̽��ֱ�� of Cambridge - Wellcome Sanger Institute

Scientists discover how aspirin could prevent some cancers from spreading

jg533 — Wed, 05 Mar 2025 16:00:58 +0000

They say that discovering the mechanism will support ongoing clinical trials, and could lead to the targeted use of aspirin to prevent the spread of susceptible types of cancer, and to the development of more effective drugs to prevent cancer metastasis.

̽��ֱ��scientists caution that, in some people, aspirin can have serious side-effects and clinical trials are underway to determine how to use it safely and effectively to prevent cancer spread, so people should consult their doctor before starting to take it.

Studies of people with cancer have previously observed that those taking daily low-dose aspirin have a reduction in the spread of some cancers, such as breast, bowel, and prostate cancers, leading to ongoing clinical trials. However, until now it wasn’t known exactly how aspirin could prevent metastases.

Professor Rahul Roychoudhuri in the Department of Pathology at the ̽��ֱ�� of Cambridge, who led the work, said: “Despite advances in cancer treatment, many patients with early stage cancers receive treatments, such as surgical removal of the tumour, which have the potential to be curative, but later relapse due to the eventual growth of micrometastases – cancer cells that have seeded other parts of the body but remain in a latent state.

“Most immunotherapies are developed to treat patients with established metastatic cancer, but when cancer first spreads there’s a unique therapeutic window of opportunity when cancer cells are particularly vulnerable to immune attack. We hope that therapies that target this window of vulnerability will have tremendous scope in preventing recurrence in patients with early cancer at risk of recurrence.”

̽��ֱ��study was published on 5 March in the journal 'Nature'.

̽��ֱ��scientists say their discovery of how aspirin reduces cancer metastasis was serendipitous. They were investigating the process of metastasis, because, while cancer starts out in one location, 90% of cancer deaths occur when cancer spreads to other parts of the body.

̽��ֱ��scientists wanted to better understand how the immune system responds to metastasis, because when individual cancer cells break away from their originating tumour and spread to another part of the body they are particularly vulnerable to immune attack. ̽��ֱ��immune system can recognise and kill these lone cancer cells more effectively than cancer cells within larger originating tumours, which have often developed an environment that suppresses the immune system.

̽��ֱ��researchers previously screened 810 genes in mice and found 15 that had an effect on cancer metastasis. In particular, they found that mice lacking a gene which produces a protein called ARHGEF1 had less metastasis of various primary cancers to the lungs and liver.

̽��ֱ��researchers determined that ARHGEF1 suppresses a type of immune cell called a T cell, which can recognise and kill metastatic cancer cells.

To develop treatments to take advantage of this discovery, they needed to find a way for drugs to target it. ̽��ֱ��scientists traced signals in the cell to determine that ARHGEF1 is switched on when T cells are exposed to a clotting factor called thromboxane A2 (TXA2).

This was an unexpected revelation for the scientists, because TXA2 is already well-known and linked to how aspirin works.

TXA2 is produced by platelets - a cell in the blood stream that helps blood clot, preventing wounds from bleeding, but occasionally causing heart attacks and strokes. Aspirin reduces the production of TXA2, leading to the anti-clotting effects, which underlies its ability to prevent heart attacks and strokes.

This new research found that aspirin prevents cancers from spreading by decreasing TXA2 and releasing T cells from suppression. They used a mouse model of melanoma to show that in mice given aspirin, the frequency of metastases was reduced compared to control mice, and this was dependent on releasing T cells from suppression by TXA2.

Dr Jie Yang in the Department of Pathology at the ̽��ֱ�� of Cambridge, first author of the report, said: “It was a Eureka moment when we found TXA2 was the molecular signal that activates this suppressive effect on T cells. Before this, we had not been aware of the implication of our findings in understanding the anti-metastatic activity of aspirin. It was an entirely unexpected finding which sent us down quite a different path of enquiry than we had anticipated.”

“Aspirin, or other drugs that could target this pathway, have the potential to be less expensive than antibody-based therapies, and therefore more accessible globally.”

In the future, the researchers plan to help the translation of their work into potential clinical practice by collaborating with Professor Ruth Langley, of the MRC Clinical Trials Unit at ̽��ֱ�� College London, who is leading the Add-Aspirin clinical trial, to find out if aspirin can stop or delay early stage cancers from coming back.

Professor Langley, who was not involved in this study, commented: “This is an important discovery. It will enable us to interpret the results of ongoing clinical trials and work out who is most likely to benefit from aspirin after a cancer diagnosis.”

“In a small proportion of people, aspirin can cause serious side-effects, including bleeding or stomach ulcers. Therefore, it is important to understand which people with cancer are likely to benefit.”

̽��ֱ��research was principally funded by the Medical Research Council, with additional funding from the Wellcome Trust and European Research Council.

̽��ֱ��Add-Aspirin clinical trial is funded by Cancer Research UK, the National Institute for Health and Care Research, the Medical Research Council and the Tata Memorial Foundation of India.

Reference: J Yang, et al: “Aspirin prevents metastasis by limiting platelet TXA2 suppression of T cell immunity.” Nature, March 2025. DOI: 10.1038/s41586-025-08626-7

Adapted from a press release by the Medical Research Council.

Scientists have uncovered the mechanism behind how aspirin could reduce the metastasis of some cancers by stimulating the immune system.

Aspirin has the potential to be less expensive than antibody-based therapies, and therefore more accessible globally.

Jie Yang

Tetra Images on Getty

̽��ֱ��text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes

Licence type:

Attribution-Noncommerical

Cartographers of the human body: the Human Cell Atlas

cjb250 — Wed, 20 Nov 2024 16:00:45 +0000

̽��ֱ��Human Cell Atlas is an ambitious project to map every cell in the human body. Its co-lead, Professor Sarah Teichmann, explains how the initiative is already changing our understanding of our bodies.

̽��ֱ��master of mutations

lkm37 — Mon, 29 Jul 2024 13:39:02 +0000

Dr Alex Cagan – illustrator, geneticist and explorer of animal DNA – is offering a new perspective on the tapestry of life. His work has profound implications for the pursuit of healthy ageing and the possibilities of cancer resistance.

Cambridge scientists elected as Members of the European Molecular Biology Organisation

jg533 — Tue, 09 Jul 2024 12:00:56 +0000

Five Cambridge researchers join the community of over 2,100 leading life scientists today as the European Molecular Biology Organisation (EMBO) announces its newest Members in its 60th anniversary year.

Cutting-edge genomic test can improve care of children with cancer

Anonymous — Tue, 02 Jul 2024 09:00:37 +0000

̽��ֱ��study, published on 2 July in Nature Medicine, is the first time that the impact of using whole genome sequencing in current NHS practice has been assessed. It was led by researchers at the ̽��ֱ�� of Cambridge, Cambridge ̽��ֱ�� Hospitals NHS Trust, Wellcome Sanger Institute and Great Ormond Street Hospital.

̽��ֱ��team analysed the use of routine genome sequencing, through the NHS Genomic Medicine Service, at Cambridge ̽��ֱ�� Hospitals, where such tests are given to all children with solid tumours, and at Great Ormond Street Hospital, which provides the test for childhood leukaemia.

̽��ֱ��researchers found that cancer sequencing gave new insights that improved the immediate clinical care of seven per cent of children, while also providing all the benefits of current standard tests.

Furthermore, in 29 per cent of cases, genome sequencing provided additional information that helped clinicians better understand the tumours of individual children and informed future management. For example, uncovering unexpected mutations that increase future cancer risk leading to preventative measures being taken, such as regular screening.

Overall, whole genome sequencing provides additional, relevant data, about childhood cancer that is useful for informing practice. ̽��ֱ��results also show that it can reduce the number of tests required, and therefore, researchers suggest it should be provided to all children impacted by cancer.

Whole genome sequencing (WGS) is a single test that provides a complete readout of the entire genetic code of the tumour and identifies every single cancer-causing mutation. Comparatively, traditional standard-of-care tests only look at tiny regions of the cancer genome, and therefore many more tests are often required per child.

Professor Sam Behjati, senior author from the Wellcome Sanger Institute, Cambridge ̽��ֱ�� Hospitals, and the ̽��ֱ�� of Cambridge: “Whole genome sequencing provides the gold standard, most comprehensive and cutting edge view of cancer. What was once a research tool that the Sanger Institute started exploring over a decade ago, has now become a clinical test that I can offer to my patients. This is a powerful example of the genomic data revolution of healthcare that enables us to provide better, individualised care for children with cancer.”

NHS England is one of the few health services in the world that has a national initiative, through the Genomic Medicine Service, offering universal genome sequencing to every child with suspected cancer. However, due to multiple barriers and a lack of evidence from real-time practice supporting its use, whole cancer genome sequencing is not yet widespread practice.

̽��ֱ��latest study looked at 281 children with suspected cancer across the two units. ̽��ֱ��team analysed the clinical and diagnostic information across these units and assessed how genome sequencing affected the care of children with cancer.

They found that WGS changed the clinical management in seven per cent of cases, improving care for 20 children, by providing information that is not possible to acquire from standard of care tests.

Additionally, WGS faithfully reproduced every one of the 738 standard of care tests utilised in these 281 cases, suggesting that a single WGS test could replace the multiple tests that the NHS currently uses if this is shown to be economically viable.

WGS provides a detailed insight into rare cancers, for example, by revealing novel variants of cancer. ̽��ֱ��widespread use of genome sequencing will enable clinicians to access these insights for individual patients while simultaneously building a powerful shared genomic resource for research into new treatment targets, possible prevention strategies, and the origins of cancer.

Dr Jack Bartram, senior author from Great Ormond Street Hospital NHS Foundation Trust and the North Thames Genomic Medicine Service, said: “Childhood cancer treatment is mostly guided by genetic features of the tumour, and therefore an in-depth genetic understanding of cancer is crucial in guiding our practice. Our research shows that whole genome sequencing delivers tangible benefits above existing tests, providing better care for our patients. We hope this research really highlights why whole genome sequencing should be delivered as part of routine clinical care to all children with suspected cancer.”

Professor Behjati at the Department of Paediatrics, ̽��ֱ�� of Cambridge, and is a Fellow of Corpus Christi College, Cambridge.

This research was supported in part by Wellcome, the Pessoa de Araujo family and the National Institute for Health and Care Research.

Reference
A Hodder, S Leiter, J Kennedy, et al. Benefits for children with suspected cancer from routine whole genome sequencing. Nature Medicine; 2 July 2024; DOI: 10.1038/s41591-024-03056-w

Adapted from a press release from Wellcome Sanger Institute

Whole genome sequencing has improved clinical care of some children with cancer in England by informing individual patient care. Research published today supports the efforts to provide genome sequencing to all children with cancer and shows how it can improve the management of care in real-time, providing more benefits than all current tests combined.

This is a powerful example of the genomic data revolution of healthcare that enables us to provide better, individualised care for children with cancer

Sam Behjati

FatCamera (Getty Images)

Boy Battling With Cancer

Eddie’s story

When he was six-years old, Eddie began to have regular low-grade fevers that seemed to affect him a lot. Even though early tests came back normal, the fevers became more frequent and his Mum, Harri, noticed that on one or two occasions he seemed out of breath while doing small things like reading a book. A chest x-ray revealed a huge mass on Eddie’s chest, and he was diagnosed with T-cell acute lymphoblastic leukemia (T-ALL). Eddie was immediately transferred to Great Ormond Street Hospital (GOSH) to begin treatment.

“I know it sounds like a cliché, but you really don’t think it will ever happen to your child. It felt like our world fell out from under us. During those first few weeks I remember wondering if this was it, I was taking so many photos of us together and wondering if it could be the last,” said Harri, Eddie's mum.

Eddie was put onto a treatment plan that included eight months of intense chemotherapy, followed by two and a half years of maintenance treatment. As part of his treatment at GOSH Eddie’s family were also offered WGS to identify any cancer-causing changes.

“When we were offered whole genome sequencing, we didn’t even hesitate. I wanted to have all the information, I wanted to have some peace of mind for the future and know that Eddie was having the right care throughout. I also wanted to make sure that Eddie’s brother, Leo, wasn’t any more likely to get T-ALL because Eddie had,” said Harri.

On his seventh birthday, Eddie’s family received the call to say he was in remission. Now, at nine years-old Eddie is nearing the end of his maintenance treatment and is doing well.

“We are trying to live each day, and this experience has really changed our outlook on life. We always try to take the positive from every situation. Words can’t explain what Eddie has been through this past three years but he has come out the other side as a sensitive, confident, and smart young man. He is mature beyond his years and he has been involved in everything, including decisions about his treatment. To say we are proud, doesn’t even come close to how we truly feel about him,” said Harri.

Their personal experience of WGS was so important on their journey that they provided support for this research.

Harri added: “I always say that having a child with a cancer diagnosis feels like you’ve been standing on a trap door all these years without knowing. Then after the diagnosis, you are in freefall. And even when things are stable again, you are constantly aware that the trap door is still there and there is a possibility it could open again at any time. Having access to whole genome sequencing gave us some sense of reassurance, it could have informed us about targeted treatments and gave us some insight into future risk. We wanted to support something that had the potential to have a real impact on treatment and outcomes so when we heard about this research project and its potential, it was very exciting that we could be a small part of it. It helped us turn something so devastating into something positive and we just hope that this research helps.”

Yes

Scientists identify genes linked to DNA damage and human disease

cjb250 — Fri, 16 Feb 2024 10:17:07 +0000

̽��ֱ��work, published in Nature, provides insights into cancer progression and neurodegenerative diseases as well as a potential therapeutic avenue in the form of a protein inhibitor.

̽��ֱ��genome contains all the genes and genetic material within an organism's cells. When the genome is stable, cells can accurately replicate and divide, passing on correct genetic information to the next generation of cells. Despite its significance, little is understood about the genetic factors governing genome stability, protection, repair, and the prevention of DNA damage.

In this new study, researchers from the UK Dementia Research Institute, at the ̽��ֱ�� of Cambridge, and the Wellcome Sanger Institute set out to better understand the biology of cellular health and identify genes key to maintaining genome stability.

Using a set of genetically modified mouse lines, the team identified 145 genes that play key roles in either increasing or decreasing the formation of abnormal micronuclei structures. These structures indicate genomic instability and DNA damage, and are common hallmarks of ageing and diseases.

̽��ֱ��most dramatic increases in genomic instability were seen when the researchers knocked out the gene DSCC1, increasing abnormal micronuclei formation five-fold. Mice lacking this gene mirrored characteristics akin to human patients with a number of rare genetic disorders, further emphasising the relevance of this research to human health.

Using CRISPR screening, researchers showed this effect triggered by DSCC1 loss could be partially reversed through inhibiting protein SIRT1. This offers a highly promising avenue for the development of new therapies.

̽��ֱ��findings help shed light on genetic factors influencing the health of human genomes over a lifespan and disease development.

Professor Gabriel Balmus, senior author of the study at the UK Dementia Research Institute at the ̽��ֱ�� of Cambridge, formerly at the Wellcome Sanger Institute, said: “Continued exploration on genomic instability is vital to develop tailored treatments that tackle the root genetic causes, with the goal of improving outcomes and the overall quality of life for individuals across various conditions.”

Dr David Adams, first author of the study at the Wellcome Sanger Institute, said: “Genomic stability is central to the health of cells, influencing a spectrum of diseases from cancer to neurodegeneration, yet this has been a relatively underexplored area of research. This work, of 15 years in the making, exemplifies what can be learned from large-scale, unbiased genetic screening. ̽��ֱ��145 identified genes, especially those tied to human disease, offer promising targets for developing new therapies for genome instability-driven diseases like cancer and neurodevelopmental disorders.”

This research was supported by Wellcome and the UK Dementia Research Institute.

Reference
Adams, DJ et al. Genetic determinants of micronucleus formation in vivo. Nature; 14 Feb 2024; DOI: 10.1038/s41586-023-07009-0

Adapted from a press release from the Wellcome Sanger Institute.

Cambridge scientists have identified more than one hundred key genes linked to DNA damage through systematic screening of nearly 1,000 genetically modified mouse lines.

Continued exploration on genomic instability is vital to develop tailored treatments that tackle the root genetic causes

Gabriel Balmus

qimono

DNA puzzle

Yes

Licence type:

Public Domain

Role of inherited genetic variants in rare blood cancer uncovered

jg533 — Wed, 17 Jan 2024 10:03:16 +0000

Large-scale genetic analysis has helped researchers uncover the interplay between cancer-driving genetic mutations and inherited genetic variants in a rare type of blood cancer.

Researchers from the ̽��ֱ�� of Cambridge, Wellcome Sanger Institute, and collaborators, combined various comprehensive data sets to understand the impact of both cancer-driving spontaneous mutations and inherited genetic variation on the risk of developing myeloproliferative neoplasms (MPN).

̽��ֱ��study, published in the journal Nature Genetics, describes how inherited genetic variants can influence whether a spontaneous mutation in a particular gene increases the risk of developing this rare blood cancer.

This analysis has an impact on current clinical predictions of disease development in individuals. Further research is required to understand the biological mechanisms behind how these inherited genetic variants influence the chances of developing rare blood cancer. In the future, this knowledge could aid drug development and interventions that reduce the risk of disease.

Myeloproliferative neoplasms, MPNs, are a group of rare, chronic, blood cancers. There are around 4,000 cases of MPN in the UK each year. These occur when the bone marrow overproduces blood cells, which can result in blood clots and bleeding. MPNs can also progress into other forms of blood cancer, such as leukaemia.

In the population, there is a large amount of natural variation between individuals’ blood cells, which can affect the amount of blood cells a person has and their particular traits. This is because multiple different genes can influence blood cell features in an individual. During routine blood tests, researchers take known information about these genes and analyse the variation to give a genetic risk score, which is how likely that individual is to develop a disease over their lifetime.

MPNs have been linked to random somatic mutations in certain genes including in a gene called JAK2. However, mutated JAK2 is commonly found in the global population, and the vast majority of these individuals do not have or go on to develop MPN.

Whilst previous studies have identified over a dozen associated inherited genetic variants that increase the risk of MPN, these studies insufficiently explain why most individuals in the population do not go on to develop MPN.

This new study, from the Wellcome Sanger Institute and collaborators, combined information on the known somatic driver mutations in MPN, inherited genetic variants, and genetic risk scores from individuals with MPN.

They found that the inherited variants that cause natural blood cell variation in the population also impact whether a JAK2 somatic mutation will go on to cause MPN. They also found that individuals with an inherited risk of having a higher blood cell count could display MPN features in the absence of cancer-driving mutations, thus, mimicking disease.

Dr Jing Guo, from the ̽��ֱ�� of Cambridge and the Wellcome Sanger Institute and first author of the study, said: “Our large-scale statistical study has helped fill the knowledge gaps in how variants in DNA, both inherited and somatic, interact to influence complex disease risk. By combining these three different types of datasets we were able to get a more complete picture of how these variants combine to cause blood disorders.”

Professor Nicole Soranzo, co-senior author from the ̽��ֱ�� of Cambridge, the Wellcome Sanger Institute, and Human Technopole, Italy, said: “There has been increasing realisation that human diseases have complex causes involving a combination of common and rare inherited genetic variants with different severity.

“We have previously shown that variation in blood cell parameters and function has complex genetic variability by highlighting thousands of genetic changes that affect different gene functions. Here, we show for the first time that common variants in these genes also affect blood cancers, independent of causative somatic mutations. This confirms a new important contribution of normal variability beyond complex disease, contributing to our understanding of myeloproliferative neoplasms and blood cancer more generally.”

Dr Jyoti Nangalia, co-senior author from the Wellcome-MRC Cambridge Stem Cell Institute at the ̽��ֱ�� of Cambridge, and the Wellcome Sanger Institute, said: “We have a good understanding of the genetic causes of myeloproliferative neoplasms. In fact, many of these genetic mutations are routine diagnostic tests in the clinic. However, these mutations can often be found in healthy individuals without the disease.

“Our study helps us understand how inherited DNA variation from person to person can interact with cancer-causing mutations to determine whether disease occurs in the first place, and how this can alter the type of any subsequent disease that emerges. Our hope is that this information can be incorporated into future disease prediction efforts.”

This research was funded by Cancer Research UK and Wellcome.

Reference

J Guo, K Walter, P M Quiros, et al. ‘Inherited polygenic effects on common hematological traits influence clonal selection on JAK2V617F and the development of myeloproliferative neoplasms.’ Jan 2024, Nature Genetics. DOI: 10.1038/s41588-023-01638-x

Adapted from a press release by the Wellcome Sanger Institute

Combining three different sources of genetic information has allowed researchers to further understand why only some people with a common mutation go on to develop rare blood cancer.

Our hope is that this information can be incorporated into future disease prediction efforts

Jyoti Nangalia

Photo by Sangharsh Lohakare on Unsplash

DNA

Yes

Licence type:

Attribution-Noncommerical

Cambridge researchers elected to Academy of Medical Sciences Fellowship 2023

lw355 — Thu, 18 May 2023 08:00:52 +0000

̽��ֱ��new Fellows have been elected to the Academy in recognition of their exceptional contributions to the advancement of biomedical and health science, cutting-edge research discoveries and translating developments into benefits for patients and wider society.

They join a prestigious Fellowship of 1,400 esteemed researchers who are central to the Academy’s work. This includes providing career support to the next generation of researchers and contributing to the Academy’s influential policy work to improve health in the UK and globally.

Professor Dame Anne Johnson PMedSci, President of the Academy of Medical Sciences, said: “These new Fellows are pioneering biomedical research and driving life-saving improvements in healthcare. It’s a pleasure to recognise and celebrate their exceptional talent by welcoming them to the Fellowship.

“This year, we are celebrating our 25th anniversary. ̽��ֱ��Fellowship is our greatest asset, and their broad expertise and dynamic ability has shaped the Academy to become the influential, expert voice of health. As we look to the future, the collective wisdom our new Fellows bring will be pivotal in achieving our mission to create an open and progressive research sector to improve the health of people everywhere.”

̽��ֱ��new Cambridge Fellows are:

Professor Charlotte Coles FMedSci

Professor of Breast Cancer Clinical Oncology, Department of Oncology, NIHR Research Professor and Director of Cancer Research UK RadNet Cambridge

Professor Coles leads practice-changing breast radiotherapy trials, has influenced international hypofractionation policy and is addressing global health, gender and equity challenges within the Lancet Breast Cancer Commission.

“It’s an honour to be elected as a new Fellow of the Academy of Medical Sciences. This is a result of research collaborations in Cambridge, the UK and internationally and I’d like to thank these wonderful colleagues, especially patient advocates,” said Coles.

“I hope to contribute to the Academy’s work to increase equity, diversity and inclusion within leadership roles, including lower- and middle-income countries, to enrich research and improve the culture in Medical Sciences.”

Professor Emanuele Di Angelantonio FMedSci

Professor of Clinical Epidemiology and Donor Health, Department of Public Health and Primary Care, and Head of Health Data Science Centre, Human Technopole (Milan)

Professor Di Angelantonio’s research has focused on addressing major clinical and public health priorities in cardiovascular disease (CVD) and transfusion medicine. His election recognises his many contributions both in helping resolve important controversies in CVD prevention strategies and in improving the safety and efficiency of blood donation.

“I am delighted and honoured to be elected to the Fellowship of the Academy of Medical Sciences, which I recognise is an outcome of the collaborations with many colleagues in UK and worldwide,” said Di Angelantonio.

“Research excellence across medical sciences and translation to health improvements has been at the centre of the Academy’s mission and I am very pleased to now be able to contribute to fulfilling this aim as a Fellow.”

Dr Rita Horvath FMedSci

Director of Research in Genetics of Rare Neurological Disorders in the Department of Clinical Neurosciences and Honorary Consultant in Neurology

Dr Horvath is an academic neurologist using genomics and biochemistry to diagnose rare, inherited neurological disorders, with a focus on mitochondrial diseases. Throughout her career she has combined fundamental experimental work with clinical studies. She pioneered the development and implementation of next generation sequencing in the diagnosis of rare neurogenetic diseases in the UK, leading to precision genetic approaches. She has established extensive international collaborations, having impact in Europe, but also for underserved groups in countries where such expertise is lacking.

“I am delighted and honoured to be elected to this Fellowship, which recognises the impact of my work. I would not have achieved it without the support of my excellent colleagues and research team, for which I give my sincere thanks,” said Horvath.

“As a Hungarian woman working in different countries before I arrived in the UK in 2007, I feel particularly proud of this award, which I recognise is an outcome of the open and fair research environment in Cambridge. This Fellowship enables me to further expand my research to develop effective treatments for patients with rare inherited neurological diseases.”

Professor Eric Miska FMedSci

Herchel Smith Chair of Molecular Genetics and Head of Department of Biochemistry, Affiliated Senior Group Leader at the Gurdon Institute, Associate Faculty at the Wellcome Sanger Institute and Fellow of St John’s College

Professor Miska is a molecular geneticist who has carried out pioneering work on RNA biology. His work led to fundamentally new insights into how small RNA molecules control our genes and protect organisms from selfish genes and viruses, and how RNA can carry heritable information across generations. Miska is Founder and Director of STORM Therapeutics Ltd, which creates novel therapies that inhibit RNA modifying enzymes for use in oncology and other diseases.

“Wonderful recognition of the work of an amazing team of researchers I have the pleasure to work with,” said Miska. “Most of our research has been done using the roundworm C. elegans. As Friedrich Nietzsche wrote in Thus Spoke Zarathustra: ‘You have evolved from worm to man, but much within you is still worm’.”

Professor Serena Nik-Zainal FMedSci

NIHR Research Professor, Professor of Genomic Medicine and Bioinformatics, Department of Medical Genetics and Early Cancer Institute, and Honorary Fellow of Murray Edwards College

Professor Nik-Zainal’s research is focused on investigating the vast number of mutations that occur in human DNA from birth, causing patterns called ‘mutational signatures’, and the associated physiological changes to cellular function, in progressive diseases such as cancer and neurodegeneration. She uses a combination of experimental and computational methods to understand biology and to develop clinical tests for early detection and precision diagnostics. Her team also builds computational tools to enable genomic advances become more accessible across the NHS.

“What an honour it is to be elected to the Fellowship. This is a wonderful recognition of the work from my team,” said Nik-Zainal. “We are thrilled and hugely indebted to all our inspiring collaborators, supporters and patients, who have shared in our passion and joined us on our path, exploring biomedical science and translating insights into patient benefit.”

Professor Julian Rayner FMedSci

Director of the Cambridge Institute for Medical Research, School of Clinical Medicine, Honorary Faculty at the Wellcome Sanger Institute, and Director of Wellcome Connecting Science

Professor Rayner’s research has made significant contributions to our understanding of how malaria parasites recognise and invade human red blood cells to cause disease. His work has helped to identify new vaccine targets, such as a protein essential for red blood cell invasion that is now in early stage human vaccine testing, and inform antimalarial drug development, through co-leading the first ever genome-scale functional screens in malaria parasites. He collaborates closely with researchers in malaria-endemic countries and is strongly committed to engaging public audiences with the process and outcomes of science.

“Malaria is a devastating and too often forgotten disease that still kills more than half a million children every year. Tackling it requires deep collaboration and working across disciplines. I’m enormously honoured by this announcement, which reflects not my work but the work of all the talented people I’ve been lucky enough to host in my lab, and collaborations with friends and colleagues across the world,” said Rayner.

“I’m excited to become a Fellow of the Academy of Medical Sciences because I strongly share their conviction that science is not just for scientists. I believe that dialogue, learning and public engagement are all fundamental and essential parts of the research process, and I look forward to contributing to their leading role in these areas.”

Professor James Rowe FMedSci

Professor of Cognitive Neurology, Department of Clinical Neurosciences, and MRC Cognition and Brain Sciences Unit

Professor Rowe leads a highly interdisciplinary research team at the Cambridge Centre for Frontotemporal Dementia and at Dementias Platform UK to improve the diagnosis and treatment of people affected by dementia. His work integrates cognitive neuroscience, brain imaging, fluidic biomarkers, computational models and neuropathology for experimental medicine studies and clinical trials. He is motivated by his busy clinical practice and the need for better diversity and inclusivity throughout medical research.

“I am delighted and honoured to be elected to the Fellowship of the Academy of Medical Sciences. It is a testament to the many wonderful colleagues and students I have been fortunate to work with, and to inspirational mentors,” said Rowe.

“Research excellence, and translation of research for direct human benefit, comes from innovation and collaboration in diverse cross-disciplinary teams. I believe in the vision and values of the Academy as the route to better health for all.”

In addition, two researchers from the wider community have also been elected:

Dr Trevor Lawley FMedSci, Senior Group Leader, Wellcome Sanger Institute and Chief Scientific Officer, Microbiotica

Professor Ben Lehner FRS FMedSci, Senior Group Leader, Human Genetics Programme, Wellcome Sanger Institute

Seven Cambridge ̽��ֱ�� researchers are among the 59 biomedical and health researchers elected to the Academy of Medical Sciences Fellowship.

As we look to the future, the collective wisdom our new Fellows bring will be pivotal in achieving our mission to create an open and progressive research sector to improve the health of people everywhere

Professor Dame Anne Johnson, President of the Academy of Medical Sciences

Clockwise from top left: E. Di Angelantonio, J. Rayner, J. Rowe, R. Horvath, S. Nik-Zainal, E. Miska, C. Coles

̽��ֱ��text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – as here, on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes