Category: Cancer

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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

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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.

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Asymptomatic Bladder Cancer Could be Unmasked by Taking Aspirin

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Photo by cottonbro studio

Haematuria, the presence of blood cells in urine, is a sign of bladder cancer. Because aspirin blocks platelets from forming harmful blood clots, the medication can cause mild bleeding or worsen existing bleeding in the urinary tract. Results from a study in the Journal of Internal Medicine suggest that this may prompt a clinician to run tests that uncover an asymptomatic bladder tumour.

For the study, investigators analysed information on 50 771 Danish adults who started taking aspirin in 2005–2023, as well as 156 191 who started non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs), which have less pronounced antiplatelet abilities than aspirin.

Compared with adults from the general population who have never used aspirin or NSAIDs, aspirin initiators received more cystoscopies – minimally invasive procedures that allow a doctor to view the inside of the bladder and urethra with a lighted tube equipped with a camera. Cytoscopy results showed that recent aspirin initiators had a similar bladder cancer prevalence, but a lower prevalence of invasive stage compared with never-users. This suggests that individuals initiating aspirin treatment represent a patient population with a higher incidence of bladder cancer, and that their higher cystoscopy rate reflects this and thus is clinically warranted. The combination of a larger proportion of relevant cystoscopies and a lower prevalence of invasive cancer stage at diagnosis may represent unmasking of otherwise asymptomatic bladder cancer.

NSAID initiators received more cystoscopies than never-users, but they had a lower bladder cancer prevalence after cystoscopy and a similar stage distribution as never-users. This suggests that the higher cystoscopy rate may not have been clinically warranted.

“We are very encouraged by these results. In the clinical setting, they underline the importance of acting on suspicious bladder cancer symptoms among aspirin initiators,” said lead author Malene Söth Hansen, MD, of Aarhus University. “The findings may further have implications for the question of whether aspirin can prevent bladder cancer, as detection in trials with short-term follow-up may appear as a higher incidence in the aspirin-exposed cohort.”

Source: Wiley

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Breakthrough Drug Nearly Doubles Survival with Advanced Pancreatic Cancer

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– an Oncologist Explains how Daraxonrasib Overcame an ‘Undruggable’ Disease

Pancreatic cancer. Credit: Scientific Animations CC BY-SA 4.0

Christopher Lieu, University of Colorado Anschutz

For a long time, the likelihood of surviving pancreatic cancer has been extremely low. For patients who were diagnosed with metastatic pancreatic cancer between 2015 and 2021, about 97% died within five years of their diagnosis.

Pancreatic cancer is so deadly in part because there are no effective screening tests, and it rarely causes noticeable symptoms in its earliest stages. By the time a patient experiences signs, such as jaundice – a yellowing of the skin – or abdominal pain, the cancer has often already spread to other organs.

As a gastrointestinal oncologist and researcher specialising in early-phase clinical trials, I have seen the critical need for more effective therapies for patients with pancreatic cancer. For decades, successfully targeting the central mechanism that causes the vast majority of pancreatic cancers was considered impossible.

However, that narrative is rapidly changing with a new drug that can shut down the key protein that drives pancreatic cancer, nearly doubling survival rates for patients with advanced stages of the disease.

‘Undruggable’ tumours

The standard treatment for advanced pancreatic cancer has historically relied on chemotherapy, potent drugs designed to kill rapidly dividing cells. While chemotherapy can slow the progression of the disease, its effectiveness is often limited by the ability of pancreatic cancer cells to develop resistance against these drugs.

Model of the 3D structure of KRAS, resembling a rough-looking blob with a molecule tucked inside
KRAS (blue) has been difficult for drugs to target. Fvasconcellos/Wikimedia Commons

Pancreatic cancer’s success lies in its genetics. More than 90% of pancreatic tumours are driven by mutations in a gene called KRAS. This gene codes for proteins that function as switches that turn cell growth on and off. When the KRAS gene is mutated, the switch becomes permanently stuck in the “on” position, commanding cancer cells to multiply endlessly.

For decades, scientists considered KRAS to be “undruggable.” The surface of the protein is exceptionally smooth, lacking the molecular pockets that standard drugs require to bind to and turn the switch off.

Because existing drugs haven’t been able to target this protein, treatment for pancreatic cancer has primarily relied on toxic drugs that act more like blunt instruments than precise tools. Chemotherapy attempts to control the disease through widespread cell destruction, causing significant collateral damage to healthy tissues that lead to side effects.

What is daraxonrasib?

A new drug called daraxonrasib offers a critical advance in treating metastatic pancreatic cancer.

Daraxonrasib is taken daily by mouth. Instead of binding to KRAS directly, it attaches to a molecule called cyclophilin A in cells that helps fold proteins into their final 3D structures. This protein complex is then able to bind to the active KRAS protein and shut down its ability to signal cancer cells to multiply.

The company developing the drug, Revolution Medicines, presented results on May 31, 2026, from its Phase 3 clinical trial of 500 patients with metastatic pancreatic cancer who had received prior treatment. Compared to standard chemotherapy, daraxonrasib nearly doubled overall survival from 6.7 months to 13.2 months after diagnosis. Overall, daraxonrasib reduced the risk of death for metastatic pancreatic cancer patients by 60%. https://www.youtube.com/embed/sIspXSWQn1w?wmode=transparent&start=0 Daraxonrasib nearly doubled survival for patients with advanced pancreatic cancer compared to chemotherapy.

The most common side effect is a prominent skin rash, which affected more than 86% of patients in the study. Patients also frequently dealt with stomatitis – painful swelling and sores inside the mouth – as well as diarrhoea, nausea and vomiting. However, patients taking daraxonrasib were far less likely to stop treatment due to severe side effects compared to chemotherapy, and they had improved quality of life with reduced pain.

Next steps for daraxonrasib

By successfully targeting the specific genetic mutation that drives the vast majority of pancreatic cancers, researchers have demonstrated that this “undruggable” disease is treatable with targeted therapy.

The immediate next step is regulatory review of the drug’s readiness for the clinic. With data now officially published, Revolution Medicines will use these findings to seek formal approval from the Food and Drug Administration and other global regulatory bodies.

Because advanced pancreatic cancer is notoriously difficult to treat, breakthrough therapies that demonstrate this kind of significant survival benefit are often granted expedited or priority review. When daroxonrasib becomes available to patients will depend on the review timeline. Should the drug obtain approval, it could be available in clinics within months.

For the broader landscape of drug development, this milestone represents a likely shift in pancreatic cancer treatment. I expect more clinical trials exploring combination therapies pairing KRAS inhibitors with other drugs to prevent tumours from developing resistance to treatment.

Should daraxonrasib succeed, it could help set the stage for more precise, personalised and effective treatments for pancreatic cancer in the years to come.

Christopher Lieu, Professor of Medical Oncology, University of Colorado Anschutz

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

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Vaccine and Immunotherapy Combo Halves Melanoma Recurrence

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3D structure of a melanoma cell derived by ion abrasion scanning electron microscopy. Credit: Sriram Subramaniam/ National Cancer Institute

The combination of a vaccine and a drug, which both harness the immune system to attack cancer cells, has proven successful in cutting the risk of skin cancer recurrence by 49% , a new study shows. This reduction, which was calculated five years after patients had their tumours surgically removed, remains unchanged.

Led by researchers at NYU Langone Health and its Perlmutter Cancer Center, the study tested the vaccine, called intismeran, in combination with the mainstay immunotherapy pembrolizumab (Keytruda) in 107 patients who had been randomly chosen after melanoma surgery to determine whether the combination therapy prevented their cancer from recurring. Intismeran is a personalized immunotherapy strategy that is developed with information from a patient’s individual tumour. These results were compared with those from a randomly selected group of 50 melanoma patients who had only received pembrolizumab postoperatively, a current standard of care.

Results of the phase 2b trial, known formally as KEYNOTE-942, are being presented at the 2026 annual meeting of the American Society of Clinical Oncology on June 1 in Chicago and simultaneously published in the society’s Journal of Clinical Oncology.

After five years of follow-up, 68.8% of patients who took the combination therapy remained cancer-free, while 49.1% of the patients in the pembrolizumab-alone group had no signs of cancer. This means that adding intismeran to pembrolizumab reduced the risk for recurrence or death by 49%. The combination therapy also reduced the risk of distant metastasis by 59%. Overall survival, meaning no death from cancer or any other cause, was 92.2%for the vaccine with immunotherapy group, while for the immunotherapy-alone group it was 71.3%.

“Our study offers strong evidence to melanoma patients that intismeran vaccine therapy, when used in combination with immunotherapy, can demonstrably reduce their risk of having their cancer return and improve clinical outcomes,” said study senior investigator Janice Mehnert, MD, a professor in the Department of Medicine at NYU Grossman School of Medicine.

“Our findings also serve as encouragement to cancer researchers globally that mRNA vaccines like intismeran could work well in combination with immunotherapy for other cancers whose high rates of mutations have proven difficult to target,” said Dr Mehnert, who also serves as director of the melanoma medical oncology program and associate director of clinical research at Perlmutter Cancer Center.

The study results highlight the role of T cells, which are capable of attacking viruses as well as cancers. To spare normal cells, the immune system uses checkpoint molecules on T cell surfaces to “turn off” their attack against viruses when they clear the infection. The body may recognide tumours as abnormal, but cancer cells hijack checkpoints to turn off and evade immune responses. Immunotherapies like pembrolizumab seek to block checkpoints, specifically the PD-1 protein receptor, making cancer cells more “visible” and vulnerable again to immune cells.

Immunotherapies, including PD-1 inhibitors like pembrolizumab, have become the mainstay for treating melanoma, although they do not work for all patients, because melanoma cells, known for their ability to evade the immune system, can become resistant to immunotherapy. For this reason, researchers have looked at adding vaccines.

The vaccine intismeran is based on messenger RNA, a chemical cousin of DNA that provides cells with instructions for making proteins. Intismeran and other mRNA cancer vaccines are meant to teach the immune system to recognize cancer cells as different from normal cells. In designing a vaccine against melanoma, researchers attempted to trigger an immune response to specific abnormal proteins, called neoantigens, made by cancer cells.

Because the study volunteers all had their tumours removed, researchers were able to analyse their cells for 34 neoantigens that were specific to each melanoma and create a personalised vaccine for each patient. As a result, T cells specific to the neoantigen proteins encoded by the mRNA were produced. Those T cells could then attack any melanoma cells trying to grow or spread.

Dr. Mehnert said that a phase 3, multicenter trial is already underway to determine if intismeran helps as a first-line therapy in combination with pembrolizumab for melanoma. Already, the vaccine is being tested to see if it also works to prevent recurrence of lung and other cancers.

For the KEYNOTE-942 trial, patients were enrolled at cancer centers in Australia and the United States from 2019 to 2021. All were men and women who had had surgery to remove their melanoma tumors. Seven patients in each treatment group died during follow-up, most from cancer. Side effects were considered manageable and included fatigue, pain at injection sites, and chills.

Source: NYU Langone Health

Categories : CancerTags :

Indigenous Plant Study Opens New Path in Cancer Treatment Research

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Prof. Chrisna Gouws and her team have been researching cancer bush for five years. Lessertia frutescens, commonly known as cancer bush.

by Phenyo Mokgothu

A plant long used in traditional medicine is now at the centre of research that could shape future cancer treatment options in South Africa and beyond.

Researchers at the North-West University(NWU) are investigating the anti-cancer potential of Lessertia frutescens, commonly known as cancer bush, after laboratory studies showed activity against several forms of cancer, including drug-resistant small cell lung cancer and colorectal cancer.

According to Prof Chrisna Gouws, a research professor in the Centre of Excellence for Pharmaceutical Sciences in the Faculty of Health Sciences, the research team tested extracts from the indigenous plant on cultured human cancer cells and more advanced laboratory-grown “mini-tumours” known as spheroids.

“Lessertia frutescens has shown significant anticancer activity against several different cancer types in our research,” she says.

Targeting cancers considered incurable

She says the findings became more important when the team observed activity in cancers that no longer respond to conventional treatment.

“What is very interesting and exciting is the apparent activity in drug-resistant cancers such as resistant small cell lung cancer where known chemotherapies have limited to no activity,” Prof. Gouws says.

“This provides us with new avenues to investigate for treatment options to treat cancers currently considered incurable.”

The research team said another factor attracting attention is the plant’s longstanding use in traditional medicine and its safety profile.

“An important consideration is that this plant has a long history of use and is considered non-toxic and safe for use,” Prof. Gouws says.

“It’s anticancer activity comes without the significant side-effects known to occur with most standard chemotherapies.”

Other systems in the body may benefit

Researchers also found that the plant may support other systems in the body during treatment.

“Lessertia has known boosting effects for the digestive and immune systems, and it can have mood-enhancing activities as well,” she says.

“It may therefore not only target the cancer but positively impact the patient as a whole at the same time.”

The team is now studying the plant’s phytochemicals to identify the molecules responsible for the anticancer activity and understand how they work.

“Although many molecules have been identified and shown to contribute to the anticancer activity of the plant, the mechanism of action remains mostly unclear,” says Prof. Gouws.

“We are therefore delving deeper now to try and understand how and why this plant works.”

The next phase of the study will include animal model testing later this year to confirm safety and efficacy before future clinical trials can be considered.

At the same time, the researchers are developing a complementary medicine product that may be available in pharmacies by 2027.

Prof. Gouws says the project could also create economic opportunities.

“Chemotherapy can be very expensive and inaccessible in rural areas. A new plant-based treatment will be much more cost-effective and may be more accessible because it can be manufactured locally,” she says. “An increase in demand for the plant material will also create economic opportunities through farming.”

More about Prof Chrisna Gouws

Prof Gouws leads the strategic project for Human-Based New Approach Methodologies for Biomedical Research. She holds a PhD in biochemistry and has more than 15 years’ experience in utilising cell culture-based models for human health and disease research, including developing new complex in vitro models for applications in drug research, including traditional medicinal remedies and plant materials for cancer treatment.

She is the founder and executive committee chair for the Society for Advanced Cell Culture Modelling for Africa, a board member of International Microphysiological Systems Society, and co-editor of the NAM Journal.

Source: North-West University

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Low Vitamin D Levels Linked to More Pain After Breast Cancer Surgery

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Patients with vitamin D deficiency may benefit from supplements before operations

Photo by Tima Miroshnichenko on Pexels

Vitamin D deficiency is associated with more moderate to severe pain following breast cancer surgery and an increased consumption of opioid drugs, finds research published online in the journal Regional Anesthesia & Pain Medicine. Breast cancer patients with low levels of vitamin D (below 30nmol/L) may benefit from taking supplements before undergoing a radical mastectomy, suggest researchers.

There is emerging evidence suggesting that vitamin D helps control how pain is felt and processed by the body. This is likely due to its anti-inflammatory effects and action on the immune system. Vitamin D deficiency is also commonly reported among patients with breast cancer. A team of researchers set out to examine the relationship between vitamin D deficiency and postoperative pain in patients undergoing breast cancer surgery.

Their prospective observational study, carried out at Fayoum University Hospital in Egypt between September 2024 and April 2025, included 184 breast cancer patients who were scheduled to undergo surgical removal of one entire breast.

Half of the patients were classified as vitamin D deficient (below 30 nmol/L) and half were classified as vitamin D sufficient (above 30nmol/L). Both groups had similar characteristics with an average age of 44 in the vitamin D deficient group and 42 in the vitamin D sufficient group.

Patients were managed according to the hospital’s routine protocol both during and after surgery. Clinical staff involved in their care were unaware of the patients’ vitamin D levels.

The opioid fentanyl was administered during the operation to manage acute pain. Following surgery, all patients were given paracetamol through a drip every 8 hours. In addition, patients could control how much tramadol (another opioid analgesic) they were given by directly pressing a button.

Patients reported their pain levels at zero, 6 hours, 12 hours, 18 hours and 24 hours after surgery. Nausea and vomiting, sedation score and days in hospital following surgery were also recorded.

Patients with vitamin D deficiency were three times more likely to report moderate to severe postoperative pain at any time point during the first 24 hours than those with sufficient vitamin D levels, the study found.

The researchers noted, however, that no patient in either group reported severe pain (7 or over on a scale of 0 to 10) so the difference was due entirely to a reduction in moderate pain (4-6 on the pain scale).

Vitamin D deficient patients received, on average, 8 μg more fentanyl during surgery, which the researchers described as a modest difference.

However, the study found those in the vitamin D deficient group used substantially more tramadol (112mg) after surgery than those who had sufficient vitamin D levels. This strong opioid was controlled directly by the patient up to a maximum dose of 50mg per hour.

Opioid drugs can cause a number of side effects including nausea, vomiting, drowsiness and confusion, while also carrying risks of dependency and addiction.

Postoperative nausea was more common in the vitamin D deficient group, and vomiting occurred only in that group, although the difference in vomiting was small and not statistically significant.

The study had some limitations. It was observational and conducted at a single centre, so no firm conclusion can be drawn about cause and effect. The researchers also did not assess inflammatory markers so could not explore the mechanisms underlying the relationship between vitamin D and pain. Data was also not collected on anxiety, depression, cancer stage, treatment or sleep disturbance before the surgery was carried out.

Nevertheless, the researchers conclude, “Vitamin D deficiency is associated with a higher occurrence of moderate to severe postoperative pain and increased opioid consumption in patients undergoing unilateral modified radical mastectomy.”

They suggest, “Preoperative vitamin D supplementation in breast cancer patients with vitamin D levels below 30 nmol/L may have a role in modulating postoperative pain.”

Source: The BMJ Group