Cancer
Researchers identify key protein in breast cancer brain metastasis
US researchers have identified a key protein whose increased presence helps promote breast cancer brain metastasis, opening a new area of research into the condition.
In their recent findings, the research team found the MUC5AC protein is upregulated in patients whose cancer has spread to the brain.
The finding provides a rationale for developing a new predictive biomarker for brain metastasis in high-risk breast cancer patients.
In addition, the researchers noted that the study offers a route to develop therapeutic targets for those cases.
Wasim Nasser, PhD, an associate professor in the UNMC Department of Biochemistry and Molecular Biology, said that the research also provides a potential platform to detect brain metastasis early in breast cancer patients.
Brain metastasis is an ominous complication that occurs in around 20-4 per cent of patients with solid tumors diagnosed with breast cancer, lung cancer or melanoma, said Dr. Nasser, who served as lead researcher and corresponding author on the study.
But with few therapies available for the affected patients with breast cancer brain metastasis, the patients typically live only for about five to 10 months, Dr. Nasser said.
According to the publication, mucin proteins previously have been implicated in cancer progression, and the researchers sought to answer whether and how they might be involved in breast cancer brain metastasis.
The study established that the secretory protein MUC5AC, through its interaction with cMET and CD44v6 receptors, is critical for breast cancer brain metastasis.
Dr. Nasser said: “It is imperative to characterise the factors responsible for brain metastasis and develop targeted therapies to challenge this complication,”
Dr. Nasser, whose research specialises in understanding the complexities that are involved in the brain metastasis pathogenesis, said the research team was intrigued to find the drivers that were potential threats to causing brain metastasis.
After analysing multiple datasets of patients with brain metastasis, Dr. Nasser said, the team found that mucins were dysregulated and MUC5AC specifically was among the top upregulated genes.
The connection was particularly strong in breast cancer patients with the HER2-positive cancer subtype, he said, and led to lower survival rates.
Having established that connection, the researchers then worked with animal models.
The researchers found that silencing MUC5AC in breast cancer brain metastatic cells for the experiment reduced brain metastasis in vivo.
In the study experiments, a cancer therapeutic already available for other uses – a cMET inhibitor known as Bozitinib, or PLB1001 – showed promise in inhibiting MUC5AC expression.
The study concluded that blocking MUC5AC and its axis with the cMET and CD44v6 proteins using a cMET inhibitor will be a novel therapeutic approach for breast cancer brain metastasis.
Dr. Nasser said the research team now is extending the study to other cancers that can metastasize to the brain, including lung cancer and melanoma.
Researchers also are hoping to push the Bozitinib therapy for clinical trials, he said.
An AI tool could help spot breast cancer risk by analysing how individual breast cells behave when squeezed under stress, research suggests.
Researchers at City of Hope and the University of California, Berkeley, created a microfluidic platform that assesses women’s breast cancer risk at the cellular level.
The platform squeezes individual breast epithelial cells, which line breast tissue, to measure how they deform, recover and behave under stress.
Because more than 90 per cent of women do not have a known genetic predisposition to breast cancer or a family history of the disease, the researchers said the approach could help fill a key gap in risk assessment.
Mark LaBarge, professor in the department of population sciences at City of Hope, said: “For women with a known genetic risk factor for breast cancer, there are things you can do like follow a higher-risk screening protocol. For everybody else, you’re left wondering, ‘Am I at high risk?’
“By translating physical changes in cells into quantifiable data, this tool gives women something tangible to discuss with their doctors, not just risk estimates, but evidence drawn directly from their own cells.”
The researchers developed a machine learning algorithm that identifies and measures cells showing signs of accelerated ageing, generating an individual breast cancer risk score.
They said the platform uses simple electronics that could be easy and affordable to replicate on a large scale.
Lydia Sohn, chair in mechanical engineering at UC Berkeley, said: “Our team isn’t the first to measure the mechanical properties of cells; however, other approaches require advanced imaging technology that’s expensive, cumbersome and has limited availability.
“In contrast, MechanoAge uses computer chips that are simpler than an Apple Watch and ‘RadioShack parts’ that are cheap and easy to assemble, potentially making the device highly scalable.”
About 6 per cent of women who develop breast cancer carry known genetic mutations.
For women outside this group, risk is usually estimated indirectly using population models or measures such as breast density, which can both overestimate and underestimate individual risk.
The researchers said there is currently no non-genetic test that can identify women at higher risk of breast cancer.
Screening mammograms can detect cancer only once it has started to grow, but the MechanoAge platform aims to assess risk earlier by looking for physical changes in individual cells.
Using the platform, the researchers found that breast cells appear to have a “mechanical age” separate from a person’s chronological age, based on how the cells respond to stress.
They said this is the first time mechanical age has been quantified in biological cells.
Sohn said: “We learned that the older the mechanical age, as determined by how cells respond to being squeezed through our microfluidic device, the higher the risk for breast cancer.”
In this type of mechano-node-pore sensing, an electrical current is measured across a liquid-filled channel.
As cells pass through, they disrupt the current, generating measurements about their size and shape. By narrowing parts of the channel, researchers squeeze the cells and then measure how long each one takes to return to its normal shape.
The team found that cells from older women were stiffer and took longer to bounce back after being squeezed.
They also identified a subset of younger women whose cells behaved more like those from older women. These cells came from women with genetic mutations linked to a higher breast cancer risk.
The researchers then refined the algorithm to assign a risk score based on the cells’ measured mechanical and physical properties. They said it successfully identified women with known genetic risks.
The team then used it to compare cells from healthy women, women with a family history of breast cancer, and cells taken from the healthy breast of women with breast cancer in the other breast.
LaBarge said: “With accuracy, we were able to figure out which women were at high risk of breast cancer and which women didn’t seem to be.”
The work grew out of more than 12 years of collaboration between the two labs, combining engineering with cancer and ageing biology.
Sohn said: “It’s a true collaboration. We’ve learned a lot from each other.
LaBarge added: “In my view, this is what happens when you have a real collaboration that develops over a long time. This result is not what we imagined at the beginning.”
An experimental drug slowed triple-negative breast cancer in mice by flooding tumour cells with toxic fats.
Triple-negative breast cancer lacks three common drug targets, making it one of the hardest-to-treat and most aggressive forms of the disease.
The compound, known as DH20931, appears to push cancer cells past their limits by triggering a surge in ceramides, fat-like molecules that place the cells under intense stress until they self-destruct.
In lab experiments, the drug also made standard chemotherapy more effective. When combined with doxorubicin, researchers were able to reduce the dose needed to kill cancer cells by about fivefold.
The drug targets an enzyme known as CerS2 to sharply increase production of these lipids and stress cancer cells. Healthy cells, by contrast, showed lower sensitivity to the drug in lab tests.
While the early results are promising, further preclinical and clinical trials would still be needed to determine the safety and effectiveness of DH20931 in humans.
Satya Narayan, a professor in the University of Florida’s College of Medicine, led the study with an international group of collaborators.
The researchers published their results on human-derived tumours on 21 April and presented their findings on combination therapy at the annual meeting of the American Association for Cancer Research in San Diego.
Narayan likened the drug’s effects to a home’s electrical system handling a power surge.
While healthy cells act like a properly grounded and installed circuit, cancer cells are more like a jumble of mismatched wires and faulty fuses. DH20931 overwhelms cells not with electricity, but with fats.
He said: “When that surge goes into the cancer cells, they cannot handle the amount of power they are getting. The fuses burn out, the cell can’t handle the surge and it dies.”
The compound was developed at the University of Florida in the lab of Sukwong Hong.
Hong, now a professor at the Gwangju Institute of Science and Technology in South Korea, created DH20931 as one of many drug candidates tested for efficacy in Narayan’s lab.
In the study, researchers implanted human triple-negative breast cancer tumours into mice and treated them with DH20931.
The drug significantly slowed tumour growth without causing noticeable weight loss or signs of toxicity in the animals. In separate lab experiments, it also showed activity against other breast cancer subtypes.
In addition to increasing lipid levels, DH20931 triggers a second stress signal by flooding cells with calcium.
Together, these effects disrupt the mitochondria, the structures that produce a cell’s energy, ultimately leading to cell death.
Narayan said: “It does not just follow one pathway but it goes through multiple pathways. It’s a two-hit hypothesis.
“These pathways are common in all breast cancer types and other solid tumours, so we think this drug can be useful not only in triple-negative breast cancer but potentially other cancers as well.”
Cervical cancer elimination in the EU is becoming achievable as HPV vaccination coverage rises, a new report says.
As Europe marks European Immunisation Week 2026, the European Centre for Disease Prevention and Control said progress in human papillomavirus vaccination is continuing across the EU and European Economic Area.
All EU and European Economic Area countries now recommend HPV vaccination for adolescent girls and boys as part of their immunisation programmes, marking a major step forward in Europe’s cancer prevention efforts.
Bruno Ciancio, head of unit, directly transmitted diseases and vaccine preventable diseases at the European Centre for Disease Prevention and Control, said: “The elimination of cervical cancer in the EU/EEA is becoming an achievable goal, thanks to the HPV vaccination programmes.
“The progress we are seeing across Europe demonstrates what can be accomplished when countries invest consistently in effective immunisation strategies.
“We are closely monitoring this progress and actively supporting countries to accelerate uptake and move faster towards cervical cancer elimination.”
According to the report, three EU and European Economic Area countries, Iceland, Portugal and Norway, have reached the 2024 EU Council Recommendation target of 90 per cent HPV vaccination coverage among girls by the age of 15.
Fifteen years after HPV vaccination programmes were introduced in Europe, a growing body of evidence confirms the vaccine is highly effective in preventing cervical cancer.
Large-scale studies from Sweden, the Netherlands and Denmark, as well as other parts of the world, have shown significant reductions in HPV infections and precancerous lesions, which are abnormal cell changes that can develop into cancer if left untreated, alongside falling cervical cancer rates among vaccinated women.
Since 2020, European countries have reported a decreased incidence of cervical cancer among vaccinated women.
Studies from Sweden, Denmark and the UK show that early administration of the vaccine increases its full protective potential.
A Swedish study suggested that vaccinating girls before their 17th birthday reduced the incidence of cervical cancer by 88 per cent.
An additional six-year follow-up found a sustained reduction in cervical cancer risk and a population-level decline in invasive cervical cancer incidence after HPV vaccination.
The report showed that vaccination programmes and health system design are critical factors in reaching high levels of HPV vaccination coverage.
Evidence from across Europe showed that school-based vaccination programmes are particularly effective and tend to reach higher levels of coverage among both girls and boys.
Entrepreneur5 days agoFuture Fertility raises Series A financing to scale AI tools redefining fertility care worldwide
Entrepreneur4 weeks agoThree sessions that show exactly where women’s health is heading in 2026
Pregnancy4 weeks agoHow NIPT has evolved and what AI NIPT means in 2026
News4 weeks agoTwo weeks left to make your mark in women’s cardiovascular health
Opinion4 weeks agoQ1 momentum: Female founders are advancing, but the system still hasn’t caught up
Fertility2 weeks agoFuture Fertility partners with Japan’s leading IVF provider, Kato Ladies Clinic
Mental health1 week agoLifting weights shows mental health and cognitive benefits in older women, study finds
Menopause2 weeks agoMore research needed to understand link between brain fog and menopause, expert says