Prof George Vassiliou reflects on the scientific milestones that shaped his career, from defining clonal haematopoiesis to identifying therapeutic vulnerabilities in AML, and outlines what may come next for prevention-focused hematology
“Curiosity and enjoyment are not optional in research, they are what sustain you. If you love what you do, that is probably the strongest predictor of success in science.”
touchHEMATOLOGY coverage from EHA 2026
It was an honour to speak exclusively with Prof George Vassiliou (University of Cambridge, UK) at the European Hematology Association (EHA) 2026 Congress on the work that underpinned his EHA Research Excellence Award, and his legacy from decades of collaborative research into the biology of myeloid malignancies. His laboratory has helped define how somatic mutations alter hematopoietic stem cells, uncovering mechanisms of leukemogenesis and therapeutic vulnerabilities in AML. More recently, his group has been central to characterising clonal haematopoiesis as a precursor state to myeloid neoplasms, developing risk prediction tools and exploring early intervention strategies, including metformin in specific molecular subtypes, to prevent progression before overt disease develops.
Congratulations on receiving the EHA Research Excellence Award. What does this recognition mean to you?
It is a tremendous honour, but it reflects the work of many people rather than any one individual. Medical science is fundamentally collaborative. Progress depends on teams, scientists, clinicians, collaborators, funding bodies, and of course patients. Patients are central to this. Many agree to contribute samples to research at a difficult moment in their lives, often knowing it will not benefit them directly. That is an extraordinary act of generosity and bravery. So while I am the person receiving the award, I see it as recognition of everyone who contributed.
Your research has significantly advanced our understanding of myeloid malignancies. What do you see as the key scientific contributions behind this award?
Early in my career, our focus was on understanding how somatic mutations alter hematopoietic stem cells, the cells of origin for many myeloid malignancies. We studied how these mutations reshape gene expression and epigenetic regulation, particularly DNA methylation and chromatin states. That work helped identify mechanisms of disease and, in some cases, therapeutic opportunities. We also used CRISPR-Cas9 screening to identify vulnerabilities in acute myeloid leukaemia (AML), several of which have become actionable drug targets. Around 2014, our focus expanded upstream, looking at what happens before patients present with overt disease. That led us into clonal haematopoiesis.
What prompted that shift toward studying pre-leukaemic states?
It was driven by a patient. He presented critically unwell with AML, but told me he had run a half marathon only weeks earlier. That contrast was striking. It made me think: if we had sampled his blood before he became unwell, what would we have seen? Could there already have been detectable abnormalities?
That led us to investigate apparently healthy individuals for mutations associated with blood cancers. We analysed samples from around 4,200 people and found that clonal hematopoiesis was surprisingly common. At the same time, several USA groups reported similar findings. Together, that established CH as a precursor state and fundamentally reframed myeloid neoplasia as an evolutionary process.
How has that changed the field?
It gave us a biological framework. Depending on the initiating mutation, CH can evolve toward different myeloid malignancies: AML, myelodysplastic syndromes or myeloproliferative neoplasms. Since then, we’ve worked to define the natural history of CH, understand how specific mutations confer fitness advantages, and develop risk stratification tools to predict progression. That is clinically important because these individuals are usually well. The challenge is to intervene safely and proportionately.
Your group recently reported metformin as a potential intervention in CH. Can you expand on that?
Yes. We identified evidence that metformin may suppress expansion of a very specific subtype of CH. It does not appear to affect most CH clones, but it may have activity against one of the most common initiating mutations in AML. That matters because around 10% of AML cases may originate from this mutation years before diagnosis. If you can suppress clonal expansion at that stage, you may reduce future AML incidence. That remains a hypothesis, but it is one we are now aiming to test prospectively.
As detection of clonal haematopoiesis improves, how close are we to reliably predicting, and preventing, blood cancers?
Prediction is already possible, but it is probabilistic. Like any predictive model, it works at the population level better than the individual level. At present, many of our tools rely on a single time point. But longitudinal monitoring will be critical. A clone that remains stable over years may behave very differently from one that is rapidly expanding. This is one of the purposes of dedicated CH clinics: serial monitoring to refine risk and identify those truly approaching transformation.
In terms of prevention, we are entering that era, but it is still early. Clinical trials are underway or in development. Routine preventive treatment is not yet here.
Which scientific or therapeutic developments are you most excited about over the next decade?
One major area is the convergence of different AML-associated mutations onto shared transcriptional programmes. We are increasingly understanding that distinct mutations can activate common gene networks through overlapping mechanisms. That is why menin inhibition is so exciting; it targets a shared dependency across molecular subtypes.
At the same time, BCL2 inhibition has transformed AML treatment paradigms. For decades, treatment centred on intensive chemotherapy and allogeneic transplantation. Now we are moving toward lower-intensity, more biologically informed approaches.
And then there is cellular immunotherapy. CAR T-cell therapy has shown that harnessing the immune system can be highly effective in hematological malignancies. That platform will continue to evolve.
What advice would you give to early-career haematologists and clinician-scientists?
The most important thing is to do something you genuinely enjoy. If you love what you are doing, you are much more likely to succeed. For me, that has always been the driving force: curiosity, science, and the possibility of helping patients. That motivation sustains you over time. More than anything else, I think that is the most important ingredient for success.
This content has been developed independently by Touch Medical Media for touchHEMATOLOGY. Views expressed are the speaker’s own and do not necessarily reflect the views of Touch Medical Media. This article was created by the editorial team utilizing AI as an editorial tool (ChatGPT 5.5 [Large language model]. https://chat.openai.com/chat.) The content was developed and edited by human editors. No funding was received in the publication of this article.
Cite: EHA Research Excellence Award 2026: Prof George Vassiliou on his legacy in clonal haematopoiesis. touchHEMATOLOGY. 1st July 2026.
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