We’re excited to announce the winners of this year’s HSDTC Science Communication Competition!
Doctoral researchers at the four King’s health faculties were invited to submit a short ‘newspaper style’ article on their research topic. The article must be based on the research they are currently engaged with, or that the research group is doing, whether that be the whole project or one aspect of it. The article should be aimed at a non-specialist audience and be understandable to an interested member of the public.
The judges were looking for articles which:
- are compelling to read and easily understandable
- clearly explain the research being done
- answer the question “why does this research matter?”
- are worthy of publication in a national newspaper.
We were really lucky to have received 20 submissions, and we’ll showcase the winning pieces and other submissions in a few blog posts.
First Prize: Gorkem Ulkar, Faculty of Life Sciences & Medicine, Randall Centre for Cell & Molecular Biophysics
The secret signals of cancer
Cancer is a master of disguise. While we often think of it as a single lump that grows, its most dangerous ability is to spread. This process, called metastasis, is what makes cancer so lethal, transforming a localized disease into a widespread, systemic threat. But what if we could understand and stop cancer cells before they make their escape?
Scientists have long known that cancer spreads not just because of genetic mutations but also because of its environment: the physical world surrounding a tumour. Just like people respond to changes in their surroundings, cancer cells sense and react to the stiffness of the tissue around them. This stiffness can trigger changes in cell behaviour, making them more aggressive and more likely to spread. But how does this happen at a molecular level? That’s the question my research aims to answer.
Using cutting-edge imaging techniques, we are peering inside breast cancer cells as they move through different environments. We use a technique called Fluorescence Lifetime Imaging Microscopy (FLIM) to measure changes in the forces inside the cells, like tension in their membranes or shifts in the DNA packaging. By studying cells in 3D models that mimic real tumours, we can see how they respond to different levels of tissue stiffness. Are cells at the tumour’s edge, in contact with surrounding tissue, acting differently from those deeper inside? Does a stiffer environment push them toward becoming more invasive?
Early results show that changes in membrane tension and DNA structure happen together, suggesting that cancer cells coordinate their escape plan in response to mechanical forces. Understanding these signals could help us develop new therapies that target not just cancer’s genes but also its physical interactions.
This research matters because stopping metastasis could mean stopping cancer in its tracks. By uncovering how cancer senses and responds to its environment, we could pave the way for treatments that prevent it from spreading in the first place. In the fight against cancer, understanding its tricks is the first step to beating it.
Second Prize: Sara Gonzalez Ortega, Faculty of Life Sciences & Medicine, School of Cardiovascular and Metabolic Medicine & Sciences
Can we teach the heart to heal itself?
Every five minutes, someone in the UK suffers a heart attack. For many, the damage is irreversible. Once heart muscle cells die, they don’t grow back. But what if we could change that? Scientists are now exploring ways to reawaken the heart’s regenerative potential using tiny molecules called microRNAs (miRNAs).
A MAJOR UNMET NEED
Heart failure affects millions worldwide and remains a leading cause of death. Unlike some animals, such as zebrafish or newborn mice, which can regenerate heart tissue, the adult human heart lacks this ability. Once heart cells are lost, the heart forms scar tissue instead of regenerating, often leading to chronic heart failure. Current treatments manage symptoms but do not repair the damaged heart.
THE POWER OF microRNAs
MicroRNAs are small molecules that regulate gene activity. At Professor Mauro Giacca lab, scientists discovered that specific miRNAs—such as miR-199a-3p and miR-1825—can push heart cells to divide and regenerate, a groundbreaking finding that could revolutionize heart failure treatment.
DELIVERING A CURE
A key challenge is safely delivering these molecules to the heart. My research at King’s College London compares two methods:
- Viral Vectors: Modified viruses introduce miRNA into heart cells for long-term effects.
- Lipid Nanoparticles: Similar to the technology behind COVID-19 mRNA vaccines, these fat-based carriers deliver miRNAs safely and temporarily.
TESTING IN A “HEART IN A DISH”
To bridge the gap between lab research and human treatment, I use human myocardial slices—thin sections of living heart tissue obtained from surgical procedures such as myectomies or heart transplants. These otherwise discarded tissues continue beating in the lab, allowing realistic testing of miRNAs and delivery strategies. Using actual human heart tissue brings our findings much closer to real-world application.
A FUTURE WITHOUT HEART FAILURE?
The ability to regrow heart muscle cells could change the future of medicine. While we must ensure miRNAs don’t cause uncontrolled growth, this research brings us closer to a future where we can teach the heart to heal itself—offering hope to millions worldwide.
Third Prize: Tiffany Baptiste, Faculty of Life Sciences & Medicine, Biomedical Engineering and Imaging Sciences
One size fits all is convenient, but is it costing lives?
As cardiovascular disease remains the world’s top killer, scientists ask: can one-size-fits-all medicine keep up?
For decades, cardiovascular disease, the world’s leading cause of death, has been treated with a one-size-fits-all approach. But what if medicine could be as personalised as a tailored suit? Researchers at the Cardiac Electro-Mechanics Research Group (CEMRG) are working to make this possible using digital twins of the human heart.
Conditions such as heart failure and atrial fibrillation affect millions in the United Kingdom. Yet treatments still rely on broad clinical guidelines, even though no two hearts are exactly alike. Factors such as sex, age, ethnicity, and lifestyle can all influence how someone responds to therapy, but these differences are often overlooked.
Digital twins aim to change that. Using detailed, patient-specific data such as heart scans and electrical recordings taken in hospital, researchers can build a computer model of an individual’s heart that mimics its unique structure and function. These virtual hearts can be used to test treatments before they are applied to the real patient, offering a safer, smarter, and more personalised approach to care.
“Doctors often prescribe treatments based on past successes, but how do we know what is best for you?” asks Dr Ludovica Cicci, postdoctoral researcher at CEMRG. “Instead of trial and error, we can now test treatments virtually, reducing unnecessary procedures and improving outcomes.”
The hope is that these models will help doctors make better, more tailored decisions, transforming how we diagnose and treat heart disease.
However, the technology is not yet ready for everyday hospital use. Creating a true digital twin requires time and computing power to run the thousands of simulations needed to match model behaviour to real-life function. However, researchers are exploring how machine learning could streamline the process and make digital twins more practical for clinics.
“If no two people are the same, why should their treatments be?”, challenges Dr. Cicci. With continued innovation, digital twins of the heart could move us beyond one-size-fits-all healthcare, towards a future where every patient receives care that truly fits.