Category: Cancer

Categories : Cancer IT in HealthcareTags :

AI Tools for Cancer Rely on Shaky Shortcuts

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Small cell lung cancer cells (green and blue) that metastasised to the brain in a laboratory mouse recruit brain cells called astrocytes (red) for their protection. Credit: Fangfei Qu

Artificial intelligence tools are increasingly being developed to predict cancer biology directly from microscope images, promising faster diagnoses and cheaper testing. But new research from the University of Warwick, published in Nature Biomedical Engineering, suggests that many of these systems may be using visual shortcuts rather than true biology – raising concerns that some AI pathology tools are currently too unreliable for real-world patient care.

“It’s a bit like judging a restaurant’s quality by the queue of people waiting to get in: it’s a useful shortcut, but it’s not a direct measure of what’s happening in the kitchen,” says Dr Fayyaz Minhas, Associate Professor and principal investigator of the Predictive Systems in Biomedicine (PRISM) Lab in the Department of Computer Science, University of Warwick, and lead author of the study.

“Many AI pathology models are doing the same thing, relying on correlations between biomarkers or on obvious tissue features, rather than isolating biomarker-specific signals. And when conditions change, these shortcuts often fall apart.”

To reach this conclusion, the researchers analysed more than 8000 patient samples across four major cancer types – breast, colorectal, lung and endometrial – and compared the performance of leading machine learning approaches. While the models often achieved high headline accuracy, the team found this frequently came from statistical “shortcuts.”

For example, instead of detecting mutations in the cancer-associated BRAF gene, a model might learn that BRAF mutations often occur alongside another clinical feature such as microsatellite instability (MSI). The system then learns to use this combination of cues to predict BRAF status rather than learning the causal BRAF signal itself – meaning accurate cancer predictions work only when these biomarkers co-occur and become unreliable when they do not.

Kim Branson, SVP Global Head of Artificial Intelligence and Machine Learning, GSK and co-author says, “We’ve found that predicting a BRAF mutation by looking at correlated features like MSI is often like predicting rain by looking at umbrellas – it works, but it doesn’t mean you understand meteorology.

“Crucially, if a model cannot demonstrate information gain above a simple pathologist-assigned grade, we haven’t advanced the field; we’ve just automated a shortcut. The roadmap for the next generation of pathology AI isn’t necessarily bigger models; it’s stricter evaluation protocols that force algorithms to stop cheating and learn the hard biology.”

When performance of AI models was assessed within stratified patient subgroups, such as only high-grade breast cancers or only MSI-positive tumours, accuracy fell substantially, revealing that the models were dependent on shortcut signals that disappear once confounding factors are controlled.

For certain prediction tasks, the performance advantage of deep learning over human-derived clinical information was modest. AI systems achieved accuracy scores of just over 80% when predicting biomarkers, compared with around 75% using tumour grade alone – a measure already assessed by pathologists.

Machine learning methods can still prove valuable for research, drug development candidate screening and for clinical triaging, screening, or supplementary decision support. However, the researchers argue that future AI tools must move beyond correlation-based learning and adopt approaches that explicitly model biological relationships and causal structure.

They also call for stronger evaluation standards, including subgroup testing and comparison against simple clinical baselines, before looking at deployment in routine care.

Dr Minhas concludes, “This research is not a condemnation of AI in pathology. It is a wake-up call. Current models may perform well in controlled settings but rely on statistical shortcuts rather than genuine biological understanding. Until more robust evaluation standards are in place, these tools should not be seen as replacements for molecular testing, and it is essential that clinicians and researchers understand their limitations and use them with appropriate caution.”

Source: University of Warwick

Categories : CancerTags :

Targeting Immune Suppression to Overcome Melanoma Resistance

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Photo by Bermix Studio on Unsplash

For patients with advanced melanoma without BRAF mutation who no longer respond to immune checkpoint inhibitors, treatment options remain frustratingly limited. A new study from Vanderbilt researchers led by Professor Emerita of Pharmacology Ann Richmond outlines a promising therapeutic strategy that may re-sensitise these resistant tumours to immunotherapy.

Figure 5b from the paper shows the difference between tumours treated with a just an antibody and vehicle (solution) or with trametinib and rigosertib and a CD40 agonist. Image cropped and shared from the paper by Yan et al. published in Nature Communications in 2026 in accordance with a CC BY-NC-ND 4.0 license.

The research introduces a three-drug combination that enhances immune activity and suppresses tumour-promoting immune cells by leveraging a low dose of the MEK inhibitor trametinib and multi-kinase inhibitor rigosertib alongside a CD40 agonist to shift the tumour microenvironment toward immune activation. Notably, all three agents have been either approved by the U.S. Food and Drug Administration or are currently in clinical trials, which may speed their path to patient testing.

“While agonist CD40 therapy can be helpful for treatment of melanoma, this therapy also induces the CD11b+ B regulatory cells that suppress the T cell response to tumours,” Richmond said. “We showed that combining CD40 therapy with trametinib and rigosertib prevents the induction of these B regulatory cells.”

Immune checkpoint inhibitors have become a mainstay of melanoma treatment, working by releasing the molecular “brakes” that prevent T cells from attacking cancer. But resistance to ICI is common in metastatic melanoma, especially in tumours that evolve immune-suppressive microenvironments. While CD40 agonists can activate immune cells, this therapy also unexpectedly expands CD11b+ regulatory B cells.

By combining CD40 activation with MEK and PI3K inhibition, the researchers blocked the expansion of suppressive B cells while retaining the benefits of CD40 stimulation. In preclinical mouse models of melanoma, the triple combination not only suppressed tumour growth but also restored responsiveness to checkpoint blockade.

Key findings

  • B cells as a resistance mechanism: CD40 therapy alone induced regulatory B cells that dampen T cell–mediated tumor immunity.
  • Triple combination prevents immune suppression: Co-treatment with trametinib and rigosertib blocked the agonist CD40 induction of regulatory B cells, allowing immune responses to proceed.
  • ICIs regain effectiveness: The drug cocktail slowed tumor progression and re-sensitized resistant melanomas to anti-PD-1 therapy.

Translational promise

Because trametinib, rigosertib, and CD40 agonists are already in human trials or approved for other indications, this therapeutic strategy may advance more quickly than approaches requiring new drug development. Richmond’s team sees potential for testing the triple therapy in clinical trials for melanoma patients who have progressed on ICI.

“This approach provides a new route to enhance antitumor immunity in patients with tumors that no longer respond to immunotherapy,” Richmond said.

By Marissa Shapiro

Source: Vanderbilt University

Categories : CancerTags :

Long-term Results Suggest that Follicular Lymphoma Is Curable

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Long-term data suggests an overall cure rate of 42%

Photo by National Cancer Institute on Unsplash

Unlike some other forms of lymphoma, advanced stage follicular lymphoma is considered incurable. But a new analysis of long-term data on patients treated for the disease years ago with standard regimens of immunotherapy and a chemotherapy combination known as CHOP suggests that many of those patients can now be considered cured.

The analysis is just published in the journal JAMA Oncology. 

“A subset of advanced-stage follicular lymphoma patients can achieve cure with CHOP-based chemoimmunotherapy, as relapse rates decline over time,” said Wilmot Cancer Institute Director Jonathan W. Friedberg, MD, MMSc, at the University of Rochester Medical Center, who is senior and corresponding author on the paper.  

“This finding represents a paradigm shift in our understanding and approach to follicular lymphoma, with broad implications for initial patient discussions and future research strategies.” 

Historically, follicular lymphoma has been considered an incurable disease, with most patients experiencing relapses even years after initial treatment.

The JAMA Oncology paper reports on an analysis of follow-up data from patients with advanced follicular lymphoma who had been treated with a standard first-line chemoimmunotherapy regimen on a large clinical trial.

Roughly 70 percent of the patients remained alive 15 years after beginning treatment, and a statistical method known as cure modelling estimated that 42% of treated patients had been cured. 

Cure modelling incorporates background mortality rates in an analysis of patient survival data to estimate what fraction of a group of patients can be considered cured of a disease. Such modelling accounts for the fact that over time some patient deaths will occur that are unrelated to the given disease.

The researchers applied a cure model to 15-year follow-up data from the S0016 clinical trial conducted by the SWOG Cancer Research Network, a clinical trials group funded by the National Cancer Institute (NCI), part of the National Institutes of Health (NIH), with the participation of other groups within the NCI-funded National Clinical Trials Network (NCTN).

This phase 3 trial, which opened in 2001, enrolled patients with untreated advanced-stage CD20-positive follicular lymphoma and randomised 531 of them to one of two treatments, both of which were built around a core chemotherapy regimen known as CHOP (cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone). One arm treated patients with rituximab plus the CHOP combination (R-CHOP), while the other arm used CHOP followed by radioimmunotherapy (CHOP-RIT). Primary results of the S0016 trial were published in 2013 (Press, OW. J Clin Oncol. 2013).

The S0016 modeling, including cure analysis, was carried out by Michael LeBlanc, PhD, a biostatistician at Fred Hutch Cancer Center and director of SWOG’s Statistics and Data Management Center (SDMC), and Hongli Li, MS, also at Fred Hutch and the SWOG SDMC.  

It showed that, with a median follow-up time of 15.5 years after a patient had begun treatment, the rate of disease relapse dropped substantially over time, falling from 6.8% of patients relapsing in the first 5 years to only 0.6% relapsing between years 15 and 20.

Fifteen years after starting treatment, about 70%of patients remained alive. The analysis also showed no statistically significant difference between the two treatment arms in the rates of 15-year overall survival.

Based on their work, the authors conclude that a substantial subset of patients with advanced-stage follicular lymphoma can, when treated with a standard regimen that includes immunotherapy and chemotherapy, achieve a functional cure – defined as having no chance of lymphoma recurring during the patient’s expected lifespan.

“These results reinforce that front-line chemoimmunotherapy remains an important option – particularly for appropriate patients – because it can deliver long-term disease control after a time-limited course of treatment, ” said first author Mazyar Shadman, MD, MPH, of Fred Hutch Cancer Center. Shadman is medical director of cellular immunotherapy at Fred Hutch, where he holds the Innovators Network Endowed Chair.

“As we bring novel agents into the first-line setting, the durability seen here sets a high benchmark; new strategies should aim not only to improve short-term response rates but to match or exceed long-term remission and cure potential.”

The idea that many of these patients can be cured could change how newly diagnosed patients are counseled and could eliminate the need for indefinite oncology and radiologic follow-up visits after treatment, with patients eventually transitioning from oncology care back to a primary care team.

Source: SWOG Cancer Research Network

Categories : CancerTags :

Hormone Therapy of Little Benefit with Radiotherapy after Prostate Surgery

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Findings could help patients avoid side significant effects and improve quality of life

Credit: Darryl Leja National Human Genome Research Institute National Institutes Of Health

A new study led by UCLA Health investigators suggests that adding hormone therapy to post-operative radiotherapy may provide little survival benefit for most men with prostate cancer, especially for those with very low PSA levels before treatment. 

The researchers found that for men with low PSA levels prior to radiotherapy, adding hormone therapy, whether short-term or long-term, did not improve overall survival. Men with higher PSA levels before radiation may see modest improvements in survival and metastasis-free survival, suggesting hormone therapy may be beneficial primarily for this higher-risk group.

The results were published in The Lancet and presented by Dr Amar Kishan, professor and executive vice chair of radiation oncology at the David Geffen School of Medicine at UCLA, during the plenary session of the American Society of Clinical Oncology Genitourinary Cancers Symposium in San Francisco. 

“Hormone therapy, which impacts the ability of testosterone to stimulate prostate cancer growth and repair, has been shown to improve outcomes when combined with radiotherapy in men whose prostates are still intact. However, whether it has a similar benefit for men receiving radiotherapy after prior surgery has remained unclear,” said Kishan, first author of the study and co-director of the cancer molecular imaging, nanotechnology and theranostics program at the UCLA Health Jonsson Comprehensive Cancer Center. “At the same time, hormone therapy carries significant side effects, including severe fatigue, hot flashes, sexual dysfunction, weight gain, bone loss and metabolic changes that can increase cardiovascular risk. Our findings show that for most men with detectable but low PSA levels (<0.5 ng/mL), after surgery to remove the prostate, post-operative radiotherapy is highly effective on its own. By safely omitting hormone therapy in these patients, we can potentially spare them months of treatment that may substantially affect their quality of life without extending survival.”

To better understand the impact of hormone therapy in this setting, the researchers conducted a large-scale, individual patient-level meta-analysis through the MARCAP Consortium, an international collaboration co-led by Kishan that is designed to evaluate long-term outcomes across randomized clinical trials.

The team analysed data from 6057 men enrolled in six randomised trials comparing post-operative radiotherapy alone to radiotherapy combined with either short-term (4-6 months) or long-term (24 months) hormone therapy. By pooling individual patient data rather than relying on summary trial results, investigators were able to examine outcomes in greater detail, including how pre-radiation PSA levels influenced treatment benefit.

Patients were followed for a median of nine years, allowing researchers to assess long-term overall survival, metastasis-free survival and recurrence outcomes. The analysis also enabled direct comparisons between short-term and long-term hormone therapy to determine whether extending treatment duration improved outcomes.

The researchers found that overall, 83.6% of men who received post-operative radiotherapy alone were alive after 10 years, compared with 84.3% for those who received post-operative radiotherapy plus hormone therapy.

Researchers found that pre-radiotherapy PSA levels, a measure of prostate-specific antigen in the blood after prostatectomy, played a crucial role. Men with low PSA levels before radiotherapy (≤0.5 ng/mL) saw no benefit from hormone therapy. In contrast, men with higher PSA levels showed modest improvements in survival, suggesting that hormone therapy may only be worthwhile for those with elevated PSA. 

The study also examined the duration of hormone therapy. Short-term therapy did not improve overall survival, though it slightly reduced the risk of cancer spreading. Long-term therapy showed a small survival benefit, particularly for men with higher PSA levels after prostatectomy. However, the team’s statistical analysis demonstrated that extending short-term therapy to long-term therapy did not further improve survival, although it did modestly lower the risk of metastasis.

“Our goal is always to treat the cancer while minimizing harm,” said Kishan. “This study helps us move toward more personalised care for men with prostate cancer. By better identifying who truly benefits from hormone therapy, we can make treatment smarter, reduce unnecessary interventions and focus on improving patients’ overall well-being.”

Building on those findings, ongoing research is working to further refine that approach. Trials such as the BALANCE Trial aim to pinpoint biomarkers that can identify which men are most likely to benefit from hormone therapy after surgery, helping tailor treatment decisions even more precisely.

Source: UCLA Health

Categories : Cancer Surgeries & ProceduresTags :

Method Spots Early Signs of Infection in Post-mastectomy Reconstruction

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Rapid detection, treatment of infections could avoid complications, additional surgeries after mastectomy

Many of those women opt to have their breasts surgically reconstructed, most commonly with implants, but a relatively high percentage develop infections after implant surgery, requiring intravenous antibiotics and often removal of the implant. This can lead to additional surgeries, delays in cancer care and increased costs, as well as added emotional distress for women already under strain from cancer diagnosis and treatment.

To address this problem, researchers at Washington University School of Medicine in St. Louis have developed a new tool to detect reconstruction-related infections early, before they cause symptoms. This method, reported in the Journal of Clinical Investigation, could allow for preemptive treatment that preserves implants, improves patient outcomes and reduces the psychological and financial burden on patients.

Led by Jeffrey P. Henderson, MD, PhD, a WashU Medicine professor, the study identified biomarkers of infection in fluid drained from reconstruction patients’ breasts days or even weeks before symptoms appeared. This represents a major opportunity for improvement over existing diagnostic methods, which rely heavily on clinical symptoms, such as redness and inflammation, that take time to appear and can overlap with normal reactions to surgery.

The findings are available online and will publish in print Feb. 16 in the Journal of Clinical Investigation.

“The ability to identify with a molecular signature early on that a patient will go on to have an infection opens up the possibility of surveillance as part of standard care,” Henderson said. “This has the potential to enable earlier treatment that would be far more effective – and potentially curative – in patients who would otherwise progress to prolonged courses of treatment and surgery, or even implant removal and reconstructive failure.”

Small molecules, big impact

The study originated when Henderson’s WashU Medicine colleague Margaret A. Olsen, PhD, a retired professor of medicine in the Division of Infectious Diseases who studies hospital infections, noticed high rates of infection among US patients who had reconstruction with implants after mastectomy. The discovery prompted Henderson and Olsen, a co-author on the study, to ask WashU Medicine plastic surgeons who performed breast reconstruction what they would need to improve outcomes in these patients. Their answer was simple: a clear yes/no test for infection.

To develop such a test, Henderson and lead author John A. Wildenthal, an MD/PhD student, leveraged their expertise in metabolomics, the study of metabolites that are created or broken down during cellular processes in the body. Metabolites can indicate the presence of an infection because they include byproducts of both the body’s response to pathogens and the metabolic activity of the pathogens themselves. By analysing changes in metabolite levels, scientists can identify patterns that are characteristic of infections, enabling early diagnosis.

Henderson and colleagues coordinated with WashU Medicine plastic surgeons to obtain fluid samples from 50 patient volunteers during several routine follow-up visits after surgery. The patients included women who later developed infections after post-mastectomy reconstruction and those who did not.

The researchers analysed the samples for differences between the two groups and identified metabolites that were significantly associated with infection and that appeared days to weeks before clinical signs and symptoms of infection. Further, they found that the presence of certain metabolites indicated more serious infections that might require more aggressive treatment.

“Originating from clinical intuition and validated through a clinical study, the evidence in this paper now supports proactive, targeted interventions to predict and address infections before they become clinically significant,” said Justin M. Sacks, MD, a co-author on the paper. “Such interventions can substantially reduce the burden of complications, implant loss and reconstructive failures in these patients.”

For instance, the findings could lead to the development of a point-of-care test that could be provided during a woman’s routine post-operative visits, noted co-author Terence M. Myckatyn, MD, a professor of surgery at WashU Medicine, who performs plastic and reconstructive surgery for breast cancer patients.

“If the test is positive, antibiotics can be started preemptively in these select patients to thwart infection,” Myckatyn said. “And perhaps just as important, we would not give antibiotics to those with a negative test, thereby adhering to a thoughtful approach for antibiotic stewardship.” Such careful use of antibiotics is important for preventing antibiotic resistance, he said.

In the near term, the team is planning additional studies to validate the results. Then a diagnostic tool could be developed and tested in clinical practice. In the future, the broader metabolomic findings about the development of tissue infection in humans could allow physicians to more selectively target a variety of post-surgical infections, for example, by revealing new drug targets.

“While better techniques are always being sought, the reality is that infections still occur despite a meticulous surgical approach,” said Myckatyn. “To be able to identify biomarkers that can portend an infection days before it develops is huge.”

Source: Washington University

Categories : CancerTags :

Aspirin not a Quick Fix for Preventing Colorectal Cancer

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Photo by cottonbro studio

Daily aspirin use does not offer a quick or reliable way to prevent colorectal cancer in the general population and carries immediate risks of serious bleeding, a new Cochrane review finds. 

Colorectal cancer is one of the most common types of cancer worldwide. Prevention typically involves following a healthy lifestyle and periodically undergoing routine screening tests. In recent years, researchers have also explored the role of off-the-shelf medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs), in reducing the incidence of colorectal cancer.

NSAIDs, which include ibuprofen and aspirin, are commonly used to reduce inflammation, fever, and pain. However, their role in the primary prevention of colorectal cancer remains uncertain and controversial.

Researchers from West China Hospital of Sichuan University in China analysed 10 randomised controlled trials including 124 837 participants, assessing whether aspirin or other NSAIDs could prevent colorectal cancer or precancerous polyps (adenomas) in people at average risk. The team found no suitable trials for non-aspirin NSAIDs, so their conclusions focus exclusively on aspirin.

Little to no short-term benefit and uncertain long-term effects

The review found that aspirin probably does not reduce the risk of colorectal cancer in the first 5 to 15 years of use. Possible protective effects after more than 10–15 years of follow-up were observed in some studies, but the certainty of this evidence is very low.

These potential long-term benefits come from observational follow-up phases of trials, in which participants may have stopped aspirin, started it independently, or begun other treatments, making the findings vulnerable to bias.

“While the idea of aspirin preventing bowel cancer in the long run is intriguing, our analysis shows that this benefit is not guaranteed and comes with immediate risks.”

— Dr Zhaolun Cai, lead author 

Immediate and well-established risks

The findings also show clear evidence that daily use of aspirin increases the risk of serious extracranial haemorrhage and probably increases the risk of haemorrhagic stroke. 

Although higher doses carry the greatest risk, low-dose (“baby”) aspirin also raises bleeding risk. Older adults and those with a history of ulcers or bleeding disorders may be particularly vulnerable.

The authors therefore caution that any potential long-term benefit must be weighed against the immediate and well-established risk of bleeding.
 

“My biggest worry is that people might assume that taking an aspirin today will protect them from cancer tomorrow. In reality, any potential preventive effect takes over a decade to appear, if it appears at all, while the bleeding risk begins immediately.”

— Dr Bo Zhang, senior author

Not a ‘one-size-fits-all’ solution

Previous evidence has shown potential benefits for people at high genetic risk of colorectal cancer, such as those with Lynch syndrome. However, this review focuses strictly on people at average risk, and the long-term evidence for them proved highly uncertain.

The authors urge that patients should not start taking aspirin for cancer prevention without a careful conversation with their healthcare professional about their personal risk of bleeding.
 

“This review reinforces that we must move away from a one-size-fits-all approach. Widespread aspirin use in the general population simply isn’t supported by the evidence. The future lies in precision prevention – using molecular markers and individual risk profiles to identify who might benefit most and who is most at risk.”

— Dr Dan Cao, senior author

The research team concludes that the story of aspirin for cancer prevention is far more complex than previously believed and that the balance of benefits and harms changes over time.

Dr Zhang adds:

“As scientists, we must follow the evidence where it leads. Our rigorous analysis of the highest-quality trials reveals that the ‘aspirin for cancer prevention’ story is more complex than a simple ‘yes or no.’ The current evidence does not support a blanket recommendation for aspirin use purely to prevent bowel cancer.” 

Read the review here.

Source: Cochrane

Categories : CancerTags :

Ibuprofen: How an Everyday Drug Might Offer Protection Against Cancer

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Photo by Towfiqu barbhuiya: https://www.pexels.com/photo/bottle-with-pills-11361813/

Dipa Kamdar, Kingston University; Ahmed Elbediwy, Kingston University, and Nadine Wehida, Kingston University

Ibuprofen is a household name – the go-to remedy for everything from headaches to period pain. But recent research suggests this everyday drug might be doing more than easing discomfort. It could also have anti-cancer properties.

As scientists uncover more about the links between inflammation and cancer, ibuprofen’s role is coming under the spotlight – raising intriguing questions about how something so familiar might offer unexpected protection.

Ibuprofen belongs to the non-steroidal anti-inflammatory drugs (NSAIDs) family. The connection between NSAIDs and cancer prevention isn’t new: as far back as 1983, clinical evidence linked sulindac – an older prescription NSAID similar to ibuprofen – to a reduced incidence of colon cancer in certain patients. Since then, researchers have been investigating whether these drugs could help prevent or slow other cancers too.

NSAIDs work by blocking enzymes called cyclooxygenases (COX). There are two main types. COX-1 helps protect the stomach lining, maintains kidney function, and plays a role in blood clotting. COX-2, on the other hand, drives inflammation.

Most NSAIDs, including ibuprofen, inhibit both, which is why doctors recommend taking them with food rather than on an empty stomach.

Ibuprofen and endometrial cancer

A 2025 study found that ibuprofen may lower the risk of endometrial cancer, the most common type of womb cancer, which starts in the lining of the uterus (the endometrium) and mainly affects women after menopause.

One of the biggest preventable risk factors for endometrial cancer is being overweight or obese, since excess body fat increases levels of oestrogen – a hormone that can stimulate cancer cell growth.

Other risk factors include older age, hormone replacement therapy (particularly oestrogen-only HRT), diabetes, and polycystic ovary syndrome. Early onset of menstruation, late menopause, or not having children also increase risk. Symptoms can include abnormal vaginal bleeding, pelvic pain, and discomfort during sex.

In the Prostate, Lung, Colorectal, and Ovarian (PLCO) study, data from more than 42,000 women aged 55–74 was analysed over 12 years. Those who reported taking at least 30 ibuprofen tablets per month had a 25% lower risk of developing endometrial cancer than those taking fewer than four tablets monthly. The protective effect appeared strongest among women with heart disease.

Interestingly, aspirin – another common NSAID – did not show the same association with reduced risk in this or other studies. That said, aspirin may help prevent bowel cancer returning.

Other NSAIDs, such as naproxen, have been studied for preventing colon, bladder, and breast cancers. The effectiveness of these drugs seems to depend on cancer type, genetics, and underlying health conditions.

Ibuprofen’s broader potential

Ibuprofen’s possible cancer-protective effects extend beyond endometrial cancer. Studies suggest it may also reduce risk of bowel, breast, lung, and prostate cancers.

For example, people who previously had bowel cancer and took ibuprofen were less likely to experience recurrence. It has also been shown to inhibit colon cancer growth and survival, and some evidence even suggests a protective effect against lung cancer in smokers.

Inflammation is a hallmark of cancer and ibuprofen is, at its core, anti-inflammatory. By blocking COX-2 enzyme activity, the drug reduces production of prostaglandins, chemical messengers that drive inflammation and cell growth – including cancer cell growth. Lower prostaglandin levels may slow or stop tumour development.

But that’s only part of the story. Ibuprofen also appears to influence cancer-related genes such as HIF-1α, NFκB, and STAT3, which help tumour cells survive in low-oxygen conditions and resist treatment.

Ibuprofen seems to reduce the activity of these genes, making cancer cells more vulnerable. It can also alter how DNA is packaged within cells, potentially making cancer cells more sensitive to chemotherapy.

A word of caution

But not all research points in the same direction. A study involving 7,751 patients found that taking aspirin after an endometrial cancer diagnosis was linked to higher mortality, particularly among those who had used aspirin before diagnosis. Other NSAIDs also appeared to increase cancer-related death risk.

Conversely, a recent review found that NSAIDs, especially aspirin, may reduce the risk of several cancers – though regular use of other NSAIDs could raise the risk of kidney cancer. These conflicting results show how complex the interaction between inflammation, immunity, and cancer really is.

Despite the promise, experts warn against self-medicating with ibuprofen for cancer prevention. Long-term or high-dose NSAID use can cause serious side effects such as stomach ulcers, gut bleeding, and kidney damage.

Less commonly, they may trigger heart problems like heart attacks or strokes. NSAIDs also interact with several medications, including warfarin and certain antidepressants, increasing the risk of bleeding and other complications.

The idea that a humble painkiller could help prevent cancer is both exciting and provocative. If future studies confirm these findings, ibuprofen might one day form part of a broader strategy for reducing cancer risk, especially in high-risk groups.

For now, experts agree it’s wiser to focus on lifestyle-based prevention: eating anti-inflammatory foods, maintaining a healthy weight and staying physically active.

Everyday medicines may yet hold surprising promise, but until the science is settled, the safest prescription for cancer prevention remains the oldest one: eat well, move often, and listen to your doctor before reaching for the pill bottle.

Dipa Kamdar, Senior Lecturer in Pharmacy Practice, Kingston University; Ahmed Elbediwy, Senior Lecturer in Cancer Biology & Clinical Biochemistry, Kingston University, and Nadine Wehida, Senior Lecturer in Genetics and Molecular Biology, Kingston University

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

Categories : Cancer Mental HealthTags :

Does Mental Health Affect Cancer Mortality?

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Study finds a link between mental health diagnoses and early death.

Photo by Alex Green on Pexels

In a study of adults with cancer, those who developed a mental health condition within the first year after their cancer diagnosis had a higher likelihood of dying over the next few years. The findings are published by Wiley online in CANCER, a peer-reviewed journal of the American Cancer Society.

In the analysis of data on all patients at University of California–affiliated hospitals, researchers identified all adult patients who were diagnosed with cancer in 2013–2023 but had no documented mental health disorder before their diagnosis.

Among 371 189 patients, 39 687 (10.6%) developed a mental health disorder within a year. After taking potentially influencing factors into account, a mental health disorder diagnosis was linked to a 51% higher risk of death in the initial 1–3 years after cancer diagnosis. This elevated risk diminished to a 17% higher risk after 3–5 years and then disappeared.

The findings support the importance of prompt screening and treatment of distress and mental health following a cancer diagnosis.

“Over the past several years, we’ve had an increasing appreciation for the important relationship between cancer, its treatment, and mental health,” said lead author Julian Hong, MD, MS, of the University of California, San Francisco. “This study reproduces our prior work by leveraging the shared experience across the University of California system, reinforcing a relationship between mental health conditions and mortality for patients with cancer and highlighting the need to prioritize and manage mental health.”

Source: Wiley

Categories : CancerTags :

The Next Cancer Breakthrough may be Stopping it Before it Starts

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Source: Unsplash CC0

Ahmed Elbediwy, Kingston University and Nadine Wehida, Kingston University

Cancer treatment follows a familiar pattern: doctors spot symptoms, diagnose the disease and start treatment. But scientists are now exploring a radical shift in how we tackle cancer. Instead of waiting for tumours to appear, they want to catch the disease decades before it develops.

This approach is called “cancer interception”. The idea is simple: target the biological processes that cause cancer long before a tumour ever forms.

Researchers are hunting for subtle early warning signs. These include genetic mutations that quietly build up in our cells, giving them advantages against our immune defences.

They’re also looking at precancerous lesions like moles or polyps, and early visible changes in tissue. All of these appear long before cancer becomes obvious.

Large genetic studies reveal that as people age, their bodies accumulate small groups of mutated cells called clones that grow silently. Scientists have studied this particularly well in blood. These clones can help predict who might develop blood cancers like leukaemia, and the genetics, inflammation and environmental factors strongly influence them.

Crucially, doctors can measure and track these changes over time. This opens up possibilities for early intervention.

A 16-year study followed around 7,000 women and uncovered how these mutations work. Some mutations helped clones multiply faster, while others made them particularly sensitive to inflammation.

When there was inflammation, these sensitive clones expanded. Breaking down these patterns helps researchers identify people with a higher chance of developing cancer later.

Not a sudden event

The research reveals something fundamental about cancer. It’s not a sudden event that instantly produces a tumour.

Instead, cancer develops through a slow, multi-step process with detectable warning signs along the way. These early signs could become powerful targets for stopping cancer before it starts.

Scientists are developing blood tests to spot cancer long before symptoms appear. These tests, called multi-cancer early detection tests (MCEDs for short), search for tiny fragments of DNA in the blood.

MCEDs work by looking for circulating tumour DNA, or ctDNA – DNA fragments that cancerous or precancerous cells release into the bloodstream. Even very early cancers shed this DNA, so the tests might detect disease long before it shows up on a scan.

The results so far look promising. MCEDs can boost survival rates through early detection, especially for colorectal cancer. When doctors diagnose colorectal cancer at stage one, 92% of patients survive five years. But when they catch it at stage four, only 18% survive that long.

If colon cancer is caught at stage one, most patients are still alive after five years. Credit: National Cancer Institute

The tests aren’t perfect, though. They miss some cancers entirely, and positive results still need follow-up tests to confirm.

Even so, research suggests MCEDs could become crucial for catching cancers that usually go unnoticed until much later. The potential to save lives is significant.

Heart doctors already use a similar approach. They calculate a person’s risk using age, blood pressure, cholesterol and family history, then prescribe drugs like statins years before a heart attack happens.

Cancer researchers want to copy this model. They envision combining genetic mutations, environmental factors and MCED results to guide early cancer prevention.

But cancer differs from heart disease in important ways. Cancer doesn’t follow a predictable path, and some early lesions shrink or never progress.

There’s also the risk of over-diagnosis. Being told you’re at higher risk when you feel perfectly healthy creates anxiety.

Cancer prevention tools also vary widely in their effectiveness, unlike statins that work broadly across different cardiovascular risk groups. The risk-based model shows promise, but needs careful handling.

Treating cancer risk instead of cancer itself raises difficult ethical questions. When someone feels completely healthy, judging whether intervention will truly help them becomes harder.

There’s a danger of causing unnecessary worry or harm. Scientists warn that doctors sometimes overestimate benefits and underestimate risks, particularly for older adults.

MCED tests bring their own ethical concerns. Accuracy isn’t the only issue that matters.

The tests sometimes flag cancer when none exists, leading to follow-up scans and biopsies that patients don’t actually need. The anxiety from all of this carries a high cost, both for patients and the healthcare system.

If these tests are expensive or only available privately, they could make health inequalities worse. This concern hits hardest in low-income countries.

In the US, the medicines regulator is investigating how MCED blood tests should work. They’re examining how reliable the tests need to be and what follow-ups doctors should require to keep patients safe.

The UK is following suit. The National Cancer Plan for England, published on February 4, 2026, commits to providing 9.5 million extra diagnostic tests through the NHS each year by March 2029.

The plan also states that ctDNA biomarker testing will continue in lung and breast cancer. It will extend to other cancers if proven to be cost effective.

What all this shows is clear. Cancer doesn’t suddenly appear; it’s a steady process that begins decades earlier. Catching it before it grows could save countless lives. The question now is how to do that safely, fairly and effectively.

Ahmed Elbediwy, Senior Lecturer in Cancer Biology & Clinical Biochemistry, Kingston University and Nadine Wehida, Senior Lecturer in Genetics and Molecular Biology, Kingston University

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

Categories : Cancer Surgeries & ProceduresTags :

Cancer Treatment Moving Towards Earlier Immunotherapy

On By ModernMedia
Killer T cells surround a cancer cell. Credit: Alex Ritter, Jennifer Lippincott Schwartz and Gillian Griffiths, National Institutes of Health (CC BY 2.0).

Immunotherapy given before or after surgery is increasingly used across several cancer areas. In an article published in the Journal of Internal Medicine, researchers at Karolinska Institutet present a comprehensive review of studies across seven tumour areas, showing how the field is moving towards earlier treatment.

For several years, immunotherapy has transformed the treatment of advanced cancer that can no longer be removed surgically. It is now used more frequently in earlier stages of disease as well – before surgery, known as neoadjuvant treatment, or after surgery, known as adjuvant treatment. In the new article, the researchers summarise findings from studies on several cancer diagnoses, grouped into seven tumour areas: skin cancer, lung cancer, breast cancer, gastrointestinal cancer, gynaecological cancer, head and neck cancer, and urological cancer.

Suggested benefits of treatment both before and after surgery

Several studies in recent years have shown that adjuvant immunotherapy after surgery can reduce the risk of the disease returning. Additional studies indicate that neoadjuvant treatment, given while the tumour is still in place, in many cases can provide the immune system with better conditions to recognise tumour cells. In several tumour areas, the results also suggest that immunotherapy given both before and after surgery may offer advantages compared with adjuvant treatment alone. 

At the same time, the authors emphasise that the results vary between different cancer types and that the treatment involves challenges, such as the risk of side effects and the possibility that some patients may receive more treatment than necessary if surgery alone would have been sufficient.

“We see that immunotherapy in early stages of disease is developing rapidly across many tumour areas. By bringing together studies from many cancer types, it becomes clearer how the field is evolving and what experiences can be shared between different specialties,” says last author Hildur Helgadottir, researcher at the Department of Oncology-Pathology at Karolinska Institutet.

How the researchers carried out the review

The work behind the article is a collaboration between 14 researchers at the Department of Oncology-Pathology, Karolinska Institutet. All of them also work with cancer treatment in clinical care. Because the researchers come from seven different tumour areas, the article gathers experiences from many parts of cancer care.

“It is valuable that we have come together from so many different tumour areas. This gives a broader understanding of how immunotherapy is used across cancer care and can, in the long term, support both clinical decision-making and future research,” says Hildur Helgadottir.

The researchers also point to areas where more knowledge is needed. One of these is the development of biomarkers, measurable characteristics that can help healthcare determine which patients benefit from immunotherapy, both before and after surgery. They also discuss how introducing immunotherapy at earlier stages raises questions about costs, side effects, and whether healthcare resources will be sufficient, questions that current studies do not yet clearly answer.

Information about funders and potential conflicts of interest can be found in the scientific publication.

Publication

Perioperative immune checkpoint inhibitor therapy across tumors: Insights and shared lessons from a rapidly evolving field.
Björkström K, Matikas A, Svedman FC, Björgvinsson E, Zupancic M, Villabona L, Eriksson H, Skribek M, Fernebro J, Lindskog M, Frödin JE, Ullén A, Ekman S, Helgadottir H
J Intern Med 2026 Feb;():

Source: Karolinska Institutet