Category: Cancer

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Epstein–Barr Virus Influences Rare Brain Lymphomas

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Primary CNS lymphomas in immunocompromised patients are among the rarest and at the same time most aggressive cancers – yet evidence-based recommendations for diagnosis and treatment have been lacking. An international research team led by Heidelberg Faculty of Medicine at Heidelberg University and the German Cancer Research Center has now identified characteristic imaging features of these tumours and developed a prognostic model to better assess disease outcomes. The researchers found that tumours positive for Epstein-Barr virus were associated with particularly poor prognosis. The findings, published in the journal Blood, may help guide future diagnostic and treatment strategies.

Primary CNS lymphoma is a rare cancer that arises from malignant white blood cells. Affected individuals develop tumours in the brain and, more rarely in the spinal cord, the eyes, or within the cerebrospinal fluid. These lymphomas can occur in people with weakened immune systems, for example after organ transplantation, in autoimmune diseases, or in association with HIV infection. This subtype, known as immunodeficiency-associated primary CNS lymphoma (ID-PCNSL) affects approximately 50 people per year in Germany. Researchers at the Heidelberg Faculty of Medicine at Heidelberg University had already shown in earlier work that ID-PCNSL is not simply a variant of classical CNS lymphoma, but a distinct disease entity characterised by specific genetic alterations.

A recent study by the International Primary CNS Lymphoma Collaborative Group – an international network dedicated to the study of CNS lymphomas – has now provided further insights into the diagnosis and treatment of ID-PCNSL. Including data from 308 patients treated at 23 hospitals across seven countries, the study is the largest conducted to date on this rare cancer. The researchers analysed clinical findings, magnetic resonance imaging scans, and tumour tissue samples. Scientists from the Heidelberg Faculty of Medicine at Heidelberg University and the German Cancer Research Center (DKFZ) played a leading role in the study.

Epstein-Barr Virus influences imaging and prognosis

Epstein-Barr virus (EBV) is known to play a central role in this cancer and was detected in 79.2 percent of the tumours examined. “Our analyses show that EBV-positive tumours often follow a more aggressive course and are associated with an unfavourable prognosis,” says first author Dr Leon Kaulen. He conducts research at the Heidelberg Faculty of Medicine at Heidelberg University and at the DKFZ and is a physician at the Department of Neurology at Heidelberg University Hospital (UKHD). EBV-positive tumours also showed characteristic imaging features including different patterns of contrast enhancement compared with EBV-negative tumours.

The researchers developed a prognostic model based on three factors that can help to better predict the course of ID-PCNSL and patient survival more accurately. The three identified factors are the detection of EBV in tumour tissue, age, and the patient’s performance status. Depending on the combination of these three factors, disease courses differed markedly among the patients studied. If only one of the three risk factors was present, the median survival was 135 months. With two risk factors, it decreased to 29 months. If all three factors were present, median survival was reduced to three months. “The prognostic model, with its clear stratification, represents a major advance. It will enable us to assess patients much more precisely in the future and to tailor therapies more effectively to the individual clinical situation,” says senior author Professor Wolfgang Wick, Heidelberg Faculty of Medicine at Heidelberg University, Chair of the Department of Neurology at UKHD, and Head of the Clinical Cooperation Unit Neurooncology at DKFZ and UKHD.

Considering immunodeficiency and cancer together

So far, no standardised therapy has been established for patients with immunodeficiency-associated primary CNS lymphoma. “Our research provides important insights into which approaches may be associated with more favourable outcomes,” says Dr Leon Kaulen. Patients whose immune system could at least partially be reconstituted – for example through adjustment of immunosuppressive medication or effective treatment of HIV infection – and who additionally received combination chemotherapy with rituximab and methotrexate typically (85 percent) responded well to treatment. In a substantial proportion of patients, the disease also remained stable in the long term and became undetectable.“ Our data suggest that the interplay between the tumour and the weakened immune system plays a central role,” says Dr Kaulen. “Both aspects should therefore be addressed together in treatment.”

“With the current study, a robust evidence base for this rare disease is now available for the first time,” summarises Professor Wick. “This represents an important step toward precision medicine even in rare diseases. Relevant research in rare tumour entities can often only be carried out in large international consortia. International scientific collaboration therefore deserves particular attention.”

Source: Heidelberg University

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Faster Aging in Younger Generations Linked to Rise in Early-onset Cancer

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Immune system aging linked to earlier lung cancer; adipose tissue aging linked to earlier colorectal cancer

Photo by Malvestida on Unsplash

Cancer is often considered a disease of aging. Older adults are at higher risk because they have had more time to accumulate cellular damage that can trigger tumour formation. But as cancer rates in younger adults rise, with each successive generation facing higher risks than the one before it, researchers are asking whether cellular damage is accumulating faster in recent generations, accelerating their body’s biological aging.

A new study led by researchers at Washington University School of Medicine in St. Louis provides evidence that younger generations are indeed aging faster biologically than their older counterparts. The causes remain under investigation around the world, including global efforts led by research members of Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine, and Cancer Grand Challenges, a global initiative co-founded by the National Cancer Institute and Cancer Research U.K.; but importantly, the new research links this accelerated aging to an increased risk of early-onset cancers in younger generations. In general, early-onset cancers are those diagnosed at age 55 or younger.

The larger the gap between biological age — that is, how old our bodies appear to be — and chronological age — which is how many years we have actually lived — the higher the cancer risk, according to the researchers. They found that people in more recent birth cohorts had larger age gaps than those in older birth cohorts, which may help explain the rise in early-onset cancer in recent generations.

Their study also identified links between faster aging in particular organ systems and increased risks for certain cancers. For instance, an immune system that appears older than its actual age was associated with early-onset lung cancer. Similarly, fat tissue that appears older than its chronological age was associated with early-onset colorectal cancer.

The study, published June 22 in the journal Nature Medicine, suggests that measures of accelerated aging could help identify individuals at higher risk of early-onset cancer and guide new strategies for cancer prevention and early detection.

“Our ultimate goal is to decode how modern environments become biologically embedded to drive cancer risk, transforming prevention from broad recommendations to personalised interventions,” said Yin Cao, ScD, a molecular epidemiologist and an associate professor of surgery and of medicine at WashU Medicine. “This brings us closer to identifying risk earlier and developing prevention strategies that are tailored to an individual’s biology.”

Exploring biological aging

Cao’s team has been at the forefront of identifying individual factors that influence cancer risk across the life course, such as obesity, metabolic dysregulation, alcohol consumption, sedentary behaviour, poor diet quality and caesarean delivery. Although these discoveries have revealed important clues to the origins of cancer at younger ages, the contribution of any single factor is modest.

With that in mind, Cao, also a research member of Siteman, and her colleagues have sought ways to capture the influence of multiple risk factors operating together to spur cancer development. With support from Cancer Grand Challenges, Cao, as co-lead of Team PROSPECT, has been able to go after this problem.

For the current study, Cao’s team analysed data from more than 154,000 young adults in the UK Biobank, a large biomedical dataset containing biological, health and lifestyle data, and from more than 10,000 individuals in the U.S. participating in the National Institutes of Health’s (NIH) All of Us Research Program, an effort to build a comprehensive health dataset on more than 1 million people living in the U.S.

To estimate the level of biological aging — or age gap — the researchers, including first author Ruiyi Tian, a doctoral student in the Cao lab, examined aging at two levels: across the body as a whole, known as systemic aging, and within individual organs, known as organ-specific aging. For systemic aging, the researchers used established measures, including clinical biomarker-based measures such as PhenoAge and the Klemera-Doubal Method, as well as a metabolomic age score, which provides a measure of individual metabolism.

PhenoAge, for example, measures nine blood biochemistry markers such as albumin, made by the liver, and creatinine, a waste product removed by the kidneys. For organ-specific aging, the researchers used blood proteomic data, which measure levels of multiple proteins linked to specific organ systems, to estimate biological aging in individual organs.

The researchers calculated the average age gap for each birth cohort and used standard deviation to describe how much each group differed from the study average. Standard deviation is a measure of how spread out data points are around the average.

The researchers found that individuals in the UK born between 1965 and 1974 had systemic aging that was 23% of one standard deviation higher compared with those born between 1950 and 1954, after accounting for chronological age. In other words, people in the younger birth cohort showed a modest shift toward older biological profiles than people in the older birth cohort when at the same chronological age.

The researchers observed a similar pattern in the U.S cohort. Participants born between 1990 and 1999 had systemic aging that was 92% of one standard deviation higher compared with those born between 1965 and 1969.

This increased systemic aging in the younger group was associated with an 8% increased risk of early-onset solid cancers, especially lung, gastrointestinal and uterine cancers. When participants were divided into three groups based on their level of systemic aging, those with the most advanced systemic aging had a 15% increased risk of early-onset solid cancer compared with those with the least advanced systemic aging. According to the analysis, the increased risk persisted even after controlling for inherited genetic risks of cancer and genetic susceptibility to accelerated aging.

By zooming into organ-specific aging, the researchers found that advanced immune system aging was associated with increased risk of early-onset lung cancer, and advanced adipose (fat) tissue aging was associated with increased risk of early-onset colorectal cancer.

“If we can identify younger people with the highest cancer risk when they are still healthy, we can focus on prevention and early-detection strategies for the individuals who will benefit most from early interventions,” Cao said.

By Julia Evangelou Strait

Source: WashU Medicine

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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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Heroes in Purple Speedos Raise R1 200 000

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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.

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Huge Genetic Study of ‘Moliness’ Helps Unravel Mysteries of Melanoma

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Photo by Bermix Studio on Unsplash

QIMR Berghofer scientists have uncovered hundreds of genes that play a role in the growth of both moles and melanoma, in a discovery that could lead to new ways of preventing and treating the deadliest form of skin cancer.

The world’s largest genetics study of ‘moliness’, published in Nature Communications, is unravelling the complex causes of both moles and melanomas that are not related to well-known risks caused by sun exposure, skin colour, and pigmentation.

The team found risk genes linked to biological pathways that could lead to the development of a mole or melanoma. These include an immune response pathway that may be failing to control cell growth, and genes implicated in harmful cell proliferation in other types of cancer, such as breast cancer, prostate, and brain cancers.

Working out how to stop these risk pathways could lead to new melanoma drug targets and prevention strategies that go beyond sun protection.

Watch the video here

Associate Professor Matthew Law, Team Head of QIMR Berghofer’s Genetics and Skin Cancer Lab, said research has made massive inroads but Australia still has the world’s highest incidence of melanoma. Around 1400 Australians lose their lives to the complex disease each year.

“We know how to reduce sun exposure and risk through SunSmart behaviours, and new immunotherapies have greatly improved survival rates. But people still get melanoma and people still die from melanoma,” A/Prof Law said.

“Existing immunotherapies fail to work for half of all patients with late-stage melanoma, so we need to find other ways to target the disease. By studying moles, we’re learning more about the biology of melanoma so we can find new ways of controlling it.”

Moles and melanomas share the same cellular origin, forming from a pigment-producing cell called a melanocyte that gives skin its colour. In moles, the cell multiplies to form a cluster then stops growing, leaving a harmless spot. In melanoma, the cell growth continues aggressively.

Moliness is strongly influenced by your genes and having a high mole count is a major risk factor for melanoma. Around a third of melanomas develop from a mole. 

The QIMR Berghofer research analysed data from more than 85000 participants of European ancestry discovering 24 new genetic regions that determine the number of moles someone has. This is a five-fold increase on the five areas found in an earlier 2018 study also led by QIMR Berghofer researchers.

All but one of the genetic regions for mole count also play a role in melanoma. The team pinpointed more than 250 key genes in these regions to prioritise for further research.

One of the new genes, SIKE1, regulates immune responses to viral infections. The researchers think it could enable the development of melanomas by malfunctioning and affecting the immune system’s ability to detect and destroy melanocytes that are multiplying abnormally. This could be a promising target for a potential immunotherapy that could possibly prevent early stage melanoma growth.

Lead author Shanika Jayasinghe from QIMR Berghofer said the study builds on decades of world-leading skin cancer research at the Institute which has been involved in every major study of the genetics of moles and melanomas from twin studies to large-scale genome-wide research.

“I’m really proud to be continuing this long legacy of research. Our study increases understanding of why some people have a lot of moles and why some people develop melanoma so we can better treat and prevent this skin cancer,” Ms Jayasinghe said.

The researchers used the study insights to create a Polygenic Risk Score (PRS) for moliness to predict those who are genetically more likely to have a large number of moles, which could be integrated into melanoma screening tools in future to improve their accuracy in finding those at high risk so they can receive extra monitoring.

The next step is to analyse even larger data sets to find more genetic regions involved in moliness and melanoma. The researchers are also searching for existing drugs that could potentially target the newly identified biological pathways.

The scientists are grateful for the contribution of the many patients who participated in the 13 studies that were analysed for this project, including QIMR Berghofer’s QSkin Sun and Health Study and the Australian Genetics of Depression Study.

The study is available in Nature Communications with DOI 10.1038/s41467-026-70368-5.

Source: QIMR Berghofer

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A New Oral Combo Drug for AML Eases Treatment Burden

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Photo by Kampus Production

The ASCERTAIN V clinical trial demonstrated that an all-oral drug combination for older patients with acute myeloid leukaemia (AML) is an effective alternative to the current standard, which requires repeated hospital or office visits for intravenous treatment. In the international phase 1/phase 2 trial, patients took a regimen of two pills, decitabine-cedazuridine and venetoclax, with strong response rates and survival outcomes. The study results were published in the New England Journal of Medicine.

Nearly half of patients (46.5%) achieved complete response, while 63% experienced either complete response or complete response with incomplete haematologic recovery, meaning cancer cells were undetectable, but the patient’s healthy blood cell counts had not yet returned to normal. The median overall survival reached 15.5 months – comparable to existing intravenous therapies.

The oral combination of decitabine-cedazuridine and venetoclax received U.S. Food and Drug Administration approval on May 13 for the treatment of AML in newly diagnosed adults 75 years or older and patients clinically unable to undergo traditional, intensive chemotherapy.

“Having received approval, we anticipate that this oral AML regimen will become the standard of care for patients who are older or more frail,” said lead author Dr Gail J. Roboz, professor of medicine and director of the Clinical and Translational Leukemia Program at Weill Cornell and a haematologist oncologist at NewYork-Presbyterian/Weill Cornell Medical Center. “We hope these results point to a future for AML patients where the treatment journey is less disruptive and less burdensome without sacrificing outcomes.”

Turning a Standard into an Oral Treatment

AML is an aggressive blood cancer that can be diagnosed at any age and is especially difficult to treat in older adults and patients with other serious health conditions. For these individuals, the current standard treatment combines venetoclax with a class of drugs known as hypomethylating agents, such as decitabine. Venetoclax inhibits Bcl-2, a protein that leukaemia cells overproduce to avoid cell death, while hypomethylating agents restore the activity of genes involved in cell growth and survival, helping slow leukaemia progression.

However, this regimen requires monthly treatment cycles that combine oral venetoclax with five to seven days of an injectable hypomethylating agent delivered in a clinic or hospital. These frequent visits create significant physical, logistical and emotional challenges for patients and families.

More recently, pharmacologists developed a pill version of decitabine by pairing it with another drug called cedazuridine that prevents decitabine from being broken down when ingested.

With the ASCERTAIN V trial, Dr Roboz and her colleagues tested whether decitabine’s oral version, combined with venetoclax, could match the efficacy of intravenous AML treatment.  

The nonrandomised phase 1/phase 2 study enrolled 189 newly diagnosed AML patients at centres across the United States, Canada and Spain. The patients took a month of venetoclax, along with five days of decitabine-cedazuridine at the start of each treatment cycle.

The oral regimen demonstrated a safety profile consistent with what doctors already expect from standard AML therapies, which commonly deplete healthy blood cells alongside leukaemia cells. The most common serious side effects included anaemia, neutropenia and fever associated with low white blood cell numbers.

Tailoring Treatment to Reduce Side Effects

During the trial, researchers also investigated how to fine-tune the treatment schedule to optimise leukaemia control, while minimising side effects related to low blood counts.

The paper offers recommendations for physicians, including careful monitoring of leukaemia cells until they reach a certain threshold and then strategically pausing venetoclax to allow the body to replenish normal white blood cells, red blood cells and platelets.

“The goal of the all-oral therapy is to keep people out of the hospital, especially once they have achieved remission,” said Dr Roboz, who is also a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell. “Patients are thrilled not to have to deal with monthly chemotherapy injections or infusions.”

Looking Ahead

For now, most patients taking the oral regimen must continue treatment to maintain remission, much like a chronic condition. “AML patients taking ongoing cycles of treatment require close monitoring but can still have an excellent quality of life,” Dr Roboz said.

In the future, the researchers hope that increasingly sensitive blood monitoring tests may identify when patients can safely stop treatment.

Dr Roboz and AML researchers worldwide are also exploring “triplet therapies,” which add additional targeted drugs to the decitabine-cedazuridine and venetoclax combination.

“The goal is to get away from treatment cycles that go on indefinitely,” said Dr Roboz. “We want to drive the leukaemic cells to such low levels that patients can discontinue therapy and be cured.”

Source: Weill Cornell Medicine

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Which Genes Contribute to Early-onset Breast Cancer in Black Women?

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Photo by National Cancer Institute

Black women experience disproportionately elevated risks of developing and dying from early-onset breast cancer. New research published by Wiley online in CANCER, a peer-reviewed journal of the American Cancer Society, reveals the genes that are most likely to be mutated to contribute to these increased risks.

In the study of 686 young Black women diagnosed in Florida and Tennessee with invasive breast cancer at age 50 or younger in 2005–2018, genetic testing showed that 15.3% of the women carried a gene variant with a suspected link to breast and/or ovarian cancer, with most occurring in the BRCA1 and BRCA2 genes and fewer in PALB2, ATM, and other genes. A family history of breast cancer was common in women with mutations in BRCA1, BRCA2, and PALB2. Triple-negative breast cancers (one of the most aggressive forms) were most often seen in women with BRCA1 mutations. Also, most of the women with BRCA1 mutations were diagnosed at or below age 40, whereas the age at diagnosis was more evenly distributed up to age 50 for women with variants in the other genes.

The study’s findings point to the importance of breast cancer genetic testing for young Black women, a group that is less likely to receive such screening compared with other racial and ethnic groups. Such tests could identify women most likely to benefit from more frequent screening and preventive measures to safeguard their health.

“We must test at-risk women across all populations – testing is essential to personalise treatment strategies and enable life-saving prevention for future cancers, and it may empower at-risk family members to get tested so they too can benefit from this information,” said senior author Tuya Pal, MD, of Vanderbilt University Medical Center. “Equitable access to inherited cancer testing ensures that all women, regardless of race, can benefit from precision medicine and take control of their genetic health.”

Source: Wiley

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Urine Test Could Help Detect Lung Cancer Years Before Symptoms Occur

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Urine samples. Credit: Cancer Research UK CC-BY4.0

Cambridge scientists hunting tell-tale killer ‘zombie’ cells that signal early lung cancer have developed a world-first urine test that could transform diagnosis and survival for thousands of patients.

[The test] could one day be used easily in GP surgeries and hospitals to help detect recurrence in this hard-to-treat cancer much earlier.

Ljiljana Fruk

As published this week in Nature Aging, the team has shown that this simple and affordable test could detect the earliest signs of lung cancer months, or even years, before symptoms appear, as well as monitor whether treatment is working and identify potential relapse.

 It works by identifying the presence of senescent cells in the lungs – so called ’zombie cells’ – that stop dividing but linger and release abnormal inflammatory signals that damage surrounding tissue and help create an environment that lowers the body’s ability to fight the cancer.

The study, funded by Cancer Research UK, marks a major leap towards more precise therapy and a test for early cancer and treatment efficiency that could be rolled out across the NHS one day.

Lung cancer is the UK’s most common cause of cancer death taking the lives of around 32,800 people every year. Thanks to huge strides in prevention, detection and treatment, in the UK, lung cancer has seen a 22% reduction in death rates in the last decade. And around two in three people (65%) with lung cancer in England survive their disease for five years or more when diagnosed at the earliest stage. But when diagnosed at the latest stage, this falls to 5 in 100 (5%).

This new test could save and improve thousands more lives in the future.  

The researchers created an injectable sensor that interacts with proteins released by senescent cells. When these proteins are present, the sensor triggers the release of a detectable compound that appears in urine – signalling the earliest biological signs of therapy resistance and lung cancer development.

The researchers say that early identification is critical to saving more lives, as the disease often relapses silently with few or no symptoms until it has already spread. By detecting signs of lung cancer development and therapy resistance early, their simple urine test can spot lung cancer and treatment resistance early, helping doctors to tailor and adapt the treatment to the patient and start that treatment earlier when it works best.

The team confirmed their results using real patient samples and large genetic datasets.

Professor Ljiljana Fruk, from the Department of Chemical Engineering and Biotechnology at Cambridge, said: “The sensor has not yet been tested in humans, next is the clinical trials and it is likely it will take few years to bring it to patients, but it is a first big step and it could one day used easily in GP surgeries and hospitals to help detect recurrence in this hard-to-treat cancer much earlier.”

Nearly half (46%) of lung cancers in England are diagnosed at the latest stage.

Professor Daniel Munoz-Espin from the Early Cancer Institute and co-lead for the Cancer Research UK Cambridge Centre Thoracic Cancer Programme, said: “Our previous studies showed that senescent cells in response to chemotherapy can cause treatment resistance and an aggressive lung cancer relapse. We also found that senescent immune system cells promote lung cancer development by causing immunosuppression.

“Our urine nano sensor may allow primary care detection of therapy resistance and lung cancer early development in future clinical settings.”

Professor Robert Rintoul of the Department of Oncology, and co-lead for the Cancer Research UK Cambridge Centre Thoracic Cancer Programme said: “Novel approaches for lung cancer detection and response to treatment are urgently needed to improve patient outcomes. This work forms the basis for testing within clinical trials with a view to future use in the clinic.”

Cancer Research UK’s spokesperson for the East of England, Patrick Keely, said: “With new technologies opening doors to new discoveries, we’re living in a golden age of research, which is powerfully underlined by this innovative new urine test to detect early lung cancer.” 

Adapted from a press release from Cancer Research UK

Reference

Hartono, M et al. Urinary detection of therapy-induced senescence and fibrosis using an injectable albumin-based nanoprobe. Nature Aging; 13 May 2026; DOI: s43587-026-01116-z

Republished from the University of Cambridge under a Creative Commons licence.

Read the original article.

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Irradiation May Help CAR-T Cell Therapy Work Better Against Solid Tumours

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New study shows focused irradiation helps immune cells keep cancer-fighting CAR T cells active and contained inside tumours

CAR-T cells (brown, arrowheads) infiltrating solid tumours. Left: unirradiated (0 Gy). Right: after focal irradiation (8 Gy).

Researchers from the Icahn School of Medicine at Mount Sinai have discovered a promising new way to improve CAR-T cell therapy for solid tumours such as lung cancer and melanoma. The study, published in Nature Cancer, found that focused irradiation, a targeted therapy that delivers high-energy beams to stun rapidly growing cells such as cancer, can help CAR-T cells survive longer and work more effectively inside tumours. 

CAR-T cell therapy involves removing the patient’s T cells (a type of immune cell), reprogramming them in the lab to fight cancer, and then infusing them back into the patient. It has transformed treatment for some blood cancers, but has not worked as well for solid tumours such as lung cancer and melanoma. Patients with solid tumours typically have bulky, treatment-resistant disease, and one of the central reasons CAR-T cells fail in this setting is that they do not persist or expand at the tumour long enough to eliminate it. Even when CAR-T cells initially reach the tumour, their numbers dwindle before they can finish the job. 

The research team discovered that tumour irradiation does something unexpected: it turns dendritic cells, the immune system’s most powerful antigen-presenting cells, into a local source of stimulation for CAR-T cells inside the tumour.  

In mouse models of advanced lung cancer and melanoma, irradiation promoted dendritic cells to capture intact tumour surface proteins and display them on their own membranes, a process called “antigen dressing.” These antigen-dressed dendritic cells then engaged the chimeric receptor on the CAR-T cells – the laboratory-engineered protein that gives these cells the ability to target specific proteins – keeping them alive and multiplying within the tumour over several weeks.  

The result was durable control of advanced lung tumors that CAR-T cells alone could not eliminate.  

“This study shows that irradiation can do more than kill cancer cells; it can enhance cell therapy,” said corresponding author Jalal Ahmed, MD, PhD, who led the study and is Assistant Professor of Immunology and Immunotherapy, and Radiation Oncology, at the Icahn School of Medicine at Mount Sinai. “We found that dendritic cells can dress themselves in tumor proteins and use them to directly expand CAR-T cells through the engineered receptor. This was completely unexpected – dendritic cells normally engage T cells through an entirely different mechanism.” 

A second finding addresses one of the most pressing safety challenges in the field. The researchers found that the CAR-T cell response stayed largely confined to the irradiated tumour. CAR-T cells expanded within the tumour but did not become more active in nearby healthy tissues, even when those tissues expressed the same protein targeted by the CAR-T cells. On-target activity against healthy organs has been one of the most serious safety barriers in solid tumour CAR-T cell therapy and has led to the termination of clinical trials. By selectively concentrating CAR-T cell activity at the tumour, focused irradiation may allow treatment of advanced tumours at lower and safer CAR-T cell doses.  

“What is striking is that irradiation does not just amplify the immune response – it tells the immune system where to act,” said study co-author Miriam Merad, MD, PhD, Robin Chemers Neustein Professor of Immunology and Chair of Immunology and Immunotherapy at the Icahn School of Medicine at Mount Sinai. “Confining CAR-T cell expansion to the tumour could open up a new generation of safer cell therapies for solid cancers.” 

This approach is particularly relevant for patients with metastatic solid tumours, who currently have few options. The irradiation treatment used in the study is available in cancer care centres around the world. This means the strategy could be tested in clinical trials without requiring new equipment, new drugs, or new infrastructure.  

“This work suggests that preparing the tumour environment is important to optimise the efficacy of CAR-T cells,” said study co-author Michel Sadelain, MD, PhD, who was previously at Memorial Sloan Kettering Cancer Center and is currently the founding director of Columbia University’s Institute for Cell Engineering and Therapy. “Irradiation may provide a practical way to help CAR-T cells succeed in solid tumours.” 

The researchers caution that the findings are still preclinical and must be tested in human clinical trials. The team is now working to define the molecular mechanism of antigen dressing, identify the signals dendritic cells use to sustain CAR-T cells, and translate the approach into trials for patients with advanced solid tumours. 

Source: Mount Sinai

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56% of New SA Stem Cell Donors Are Under 25 and Saving Lives

On By ModernMedia
Photo by Elizeu Dias on Unsplash

More than half of all new stem cell donors registered in South Africa in 2025 were between the ages of 17 and 25. And, according to a growing body of medical research, they are also the most valuable donors on the planet.

Research analysing more than 10 000 stem cell transplants has found that for every ten-year increase in donor age, patient survival rates two years after transplant decline by approximately 6 to 7%. Donors aged 17 to 25 consistently provide patients with the best chance of survival. A separate long-term study found that transplants from younger donors successfully engrafted up to 30 000 stem cells that continued contributing to blood production for decades, compared to a tenfold decrease in transplants from older donors. It has also been confirmed that donor age has a greater influence on transplant success than previously assumed, with younger donors associated with improved overall survival and reduced relapse risk.

The evidence is bearing out in South Africa’s own numbers. DKMS Africa’s donor base has grown from 18 801 in 2021 to more than 173 000 by the end of 2025, a ninefold increase in four years. New sign-ups in 2025 alone reached more than 60 000, nearly double the 2023 figure. The 17 to 25 age group has led that charge, growing from 19% of new donors in 2021 to 56% in 2025. Forty percent of last year’s new donors were between 17 and 21.

Context matters: every hour, someone in South Africa is diagnosed with blood cancer. For many patients, a stem cell transplant from a matched, unrelated donor is the only viable path to survival. The match they need may already be on the registry. Or it may not exist yet.

“In South Africa, finding a compatible donor depends on human leukocyte antigen (HLA) characteristics that are inherited and vary significantly across ethnic groups. Patients have the highest probability of finding a match within a registry that reflects their own background. Currently, patients from black, coloured and Indian communities face considerably lower odds than those from communities better represented in local and international registries. A registry that grows without also diversifying fails the patients who need it most. That is why more young people of diverse backgrounds need to step forward and close this gap,” says Palesa Mokomele, Head of Community Engagement and Communications at DKMS Africa.

She adds, “This Youth Month, we need every young person who has not yet registered to know that their moment is now, and every adult who has not yet registered to ask themselves honestly: what is my excuse?”

The registration process takes minutes: a free swab kit arrives by post, is completed at home, and returned. No blood is drawn. No appointment is made. A registered donor is only contacted if they prove to be a genetic match for a patient in need, and even then, the decision to proceed remains entirely theirs. Registering is the first step. Following through, if called upon, is the one that saves a life.

To register, visit www.dkms-africa.org.