Insight
Three women named Britain’s Brightest Young Scientists
Three women have been named winners of the UK young scientist awards, the country’s largest unrestricted prize for young researchers, marking only the second time all laureates have been female.
Thi Hoang Duong (Kelly) Nguyen, Maxie M. Roessler and Paola Pinilla each received £100,000 at a ceremony held at Banqueting House in London on 24 February 2026.
The remaining six finalists were awarded £30,000 each.
The winners were selected from nine finalists and a wider field of 91 nominees drawn from 46 academic and research institutions across the UK.
An independent jury chose one laureate in each of three categories: life sciences, chemical sciences, and physical sciences and engineering.
Nicholas B. Dirks is president and chief executive of The New York Academy of Sciences and chair of the awards’ scientific advisory council.
Dirks said: “This is a remarkable group of laureates whose work reflects both scientific brilliance and real-world impact.
“Notably, this marks the second time in the history of the Blavatnik Awards in the United Kingdom that all three laureates are women scientists.
“On behalf of The New York Academy of Sciences, we celebrate the representation and success of women in science and congratulate these winning laureates.”
Nguyen, a molecular biologist at the MRC Laboratory of Molecular Biology, was recognised for research into telomerase, an enzyme that helps protect the ends of chromosomes during cell division.
Her work sheds light on how disruptions in telomerase activity are linked to premature ageing and cancer.
She used cryo-electron microscopy, a technique that allows scientists to visualise biological structures at extremely high resolution, to produce the first atomic-level model of the enzyme.
Roessler, a bioinorganic chemist at Imperial College London, was recognised for developing new methods that reveal how cells generate energy through rapid electron transfer.
Her findings could inform future work on catalysts and the development of new functional materials.
Pinilla, an astrophysicist at University College London, was recognised for research into how planets form.
Using telescope data and computer modelling, she identified structures in protoplanetary discs, rings of gas and dust around young stars, that trap dust and support planet formation.
Sir Leonard Blavatnik, founder of Access Industries and the Blavatnik Family Foundation, said: “The exceptional talent celebrated through these awards reflects the creativity and ambition that continue to place the UK at the forefront of scientific advancement.
“It is a privilege to recognise their work and to support the next stage of their scientific journeys.”
The Blavatnik Awards for Young Scientists are open to UK-based researchers aged 42 or under.
Now in their ninth year in the UK, the awards also run parallel programmes in the US and Israel.
Since launching in the UK in 2017, 73 honourees have received nearly £3.3m in prize funding.
By the end of 2026, the awards are expected to have distributed more than US$20m to over 500 scientists and engineers worldwide.
An early PET scan after one cycle of chemotherapy may help predict how aggressive breast cancer responds to treatment, a study suggests.
Research led by The Institute of Cancer Research, London and King’s College London suggests that an early scan taken after one cycle of chemotherapy could help predict how well a patient’s cancer will respond to treatment.
The study focused on patients with triple-negative breast cancer (TNBC), an aggressive form of the disease in which cancer cells lack receptors for the hormones oestrogen and progesterone, as well as the HER2 protein.
Patients with TNBC are usually treated with chemotherapy prior to surgery. While many respond well, residual disease at surgery, typically around six months later, is associated with a significantly poorer prognosis. Identifying people sooner who are unlikely to respond remains a major clinical challenge.
The research explored whether using PET imaging shortly after treatment begins, rather than relying only on MRI scans later in the treatment process, could provide earlier insight into how a patient’s cancer is responding. Twenty-two patients were recruited, with fourteen undergoing FDG-PET scans before treatment and after the first cycle of chemotherapy.
The findings, published in Clinical Cancer Research, showed that changes seen on PET scans after just one cycle of chemotherapy were strongly associated with subsequent response, including whether there was no detectable cancer, known as a complete response, by the end of treatment. Importantly, early PET response showed stronger associations with treatment outcomes than standard mid-treatment MRI scans in this study.
Being able to identify patients who are not responding well at an early stage could allow clinicians to adjust treatment sooner or consider alternative approaches. These findings may also support future strategies to better tailor treatment intensity to individual patients.
The study also compared two types of PET tracers, FDG and FLT, to determine which was most suitable. While both met the study’s technical criteria, FDG-PET was selected for further evaluation due to its better image quality, greater consistency and wider use in clinical practice.
The research also explored how imaging changes after just one cycle of chemotherapy relate to the body’s immune response to treatment. Biopsies taken before and after the first cycle of chemotherapy showed that an increase in immune cells within the tumour was strongly associated with both early PET changes and improved treatment outcomes.
The researchers emphasise that these findings now need to be validated in larger studies. Future work will aim to confirm these results in broader patient groups and explore more accessible imaging approaches, such as ultrasound, alongside PET and MRI.
Sheeba Irshad, professor of cancer immunology at King’s College London and lead of the Breast Cancer Now KCL Research Unit, said:
“In patients who had PET scans both before treatment and after the first cycle, we found that this early scan could predict whether they were likely to achieve a complete response by the end of treatment. These findings highlight the potential of early imaging to guide treatment decisions, and now need to be validated in larger, modern clinical trials.”
Andrew Tutt, professor of breast oncology at The Institute of Cancer Research, London, said:
“Research that helps us determine early who is already benefitting from standard neoadjuvant chemotherapy and who might benefit from clinical trials to find better treatments is vital. This study shows that FDG-PET may have great value in this regard. We hope to be able to design studies that further investigate and validate these findings.”
The study was supported by funding from King’s College London and Guy’s and St Thomas’ NHS Foundation Trust, Breast Cancer Now, Cancer Research UK, and Guy’s and St Thomas’ Charity.
Ki-67, a protein used to measure tumour growth, may also help prevent chromosome errors that drive cancer, a study suggests.
The findings could change how scientists view Ki-67, a marker commonly used in breast cancer and other tumours to assess how quickly cancer cells are growing.
Researchers found the protein may help preserve genome stability by maintaining the structural integrity of centromeres, key parts of chromosomes that help ensure DNA is shared correctly during cell division.
The research was led by professor Paola Vagnarelli at Brunel University of London in collaboration with scientists at the University of Edinburgh and the Technical University of Berlin.
Professor Vagnarelli said: “Doctors already measure Ki-67 to see how aggressive a cancer might be. But our results suggest it is actually helping maintain genome stability.
“That means it may be more than a marker. It could potentially also be a therapeutic target.”
The study examined three proteins that attach to chromosomes during cell division and help rebuild the molecular system that tells each new cell what kind of cell it is.
Every human cell carries identical DNA. What makes a liver cell different from a brain cell is which genes are switched on and which are kept inactive.
When a cell divides, that entire system of switches must be rebuilt. The three proteins involved in this process were Ki-67, Repo-Man and PNUTS.
Vagnarelli’s team developed a method that individually removes each protein from a living cell at the precise point of division. Older techniques could not isolate that moment cleanly.
They found that cells rely on all three proteins to reset themselves after division, but each failed in a different way when removed.
Without PNUTS, gene activity spiralled out of control and thousands of genes switched on at once.
Without Repo-Man, cells escaped safety checkpoints that usually stop damaged or abnormal cells from continuing to divide.
“What we didn’t expect was how clean the separation was,” said Vagnarelli.
Each protein fails in its own specific way. There is no redundancy, no safety net. Which means there are three separate points at which this process can go wrong.
“When the system breaks down, cells can emerge with the wrong number of chromosomes. That condition, called aneuploidy, is seen in disorders such as Down syndrome and in many cancers.
“We also found that these chromosome errors can trigger inflammatory signals inside the cell.”
Aneuploidy means a cell has too many or too few chromosomes, which can disrupt normal growth and function.
Inflammatory signals are chemical messages that can make a cell behave as if it is responding to injury or infection.
“These cells behave almost as if they are under attack,” said Vagnarelli.
“The immune response switches on because the genome is unstable.
“That link between chromosome imbalance and inflammation could help explain patterns we see in several diseases.”
The researchers said the findings may help cancer scientists better understand how chromosome instability, loss of gene regulation and cells dividing before they are ready contribute to tumour growth.
They said understanding the normal machinery that prevents these errors may help researchers find ways to push cancer cells into making mistakes they cannot survive.
“We now have a clearer map of the machinery that resets the cell after division,” said Vagnarelli.
“That knowledge gives us a starting point for thinking about new therapeutic approaches.”
After more than a decade of campaigning, doctors around the world have agreed to rename polycystic ovary syndrome (PCOS).
It is hoped the new name, polyendocrine metabolic ovarian syndrome, or PMOS, will help end the misconception that the condition is all about cysts, which campaigners say has contributed to missed diagnoses and inadequate treatment.
The condition affects one in eight women, or 3.1m women and girls in the UK, and is linked to hormone fluctuations that can affect weight, mental health, skin and the reproductive system.
The renaming was spearheaded by UK patient charity Verity alongside Professor Helena Teede, director of Melbourne’s Monash Centre for Health Research and Implementation.
It followed 14 years of consultation with clinicians and patients around the world.
The new name was published in a consensus statement on May 12 and announced at the European Congress of Endocrinology in Prague.
The paper states that PCOS should now be referred to as PMOS.
“This is a landmark moment that will lead to desperately-needed worldwide advancements in clinical practice and research,” said Professor Teede.
“It was heart-breaking to see the delayed diagnosis, limited awareness and inadequate care afforded those affected by this neglected condition.”
When doctors first named PCOS in 1935, they thought it was mainly caused by physical changes to the ovaries.
Decades of research have since changed that understanding, with clinicians now agreeing the condition is far more complex.
“What we now know is that there is actually no increase in abnormal cysts on the ovary and the diverse features of the condition were often unappreciated,” Professor Teede added.
“A name change was the next critical step towards recognition and improvement in the long term impacts of this condition.”
The exact cause of the condition is still unknown, though it is thought to be linked to abnormal hormone levels and is associated with insulin resistance and raised levels of testosterone and luteinising hormone.
Insulin resistance means the body does not respond properly to insulin, the hormone that helps control blood sugar. Luteinising hormone helps regulate ovulation.
Common symptoms listed by the NHS include irregular periods or no periods at all, difficulty getting pregnant, excessive hair growth, weight gain, thinning hair, oily skin and acne.
Campaigners have acknowledged that the name change could cause temporary confusion.
“Despite decades of tireless advocacy to improve awareness, we recognised that the risk of change would be worth the reward,” said Rachel Morman, chairwoman of Verity.
“This shift will reframe the conversation and demand that it is taken as seriously as the long-term, complex health condition it is.”
It is also unclear if, or when, the NHS will change the language it uses.
An NHS England spokesperson said: “We routinely review and update content on the NHS website to ensure it reflects the latest clinical advice and will carefully consider these recommendations.
“The NHS will also continue our work to improve women’s healthcare, including for this important group, which involves giving women more choice over their care, bringing down waiting times, and delivering more care in communities.”
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