMPIC®, Wegovy® and MOUNJARO® is not driven by their active ingredients alone.

Through years of clinical research, regulatory scrutiny and market presence, these brands have accumulated significant reputational capital. Consumers are not simply looking for semaglutide or tirzepatide—they are looking for certainty.

Consumers want products backed by known standards of safety, tested efficacy and regulatory oversight.

In this context, the goodwill attached to a pharmaceutical trade mark reflects far more than brand recognition. It represents confidence in the entire lifecycle of the product—from development and approval to manufacture and distribution.

Reputation Laundering: Trading on Trust Without Earning It

In the current GLP-1 market, misuse of reputation does not always take the form of direct counterfeiting or even traditional trade mark infringement.

More often, products are marketed as alternatives, equivalents or substitutes for well-known medicines. Advertising often references established brands to attract consumer attention and to confer an aura of legitimacy on products that may not have undergone the same level of regulatory scrutiny.

This is where a more subtle form of exploitation emerges.

Even without reproducing a trade mark, these practices appropriate the trust associated with it. The result is what can aptly be described as reputation laundering, being the transfer of credibility from a trusted product to one that has not independently earned it.

From a trade mark perspective, the damage goes far beyond lost sales. It weakens the link between the brand and the qualities consumers expect from it.

The Consequences for Consumer Trust

The risks become most apparent when products fail to meet expectations- or worse, raise safety concerns.

If a consumer experiences harm after using a product marketed with reference to a well-known brand, the reputational fallout rarely remains confined to the seller. It can spill over to the genuine product.

This is what makes pharmaceutical trade marks unique. The goodwill they embody is inseparable from consumer trust in the safety and reliability of medicines.

Once that trust is compromised, the consequences extend beyond individual brand owners. They can influence patient behaviour, clinical decision and confidence in an entire class of treatments.

The Growing Union Between Regulatory Enforcement and Trade Mark Protection

Historically, regulatory compliance and trade mark enforcement have been treated as distinct legal disciplines. Increasingly, however, the two are becoming interconnected.

Regulatory authorities seek to protect consumers from unsafe or unapproved products. Trade mark owners seek to protect the reputation and goodwill associated with their brands. In many cases, these objectives are aligned.

SAHPRA’s recent focus on unregistered GLP-1 products illustrates this convergence. Both regulators and trade mark proprietors share an interest in ensuring that consumers are not misled regarding the nature, origin or reliability of pharmaceutical products.

As pharmaceutical brands continue to acquire substantial reputational capital, the distinction between consumer protection and brand protection becomes increasingly difficult to draw.

It is clear that pharmaceutical trade marks are no longer simply badges of origin. They have become proxies for trust. As the current GLP-1 market demonstrates, protecting that trust is not only a commercial imperative- it is increasingly a matter of public health.

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Abatacept Trumps Hydroxychloroquine in Cutting Risk of Rheumatoid Arthritis

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Rheumatoid arthritis. Credit: Scientific Animations CC4.0

A clinical trial led by researchers from Hospital Clínic de Barcelona, the August Pi i Sunyer Biomedical Research Institute (IDIBAPS) and the Institute of Advanced Chemistry of Catalonia (IQAC-CSIC) has compared the effectiveness of abatacept and hydroxychloroquine in preventing the development of rheumatoid arthritis in patients with palindromic rheumatism, an autoimmune disease that progresses to arthritis in approximately half of all patients. The trial was conducted over two years across 14 hospitals throughout Spain and involved 70 patients with palindromic rheumatism. The findings, published in Nature Medicine, indicate that abatacept is significantly more effective than hydroxychloroquine in preventing the onset of arthritis.

Palindromic rheumatism is characterised by intermittent episodes of joint inflammation, with acute flare-ups lasting a few days and resolving spontaneously. However, around half of patients eventually develop rheumatoid arthritis, a chronic disease that causes irreversible joint damage. This risk is particularly high in individuals with biomarkers such as rheumatoid factor and anti-citrullinated peptide antibodies. The presence of these two autoantibodies is used in the diagnosis of the disease.

Until now, in the absence of clinical trial evidence, the standard approach has been to treat patients with palindromic rheumatism using hydroxychloroquine, a drug with anti-inflammatory and immunosuppressive properties aimed at improving disease symptoms. In this context, the team led by Raimon Sanmartí, head of the Inflammatory Arthropathies Research Group at IDIBAPS, conducted a two-year clinical trial involving 70 patients with palindromic rheumatism. The objective was to compare the effectiveness of hydroxychloroquine with abatacept, a lymphocyte inhibitor – a type of white blood cell that attacks the joints after mistakenly identifying them as a threat – in reducing progression from palindromic rheumatism to rheumatoid arthritis

The results show that treatment with abatacept significantly reduces progression to rheumatoid arthritis. Only 20% of patients receiving abatacept developed arthritis, compared with 50% of those treated with hydroxychloroquine. Furthermore, patients treated with abatacept not only avoided progression to rheumatoid arthritis in most cases, but also experienced a significant improvement in palindromic rheumatism symptoms. “The study shows that patients treated with abatacept are more likely to achieve complete remission of attacks associated with acute pain and joint swelling, and that their inflammatory episodes are less severe,” explains Isabel Haro, Head of the Peptide Synthesis and Biomedical Applications Unit at IQAC-CSIC. The research team also highlights that both drugs proved safe and well tolerated throughout the trial.

Early intervention

“The results of this study indicate that we can intervene at an early stage to modify the natural course of the disease and reduce the risk of patients developing more severe and irreversible conditions,” says Sanmartí. “This opens the door to a paradigm shift in the treatment of these patients.”

The study, which involved several national research centres, also analysed the evolution of a number of biomarkers (autoantibodies) developed by the CSIC research group during patient follow-up. “Although no significant differences were observed between abatacept and hydroxychloroquine in terms of autoantibody responses, this work demonstrates the value of immunomodulatory approaches in the early stages of disease, when it is still possible to prevent progression to more severe and chronic forms,” notes Haro.

Source: Spanish National Research Council 

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Fish Oil Supplements May Not Prevent Alzheimer’s-related Decline

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New clinical trial results show supplements with omega-3s have no effect on memory or cognitive function in older adults at risk for Alzheimer’s disease

Photo by Aleksander Saks on Unsplash

Fish oil supplements are purported to have cognitive benefits from the omega-3 fatty acids they contain, essential nutrients that help form neuron connections. But a new Keck Medicine of USC study published in eBioMedicine suggests that increasing omega-3 levels via supplements has little effect on brain health despite showing evidence that the nutrients directly reach the brain. 

The two-year, placebo-controlled, double-blinded study of older adults with an elevated risk of developing Alzheimer’s showed that high doses of omega-3s did not improve memory, cognitive function or brain cell loss in areas of the brain related to Alzheimer’s. 

“We all wish there was a silver bullet for preventing Alzheimer’s, but our findings showed that fish oil supplements do not appear to protect brain health,” said Hussein Naji Yassine, MD, director of the USC Center for Personalized Brain Health and lead investigator of the study. “While omega-3s play an important role in forming brain cell connections needed for cognition, our results do not support fish oil supplements as a preventive measure against Alzheimer’s.” 

How the study was conducted 

Researchers recruited 365 adults, ages 55 to 80 who rarely ate fish, which is rich in omega-3s, and who study authors considered at risk for Alzheimer’s. About half (47%) carried an APOE4 gene, the strongest genetic risk factor for late-onset Alzheimer’s. Participants were randomly chosen to receive either daily fish oil supplements or a placebo. The supplements contained 2000mg of docosahexaenoic acid (DHA), a key omega-3 involved in brain function. 

Researchers were first interested to learn whether the omega-3 in the supplement was able to reach the brain.  

They measured DHA levels in cerebrospinal fluid, which surrounds the brain, and found an average 17% increase of DHA levels in patients’ brains after six months, confirming the omega-3 reached its intended target. 

Next, researchers tested participants’ memory and cognitive abilities at the beginning of the study and again two years later. Study participants who took DHA supplements did no better on the tests than those who took a placebo. Brain scans also showed that supplements did not prevent shrinkage of the hippocampus, a brain region important for memory that is often used as a marker of brain aging and Alzheimer’s risk. 

Looking beyond supplements 

Now, Yassine and his team are focused on solving why omega-3 supplements can reach the brain but not affect brain health. Based on their previous research, they believe omega-3s may work better as a part of a Mediterranean-style diet, which is naturally rich in omega-3s and linked with lower Alzheimer’s risk, than in a standalone supplement. 

“We’re focused on better understanding how the brain processes omega-3s and whether factors, such as poor health, dietary pattern, genetic risk and age, may change the brain’s ability to effectively absorb and use omega-3s,” said Yassine. “We are working to develop medications that may help the brain better utilise these nutrients to preserve cognitive function.”  

Holistic lifestyle remains the best prevention  

While out of scope of the study, the researchers stress that overall healthy living – rather than relying on fish oil supplements alone – is the best way to protect brain health.

“Staying healthy throughout life remains the most powerful tool we have for reducing Alzheimer’s risk, including regular exercise, quality sleep and a balanced diet,” said Yassine. “Living a healthy lifestyle is the brain’s equivalent of getting regular car maintenance and high-quality oil changes. The brain is more likely to lose greater function if health issues in other parts of the body go unaddressed, in the same way that car engines stop working if regular maintenance is skipped.”

Source: Keck Medicine of USC

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Early-onset Colorectal Cancer Risks Also Linked to Parental Characteristics

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Photo by LOGAN WEAVER | @LGNWVR on Unsplash

A recent study found that factors such as a person’s birthweight, sex, ethnicity, and father’s age may affect the risk of being diagnosed with colorectal cancer at a young age. The findings are published by Wiley online in CANCER, a peer-reviewed journal of the American Cancer Society.

In the study of 1,221 people born and diagnosed with early-onset colorectal cancer – defined as being diagnosed before age 50 – in California in 1988–2021 and 61 050 matched individuals without cancer, men had a 34% higher risk of early-onset colorectal cancer compared with women. Also, Hispanic ethnicity was linked with a 43% higher risk compared with white ethnicity. Having a foreign-born mother was associated with a 15% lower risk of early-onset colorectal cancer. Among females, every 500g increase in birthweight was associated with a 10% increase in early-onset colorectal cancer risk and having a father aged 35 years or older was associated with a 56% higher risk. Investigators did not observe any links between early-onset colorectal cancer risk and other demographic, birth, and parental characteristics.

Additional research is needed to uncover potential mechanisms behind these associations.

“Evaluating demographic, birth, and parental characteristics is important in understanding what’s causing the rising incidence of early-onset colorectal cancer,” said lead author Sunny Siddique, MPH, PhD, of the Yale School of Public Health. “Our findings warrant future studies aimed to understand the mechanisms through which factors such as male sex, Hispanic ethnicity, birthweight, maternal birthplace, and paternal age may influence risk of early onset colorectal cancer.”

Source: Wiley

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Discovery of 3 Severe Pneumonia Subtypes Could Lead to Tailored Treatments

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Photo by engin akyurt on Unsplash

Cambridge researchers have shown that severe pneumonia has three different subtypes, helping explain why some patients in intensive care units (ICUs) recover from their illness faster than others, while for other patients the disease can be life-threatening.

Their findings could in future help inform tailored treatments, allowing individual patients to receive the most appropriate therapies.

The current approach of classifying patients by their clinical syndromes without looking at the underlying biology risks missing what’s key

Andrew Conway Morris

Pneumonia is the commonest infectious cause of death worldwide, responsible for an estimated 2.5 million deaths per year. In severe cases, patients may need to be admitted to an ICU and given mechanical ventilation. Severe pneumonia accounts for six in 10 infections managed in intensive care, and spread of the infection within ICUs is a significant concern. 

Doctors have long struggled to understand why patients whose condition looks similar clinically can have very different recoveries. Some respond quickly to treatment, while others remain critically ill for weeks or even die.

Dr Andrew Conway Morris from the Department of Medicine at the University of Cambridge and an ICU consultant at Addenbrooke’s Hospital, Cambridge, said: “Even though we’re able to treat the initial infection, many patients with severe pneumonia still struggle to come off the ventilator and can develop lung failure. Therapies to tackle inflammation in the lungs have had mixed results in clinical trials – some suggest they are beneficial, others that they’re harmful. 

“The current approach of classifying patients by their clinical syndromes – sepsis, acute respiratory distress syndrome and so on – without looking at the underlying biology risks missing what’s key. Instead of asking ‘Does this patient have pneumonia?’, we should be asking ‘What’s the inflammatory pattern in this patient’s lungs?’”

In findings published today in Nature Communications, Professor Conway Morris and team recruited patients admitted with suspected severe pneumonia to the ICU at Addenbrooke’s Hospital, part of Cambridge University Hospitals NHS Foundation Trust.

Severe pneumonia is usually diagnosed through a combination of symptoms, imaging and blood tests. Symptoms typically include fever or hypothermia, low oxygen levels, breathing difficulties and confusion.

Instead of relying only on blood tests or scans, however, the Cambridge team analysed immune cells, inflammatory signals, and gene activity in fluid taken from the lungs of the patients. They discovered that there are three distinct biological types – or ‘pneumotypes’ – of severe pneumonia, none of which could be reliably detected using standard blood tests, even though they were strongly linked to how patients recovered.

The most common pneumotype – accounting for almost half (49%) of cases – was characterised by immune suppression, significant damage to the lining of the lungs, and bleeding in the alveoli (tiny air sacs within the lungs). There were fewer signs of inflammation, which may explain why treatments targeting inflammation can fail or even harm some patients. 

The second pneumotype – accounting for just under a quarter (23%) of cases – was characterised by a balanced immune response and active repair of damage to the lungs. Patients were most likely to recover faster from this pneumotype and require the shortest time on the ventilator, even though they initially looked just as ill as the others.

Patients with the most dangerous pneumotype – the one that most resembles ‘classic’ pneumonia – spent longest on mechanical ventilation and had prolonged critical illness. They had severe and persistent inflammation, with a flood of immature immune cells in the lung. This group may be most likely to respond to anti-inflammatory therapies, say the team.  

Dr Mark Jeffrey from the Department of Medicine at the University of Cambridge, the study’s first author, said: “Even though on the surface, all of the patients seemed to have similar types of pneumonia, with comparable illness severity, oxygen levels and clinical diagnoses, their outcomes were very different.

“It was only when we drilled down and looked at patterns of inflammation that the differences became apparent. Severe pneumonia is not a single disease, but several biologically distinct conditions that happen to look alike. This helps explain why ‘one-size-fits-all’ treatments – including some immune-modulating drugs – have often failed in clinical trials.”

The tests used to determine the pneumotypes are too complex to enable rapid classification, but the researchers hope to develop a simplified tool that could help them stratify the patients and ultimately offer tailored treatments.

Dr Vilas Navapurkar from the John Farman Intensive Care Unit at Addenbrooke’s Hospital said: “If we know which subtype of pneumonia an individual has, we can potentially tailor their treatment more precisely, boosting the immune response in some, while calming harmful inflammation in others. This has the potential to help critically ill patients, reduce deaths from pneumonia, shorten ICU stays and cut unnecessary antibiotic use.”

The study was funded by Addenbrooke’s Charitable Trust, the National Institute for Health and Care Research Cambridge Biomedical Research Centre, and The Forster Foundation. Professor Conway Morris is a Fellow at Emmanuel College, Cambridge.

Reference

Jeffrey, M et al. Pulmonary inflammation in severe pneumonia is characterised by compartmentalised and mechanistically distinct sub-phenotypes. Nat Comms; 23 Jun 2026; DOI: 10.1038/s41467-026-74190-x

Source: University of Cambridge

Categories : CancerTags : Leave a comment

Heroes in Purple Speedos Raise R1 200 000

On By ModernMedia

Hollard Daredevil Run Hands over Funds Raised and Launches 2026 Campaign

Hollard has donated R1 200 000 to the Cancer Association of South Africa (CANSA) and the Prostate Cancer Foundation, with every rand raised by the purple speedo-clad heroes who took part in the 2025 Daredevil Run. At the same event, the 2026 campaign was officially launched and South African men will be called upon to lace up, strip down and do it all again!

Seventeen years in and the Hollard Daredevil Run shows no signs of putting its trousers back on. Under this year’s tagline “Lekker Balls; Lekker Life”, the 2026 cheque handover and campaign launch took place today at Hollard Campus in Parktown, Johannesburg.

The R1.2 million raised in the 2025 Hollard Daredevil Run was formally handed over to CANSA and the Prostate Cancer Foundation (PCF) to fund awareness campaigns, Prostate-Specific Antigen (PSA) screening and patient support. “The Hollard Daredevil Run is an unforgettable experience that raises awareness in a fun, engaging manner and sparks dialogue about men’s health in a non-threatening way,” saysHazel Chimhandamba, Group Chief Marketing Officer at Hollard.

“In 2024, we raised R1 million, 100% of which went directly to supporting prostate and testicular cancer awareness programmes. We are incredibly grateful to every Daredevil who dared to run in a purple speedo. It takes a special kind of bravery to turn heads for something that truly matters. Because behind all the laughs is a very serious mission: getting more men to check in on their health and each other,” adds Hazel.

The stakes are real. Prostate cancer remains one of the leading causes of cancer-related deaths in South African men. One in eight men is expected to be diagnosed with prostate cancer in their lifetime, with Black African men facing a 60% higher risk than other population groups. South Africa’s mortality rate due to prostate cancer is particularly high, largely due to underscreening, sociocultural stigmas and lack of health education.

Testicular cancer, while less widespread, is most common in young men aged 15-49, affecting approximately 1 in every 250 males. When caught early, it is highly treatable. A two-minute self-examination can detect lumps, swelling, or changes early, that’s considerably less time than it takes to run 5km in a purple speedo and the payoff is just as big.

A simple Prostate Specific Antigen (PSA) blood test for men over 40 can detect elevated protein levels before a single symptom appears. “The Hollard Daredevil donation is the largest single donation the PCF receives each year,” says Andrew Oberholzer, CEO of the Prostate Cancer Foundation of South Africa. “The funds help PCF distribute accurate, multilingual educational material and keep free PSA screening programmes running nationwide.”

He goes on to say that the run has also contributed to the development of South Africa’s first comprehensive prostate cancer registry, launching in 2026, which will track incidence, treatment and outcomes. The campaign further funds PCF’s helpline and support networks for men and families navigating a diagnosis.

Lorraine Govender, National Manager: Health Programmes of CANSA states, “The Hollard Daredevil Run has become far more than a fundraising event – it’s helped build a national movement that encourages men to speak openly about their health and seek help sooner. We are incredibly grateful to Hollard and every participant whose courage and commitment enable CANSA to continue providing awareness, early detection, screening and support services to men across South Africa.”

The event returns to Zoo Lake in Johannesburg on Friday, 23 October at 3pm with participants elsewhere able to register and run in their own neighbourhoods, workplaces, schools or universities anywhere in the country.

Registrations for the 2026 Hollard Daredevil Run open from 1 July and tickets will be available from Ticketpro at R200, which includes the courier of a registration pack and a complimentary purple speedo.

For more information, go to www.hollard.co.za/daredevilrun.