̽��ֱ�� of Cambridge - Wellcome Trust-CRUK Gurdon Institute

One man, three companies, tens of thousands of lives...

skbf2 — Fri, 22 Oct 2021 08:12:28 +0000

Professor Steve Jackson talks about drug discovery, serial entrepreneurship and the enterprising mindset.

Scientists identify 160 new drugs that could be repurposed against COVID-19

cjb250 — Wed, 30 Jun 2021 18:00:28 +0000

In a study published today in Science Advances, a team led by researchers at the ̽��ֱ�� of Cambridge’s Milner Therapeutics Institute and Gurdon Institute used a combination of computational biology and machine learning to create a comprehensive map of proteins that are involved in SARS-CoV-2 infection – from proteins that help the virus break into the host cell to those generated as a consequence of infection. By examining this network using artificial intelligence (AI) approaches, they were able to identify key proteins involved in infection as well as biological pathways that might be targeted by drugs.

To date, the majority of small molecule and antibody approaches for treating COVID-19 are drugs that are either currently the subject of clinical trials or have already been through clinical trials and been approved. Much of the focus has been on several key virus or host targets, or on pathways – such as inflammation – where a drug treatment could be used as an intervention.

̽��ֱ��team used computer modelling to carry out a ‘virtual screen’ of almost 2,000 approved drugs and identified 200 approved drugs that could be effective against COVID-19. Forty of these drugs have already entered clinical trials, which the researchers argue supports the approach they have taken.

When the researchers tested a subset of those drugs implicated in viral replication, they found that two in particular – an antimalarial drug and a type of medicine used to treat rheumatoid arthritis – were able to inhibit the virus, providing initial validation of their data-driven approach.

Professor Tony Kouzarides, Director of the Milner Therapeutics Institute, who led the study, said: “By looking across the board at the thousands of proteins that play some role in SARS-CoV-2 infection – whether actively or as a consequence of infections – we’ve been able to create a network uncovering the relationship between these proteins.

“We then used the latest machine learning and computer modelling techniques to identify 200 approved drugs that might help us treat COVID-19. Of these, 160 had not been linked to this infection before. This could give us many more weapons in our armoury to fight back against the virus.”

Using artificial neural network analysis, the team classified the drugs depending on the overarching role of their targets in SARS-CoV-2 infection: those that targeted viral replication and those that targeted the immune response. They then took a subset of those involved in viral replication and tested them using cell lines derived from humans and from non-human primates.

Of particular note were two drugs, sulfasalazine (used to treat conditions such as rheumatoid arthritis and Crohn’s disease) and proguanil (an antimalarial drug), which the team showed reduced SARS-CoV-2 viral replication in cells, raising the possibility of their potential use to prevent infection or to treat COVID-19.

Dr Namshik Han, Head of Computational Research and AI at the Milner Therapeutics Institute, added: “Our study has provided us with unexpected information about the mechanisms underlying COVID-19 and has provided us with some promising drugs that might be repurposed for either treating or preventing infection. While we took a data-driven approach – essentially allowing artificially intelligent algorithms to interrogate datasets – we then validated our findings in the laboratory, confirming the power of our approach.

“We hope this resource of potential drugs will accelerate the development of new drugs against COVID-19. We believe our approach will be useful for responding rapidly to new variants of SARS-CoV2 and other new pathogens that could drive future pandemics.”

̽��ֱ��research was funded by LifeArc, the LOEWE Center DRUID, the Bundesministerium für Bildung und Forschung, the European Union’s Horizon 2020 programme, Wellcome and Cancer Research UK.

Reference
Han, N, Hwang, W, Tzelepis, K, & Schmerer, P, et al. Identification of SARS-CoV-2 induced pathways reveal drug repurposing strategies. Sci Adv; 30 June 2021

Cambridge scientists have identified 200 approved drugs predicted to work against COVID-19 – of which only 40 are currently being tested in COVID-19 clinical trials.

We hope this resource of potential drugs will accelerate the development of new drugs against COVID-19. We believe our approach will be useful for responding rapidly to new variants of SARS-CoV2 and other new pathogens that could drive future pandemics

Namshik Han

geralt

Graphical representation of COVID-19 and networks

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 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

Licence type:

Public Domain

Switching off heart protein could protect against heart failure

cjb250 — Thu, 27 May 2021 07:42:12 +0000

There is an unmet need to find drugs that can successfully improve the heart’s ability to pump blood efficiently after it’s been damaged following a heart attack. However, many drugs that make failing heart muscle contract more strongly have been deemed unsafe, leaving a huge gap in heart attack and heart failure treatment. Scientists now believe that they might have identified a new drug target – a protein called MARK4.

In research funded by the British Heart Foundation (BHF), Cambridge scientists found levels of MARK4 were elevated in mouse hearts after a heart attack. When they compared mice with and without MARK4 in the heart, they found hearts without the protein were 57 per cent better at pumping blood. This protective effect was seen 24 hours after a heart attack and lasted for the entire follow-up period of four weeks.

̽��ֱ��team identified for the first time that MARK4 fine-tunes a structural network within the heart muscle cell – called the microtubule network – that attaches to the machinery which makes heart muscle cells contract and relax. When MARK4 levels were increased after a heart attack, microtubules were tightly anchored onto the contractile machinery in the heart, causing more resistance and preventing them from functioning normally. When MARK4 levels were reduced, microtubules were loosely anchored, making it easier for the heart to contract and relax.

After a heart attack, in the heart muscle cells of mice without MARK4, the speed of contraction increased by 42 per cent and the speed of relaxation increased by 47 per cent, compared to muscle cells from mice with the MARK4 protein. They were also close to functioning at the same level as healthy heart muscle cells, showing the power of lowering levels of MARK4.

Now, the researchers suggest that drugs to switch off MARK4 could provide a promising new way to improve recovery and help the heart to pump blood more efficiently in people with failing hearts.

Dr Xuan Li, BHF Intermediate Research Fellow at ̽��ֱ�� of Cambridge BHF Centre of Research Excellence, said: “After years of research we’ve revealed an entirely new and promising way that could help the recovery of failing hearts.

“It’s early days, and we now need to test the longer-term effects of switching off MARK4. But if drugs to do that prove successful, the life-changing benefits could be seen in people with other types of heart disease as well as those who’ve had a heart attack and developed heart failure.”

Professor Metin Avkiran, Associate Medical Director at the British Heart Foundation, said: “Heart attacks are a major cause of disability worldwide - people who’ve had a major heart attack are at much greater risk of developing chronic heart failure. There are around 920,000 people living with heart failure in the UK, and we desperately need drugs to drastically improve the heart’s function in these patients.

“These findings are a positive step forward. Further research is needed to refine and test drugs that can target MARK4 before we’ll see them given to people who’ve had a heart attack and develop heart failure.”

This study was also supported by the Isaac Newton Trust, Wellcome, Cancer Research UK and the German Research Foundation.

Reference
Yu, X et al. MARK4 controls ischaemic heart failure through microtubule detyrosination. Nature; 26 May 2021; DOI: 10.1038/s41586-021-03573-5

Adapted from a press release by the British Heart Foundation.

Switching off a heart muscle protein could provide a new way for drugs to combat heart failure in people who’ve had a heart attack, according to research led by the ̽��ֱ�� of Cambridge and published in the journal Nature.

After years of research we’ve revealed an entirely new and promising way that could help the recovery of failing hearts

Xuan Li

geralt

Heart graphic

Yes

Licence type:

Public Domain

̽��ֱ��Academy of Medical Sciences announces election of new Fellows 2021

cg605 — Wed, 12 May 2021 09:39:48 +0000

̽��ֱ��Academy of Medical Sciences has elected 50 prominent biomedical and health scientists to its respected and influential Fellowship. ̽��ֱ��new Fellows have been selected for their exceptional contributions to the advancement of medical science through innovative research discoveries and translating scientific developments into benefits for patients and the wider society.

Professor Dame Anne Johnson, President of the Academy of Medical Sciences, said: “I am truly delighted to welcome these 50 new Fellows to the Academy’s Fellowship, and I offer my congratulations to each of them on their exceptional contribution to biomedical and health science. ̽��ֱ��knowledge, skill and influence that each brings to the Fellowship is the Academy’s most powerful asset.

“ ̽��ֱ��last year has clearly demonstrated the power and prowess of UK biomedical science, and I am proud of how many Fellows, new and old, have been at the forefront of the COVID-19 response in the UK and globally.

“Although it is hard to look beyond the pandemic right now, I want to stress how important it is that the Academy Fellowship represents the widest diversity of biomedical and health sciences. ̽��ֱ��greatest health advances rely on the findings of many types of research, and on multidisciplinary teams and cross-sector and global collaboration.”

Professor Franklin Aigbirhio FRSC

Professor of Molecular Imaging Chemistry, Department of Clinical Neurosciences and the Department of Chemistry, Senior Research Fellow, Magdalene College

Professor Aigbirhio’s research focuses on the development and application of new biomedical imaging technologies for clinical research in areas such as dementia, acute brain injury and hypertension. His research seeks to enable earlier detection and a greater understanding of the disorders, thereby aiding the development of new treatments. A further objective of Professor Aigbirhio’s work is to enable these new imaging technologies to be more accessible and widely applied throughout the NHS.

“It’s a pleasure and honour to be elected to this Fellowship, which I recognise is an outcome of the collaborations with many talented colleagues at Cambridge and further afield, for which I give my sincere thanks,” said Aigbirhio.

“Going forward my election to the Fellowship provides a platform to highlight the role of black researchers and participants in biomedical and health research and to increase their involvement.”

Professor Ravindra Gupta

Professor of Clinical Microbiology at the Cambridge Institute of Therapeutic Immunology and Infectious Diseases, Fellow, Homerton College

Professor Gupta has worked extensively in HIV, both at molecular and population levels, and his work demonstrating escalating global resistance led to change in WHO treatment guidelines for HIV. He led the team that demonstrated HIV cure in the ‘London Patient’ – only the second in history.

In 2020 he was named as one of the 100 most influential people worldwide by TIME Magazine. Gupta deployed his expertise in RNA virus genetics and biology during the COVID-19 pandemic to report the first evidence for immune escape of SARS-CoV-2 within an individual, defining the process by which new variants likely arise, and also reporting the first data on Pfizer BioNTech vaccine-induced antibody responses against the B.1.1.7 ‘Kent UK’ variant.

“I am honoured to have been elected to Fellowship of the Academy of Medical Sciences,” said Gupta. “ ̽��ֱ��COVID-19 pandemic has demonstrated the importance of cross-disciplinary science. 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.”

Professor Brian Huntly

Head of the Department of Haematology and Professor of Leukaemia Stem Cell Biology, Group Leader at the Wellcome – MRC Cambridge Stem Cell Institute

Professor Huntly’s research focuses on the stem cell aspects of the evolution of haematological malignancies, in particular acute myeloid leukaemia and lymphoma. His election recognises his many contributions to the understanding and treatment of blood cancers.

“I am delighted and honoured to be elected to the Fellowship of the Academy of Medical Sciences,” said Huntly. “ ̽��ֱ��Academy’s aims of bringing the best minds in biomedical research together, supporting talent, asking challenging questions and sharing our work so that all can benefit from it mirror very much our own aims here in Cambridge. Biomedical research is a hugely collaborative endeavour and I see my election as recognition of the hard work of many people who have contributed to my research and also highlighting the tremendous work we are doing at the ̽��ֱ�� of Cambridge Department of Haematology.”

Professor Adrian Liston

Senior Group Leader, Babraham Institute, Senior Research Fellow, Churchill College

Professor Adrian Liston works in the field of immunology, based around the question of the biological checkpoints that restrain immune activation. His research investigates the basis for pathological immune activation in the contexts of autoimmune diseases, primary immunodeficiencies and neuroinflammation. By understanding the genetic, molecular and cellular basis of immune checkpoint failure in these conditions, the rationale selection of therapeutics can help prevent or treat pathologies.

“This is a really wonderful recognition of the work from my team”, Liston said. “I’ve been lucky to work with an outstanding team of scientists, able to work on immune pathology from different angles – from the clinic or the lab, as an immunologist or a neuroscientist, in advanced techniques ranging from cytometry through to computational modelling. ̽��ֱ��curiosity and interdisciplinarity of the team are what has let us explore new fields and push the boundaries forwards.”

Professor Benjamin Simons FRS

Royal Society EP Abraham Professor, Department of Applied Mathematics and Theoretical Physics and Senior Group Leader of the Gurdon Institute, Group Leader at the Wellcome – MRC Cambridge Stem Cell Institute, Fellow, St John's College

As a theorist, Professor Simons has contributed to a diverse range of fields, from quantum condensed matter physics to developmental and cancer biology. His research translates concepts and approaches from statistical physics to gain predictive insights in the collective dynamics of complex systems. In biology, his studies have revealed common mechanisms of stem cell regulation, and how these programmes become subverted during the early phase of tumour growth.

Simons said: “As a theorist, and relative newcomer to the field of biomedical sciences, it is a great honour to be elected as a Fellow of the Academy of Medical Sciences.”

Cambridge scientists are among the new Fellows announced today by the Academy of Medical Sciences.

̽��ֱ��greatest health advances rely on the findings of many types of research, and on multidisciplinary teams and cross-sector and global collaboration.

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

Yes

̽��ֱ��Royal Society announces election of new Fellows 2021

cg605 — Thu, 06 May 2021 10:48:11 +0000

Over 60 outstanding scientists from all over the globe have joined the Royal Society as Fellows and Foreign Members. ̽��ֱ��distinguished group of scientists consists of 52 Fellows, 10 Foreign Members and one Honorary Fellow and were all selected for their exceptional contributions to science.

̽��ֱ��Royal Society is a self-governing Fellowship made up of the most eminent scientists, engineers and technologists from the UK and the Commonwealth. Its Foreign Members are drawn from the rest of the world.

̽��ֱ��Society’s fundamental purpose is to recognise, promote, and support excellence in science and to encourage the development and use of science for the benefit of humanity.

“ ̽��ֱ��global pandemic has demonstrated the continuing importance of scientific thinking and collaboration across borders,” said President of the Royal Society, Sir Adrian Smith.

“Each Fellow and Foreign Member bring their area of scientific expertise to the Royal Society and when combined, this expertise supports the use of science for the benefit of humanity.

“Our new Fellows and Foreign Members are all at the forefronts of their fields from molecular genetics and cancer research to tropical open ecosystems and radar technology. It is an absolute pleasure and honour to have them join us.”

̽��ֱ�� of Cambridge:

Professor Julie Ahringer FMedSci FRS

Director and a Senior Group Leader of the Gurdon Institute

Professor Ahringer has made wide-ranging contributions to molecular genetics through her work on the nematode C. elegans. She carried out the first systematic inactivation of all the genes in any animal, which pioneered genome-wide reverse genetic screening.

Her research has illuminated our understanding of the processes underlying cell polarity and gene expression. This includes showing that spindle positioning is controlled by heterotrimeric G protein signalling, discovering a connection between chromatin marking and mRNA splicing, and most recently revealing mechanisms and principles of genome organisation and gene expression regulation.

“I am honoured to be elected as a Fellow of the Royal Society,” said Ahringer. “Much of science today is done in teams, and this reflects the tremendous contributions of my past and present lab members.”

Professor Sadaf Farooqi FRCP FMedSci FRS

Wellcome Principal Research Fellow and Professor of Metabolism and Medicine, Wellcome-MRC Institute of Metabolic Science

Professor Farooqi is distinguished for her discoveries of fundamental mechanisms that control human energy homeostasis and their disruption in obesity. Farooqi discovered that the leptin-melanocortin system regulates appetite and weight in people and that genetic mutations affecting this pathway cause severe obesity. Findings by her team have directly led to diagnostic testing for genetic obesity syndromes world-wide and enabled life-saving treatment for some people with severe obesity.

Farooqi said: “As a clinician scientist, I am absolutely delighted to be elected to the Fellowship of the Royal Society. This prestigious honour recognises the work of many team members past and present, our network of collaborators across the world and the patients and their families who have contributed to our research.”

Professor Usha Goswami CBE FBA FRS

Professor of Cognitive Developmental Neuroscience, Department of Psychology, and Director of the Centre for Neuroscience in Education

Professor Goswami has pioneered the application of neuroscience to education. Her research investigates the sensory and neural basis of childhood disorders of language and literacy, which are heritable and found across languages. Goswami's research shows a shared sensory and neural basis in auditory rhythmic processing. ̽��ֱ��acoustic ‘landmarks’ for speech rhythm provide automatic triggers for aligning speech rhythms and brain rhythms, and Goswami has shown that this automatic process can be disrupted, thereby disrupting speech encoding for these children.

“It is a huge honour to be elected to the Royal Society and a wonderful acknowledgement of our research in the Centre for Neuroscience in Education,” said Goswami. “I have been interested in children's reading and language development since training as a primary school teacher, and we have used neuroscientific insights to understand the mechanisms underpinning developmental language disorders. It is fantastically rewarding for our work to be recognised in this way.”

Professor Rebecca Kilner FRS

Professor of Evolutionary Biology and Director of the ̽��ֱ�� Museum of Zoology

Professor Kilner researches the evolution of animal behaviour, and how this behaviour then affects the pace and scope of subsequent evolutionary change. Using experimental evolution, her current work investigates how quickly populations can adapt when environmental conditions change.

Kilner discovered novel ways in which social behaviour drives evolutionary change. She used elegant cross-fostering experiments in birds and insects to expose how family members exert selection on each other, and discovered hidden evolutionary conflicts between parents and their offspring, and among adults caring together for offspring.

Kilner said: “I’m astonished, honoured and delighted to be elected to the Fellowship of the Royal Society. This honour is shared with everyone I have ever worked with. Science is a team effort and I’ve been incredibly lucky to collaborate with brilliant colleagues throughout my career.”

Professor David Rowitch FMedSci FRS

Professor and Head of the Department of Paediatrics, Wellcome Trust Senior Investigator

Professor Rowitch’s basic and translational research on glial cells, comprising 90% of cells in the human brain, has been transformative. Rowitch’s established how embryonic central nervous patterning specifies myelinating oligodendrocytes through essential functions of Olig2, a study that helped initiate genetic methodologies in glial biology, and how astrocyte functional diversification is critical for support of neural circuits in the spinal cord. He has applied a developmental neuroscience perspective to better understand human neonatal brain development and white matter injury in premature infants, multiple sclerosis and leukodystrophy.

Rowitch said: “It is a great honour to be elected to the Fellowship of the Royal Society, joining many of my esteemed Cambridge, and other scientific, colleagues.”

Professor Richard Samworth FRS

Professor of Statistical Science and Director of the Statistical Laboratory

Professor Samworth has made fundamental contributions to the development of modern statistical methodology and theory. His research concerns the development of statistical methods and theory to address contemporary data challenges, often posed by the large volumes of data that are routinely collected in today's Big Data era.

“I was incredibly honoured when I found out I'd been elected a Fellow of the Royal Society,” said Samworth. “It's a real thrill to become a small part of such a respected institution.”

Professor Benjamin Simons FRS

Royal Society EP Abraham Professor, Department of Applied Mathematics and Theoretical Physics and Senior Group Leader of the Gurdon Institute

Simons said: “I am delighted to be elected to the Fellowship. I hope that my election may serve to emphasise the value of multidisciplinary research that stands at the interface between physics and the life sciences.”

Wellcome Sanger Institute:

Dr Peter Campbell FMedSci FRS, Head, Cancer, Ageing, and Somatic Mutations Programme, Wellcome Sanger Institute (and Wellcome-MRC Stem Cell Institute, ̽��ֱ�� of Cambridge).

MRC Laboratory of Molecular Biology:

Dr Christopher Tate FRS, MRC Investigator, MRC Laboratory of Molecular Biology

Dr Sjors Scheres FRS, Group Leader, Structural Studies Division, MRC Laboratory of Molecular Biology

British Antarctic Survey:

Professor Dame Jane Francis DCMG FRS, Director, British Antarctic Survey

Professor Richard Horne FRS, Head, Space Weather and Atmosphere, British Antarctic Survey

Cambridge scientists are among the new Fellows announced today by the Royal Society.

Our new Fellows and Foreign Members are all at the forefronts of their fields from molecular genetics and cancer research to tropical open ecosystems and radar technology.

Sir Adrian Smith, President of the Royal Society

Yes

Scientists develop new class of cancer drug with potential to treat leukaemia

cjb250 — Mon, 26 Apr 2021 15:00:17 +0000

Our genetic code is written in DNA, but in order to generate proteins – molecules that are vital to the function of living organisms – DNA first needs to be converted into RNA. ̽��ֱ��production of proteins is controlled by enzymes, which make chemical changes to RNA. Occasionally these enzymes become mis-regulated, being produced in over-abundance.

In a study published in 2017, a team led by Professor Tony Kouzarides from the Milner Therapeutics Institute and the Gurdon Institute at the ̽��ֱ�� of Cambridge showed how one such enzyme, METTL3, plays a key role in the development and maintenance of acute myeloid leukaemia. ̽��ֱ��enzyme becomes over-expressed – that is, over-produced – in certain cell types, leading to the disease.

Acute myeloid leukaemia (AML) is a cancer of the blood in which bone marrow produces abnormal white blood cells known as myeloid cells, which normally protect the body against infection and against the spread of tissue damage. AML proceeds rapidly and aggressively, usually requiring immediate treatment, and affects both children and adults. Around 3,100 people are diagnosed with the condition every year in the UK, the majority of whom are over 65 years of age.

Now, Professor Kouzarides and colleagues at STORM Therapeutics, a Cambridge spinout associated with his team, and the Wellcome Sanger Institute, have identified a drug-like molecule, STM2457, that can inhibit the action of METTL3. In tissue cultured from individuals with AML and in mouse models of the disease, the team showed that the drug was able to block the cancerous effect caused by over-expression of the enzyme.

Professor Kouzarides said: “Proteins are essential for our bodies to function and are produced by a process that involves translating our DNA into RNA using enzymes. Sometimes, this process can go awry with potentially devastating consequences for human health. Until now, no one has targeted this essential process as a way of fighting cancer. This is the beginning of a new era for cancer therapeutics.”

To investigate the anti-leukaemic potential of STM2457, the researchers tested the drug on cell lines derived from patients with AML and found that the drug significantly reduced the growth and proliferation of these cells. It also induced apoptosis – ‘cell death’ – killing off the cancerous cells.

̽��ֱ��researchers transplanted cells from patients with AML into immunocompromised mice to model the disease. When they treated the mice with STM2457, they found that it impaired the proliferation and expansion of the transplanted cells and significantly prolonged the lifespan of the mice. It reduced the number of leukaemic cells in the mouse bone marrow and spleen, while showing no toxic side effects, including no effect on body weight.

Dr Konstantinos Tzelepis from the Milner Therapeutics Institute at the ̽��ֱ�� of Cambridge and the Wellcome Sanger Institute added: “This is a brand-new field of research for cancer and the first drug-like molecule of its type to be developed. Its success at killing leukaemia cells and prolonging the lifespans of our mice is very promising and we hope to begin clinical trials to test successor molecules in patients as early as next year.

“We also believe that this approach – of targeting these enzymes – could be used to treat a wide range of cancers, potentially offering us a new weapon in our arsenal against these terrible diseases.”

Michelle Mitchell, Chief Executive of Cancer Research UK, said: "This work is yet another example of how our researchers strive to get new cancer treatments into the clinic and improve outcomes for cancer patients.

"Acute myeloid leukaemia is an aggressive form of cancer which grows rapidly. Treatment is required as soon as possible after diagnosis, which means research like this can't come soon enough.

"We look forward to seeing the outcomes of the phase 1 trial and the benefits it may have for AML sufferers and their families in the future."

̽��ֱ��research was supported by Cancer Research UK, the European Research Council, Wellcome, the Kay Kendall Leukaemia Fund, and Leukaemia UK.

STORM Therapeutics is a ̽��ֱ�� of Cambridge spin-out, supported by Cambridge Enterprise. It specialises in translating research in RNA epigenetics into the discovery of first-in-class drugs in oncology and other diseases.

Reference
Yankova, E, et al. Small molecule inhibition of METTL3 as a therapeutic strategy for acute myeloid leukaemia. Nature; 26 Apr 2021; DOI: 10.1038/s41586-021-03536-w

Scientists have made a promising step towards developing a new drug for treating acute myeloid leukaemia, a rare blood disorder. In a study published today in Nature, Cambridge researchers report a new approach to cancer treatment that targets enzymes which play a key role in translating DNA into proteins and which could lead to a new class of cancer drugs.

Until now, no one has targeted this essential process as a way of fighting cancer. This is the beginning of a new era for cancer therapeutics

Tony Kouzarides

National Cancer Institute

Human cells with acute myelocytic leukemia, shown with an esterase stain at 400x

Yes

Licence type:

Public Domain

HeLa: the cells that changed science

zs332 — Thu, 25 Feb 2021 09:14:42 +0000

Discover the incredible story of Henrietta Lacks, an African American woman whose cells enabled a scientific revolution and contributed to numerous incredible developments and life-saving treatments in a special book club as part of the Cambridge Festival.

Set up for life

cjb250 — Wed, 25 Nov 2020 08:13:14 +0000

We’re used to the idea that as adults we have some control over our destiny: what we eat and drink and how much we exercise can affect our health. But the risks of heart disease and diabetes can be programmed much earlier – even before we are born.