��Ī - immunotherapy

Supertroopers: CAR-T cell cancer therapy

lw355 — Wed, 16 Oct 2024 08:00:15 +0000

A life-saving cancer therapy is being scaled up in ��Ī to deliver more treatments to more patients for more cancers.

Sir Greg Winter wins the 2018 Nobel Prize in Chemistry

Anonymous — Wed, 03 Oct 2018 09:58:49 +0000

The first pharmaceutical based on this method, adalimumab, was approved in 2002 and is used for rheumatoid arthritis, psoriasis and inflammatory bowel diseases. Since then, phage display has produced antibodies that can neutralise toxins, counteract autoimmune diseases and cure metastatic cancer.

The Royal Swedish Academy of Sciences announced the 2018 Prize this morning with one half to Frances H. Arnold and the other half jointly to George P. Smith and Sir Gregory P. Winter.

The Nobel Assembly said: “The 2018 Nobel Laureates in Chemistry have taken control of evolution and used it for purposes that bring the greatest benefit to humankind. Enzymes produced through directed evolution are used to manufacture everything from biofuels to pharmaceuticals. Antibodies evolved using a method called phage display can combat autoimmune diseases and in some cases cure metastatic cancer.”

Winter, the Master of Trinity College, is a genetic engineer and is best known for his research and inventions relating to humanised and human therapeutic antibodies. Sir Gregory is a graduate of Trinity College and was a Senior Research Fellow before becoming Master.

His research career has been based almost entirely in ��Ī at the Medical Research Council’s Laboratory of Molecular Biology and the Centre for Protein Engineering, and during this time he also founded three ��Ī biotech companies based on his inventions: ��Ī Antibody Technology (acquired by AstraZeneca), Domantis (acquired by GlaxoSmithKline) and Bicycle Therapeutics.

Winter becomes the 107th Affiliate of ��Ī to be awarded a Nobel Prize. Born in 1951 in Leicester, Sir Greg studied Natural Sciences at Trinity College, ��Ī, and was awarded his PhD, also from ��Ī, in 1977.

"It came as a bit of a shock, and I felt a bit numb for a while. It's almost like you're in a different universe," said Winter, on hearing he had been jointly awarded the Prize.

"For a scientist, a Nobel Prize is the highest accolade you can get, and I'm so lucky because there are so many brilliant scientists and not enough Nobel Prizes to go around."

The University's Vice-Chancellor, Professor Stephen Toope, said: "I am thrilled to hear that Sir Greg Winter has been awarded this year’s Nobel Prize in Chemistry. Greg’s work has been vital in the development of new therapies for debilitating health conditions such as rheumatoid arthritis, and has led to breakthroughs in cancer care. These advances continue to transform the lives of people across the world.

"It gives me the greatest pleasure, on behalf of our community, to congratulate the ��Ī’s latest Nobel Prize winner.”

Patrick Maxwell, Regius Professor of Physic and Head of the School of Clinical Medicine at the ��Ī, said: “I am absolutely delighted that Sir Greg’s work has been recognised with a Nobel Prize. The work for which the prize is awarded was carried out on the ��Ī Biomedical Campus. It directly led to the power of monoclonal antibodies being harnessed for treatment of disease. His inventions really have produced silver bullets that have transformed the way medicine is practised.”

Professor Sir Alan Fersht, former Master of Gonville and Caius, collaborated with Winter on early protein engineering work. "Greg Winter is an outstandingly creative scientist of a practical bent," he said.

"He has applied his skills and imagination to the benefit of humankind to create, amongst other inventions, novel engineered antibodies that have formed the basis of a new pharmaceutical industry to treat disease and cancer. It is a thoroughly worthy Nobel Prize."

Professor Dame Carol Robinson, Royal Society of Chemistry president, said: “Today’s Nobel Prize in chemistry highlights the tremendous role of chemistry in contributing to many areas of our lives including pharmaceuticals, detergents, green catalysis and biofuels. It is a great advert for chemistry to have impact in so many areas.

“Directed evolution of enzymes and antibody technology are subjects that I have followed with keen interest; both are now transforming medicine. It would have been hard to predict the outcome of this research at the start – this speaks to the need for basic research.

“I am delighted to see these areas of chemistry recognised and congratulate all three Nobel Laureates.”

Frances H. Arnold, who also shared today's Prize, conducted the first directed evolution of enzymes, which are proteins that catalyse chemical reactions. Since then, she has refined the methods that are now routinely used to develop new catalysts. The uses of Frances Arnold’s enzymes include more environmentally friendly manufacturing of chemical substances, such as pharmaceuticals, and the production of renewable fuels for a greener transport sector.

In 1985, George Smith developed an elegant method known as phage display, where a bacteriophage – a virus that infects bacteria – can be used to evolve new proteins.

More details on previous ��Ī winners can be found here: /research/research-at-cambridge/nobel-prize

You can read more about the 2018 Nobel Prize in Chemistry here: https://www.nobelprize.org/uploads/2018/10/popular-chemistryprize2018.pdf

Sir Gregory Winter, awarded the #NobelPrize in Chemistry, has used phage display to produce new pharmaceuticals. Today phage display has produced antibodies that can neutralise toxins, counteract autoimmune diseases and cure metastatic cancer. pic.twitter.com/p5fOfo0DwJ
— The Nobel Prize (@NobelPrize) October 3, 2018

Sir Greg Winter, of the ��Ī, has been jointly awarded the 2018 Nobel Prize in Chemistry, along with Frances Arnold and George Smith, for his pioneering work in using phage display for the directed evolution of antibodies, with the aim of producing new pharmaceuticals.

It came as a bit of a shock, and I felt a bit numb for a while. It's almost like you're in a different universe.

Greg Winter on finding out about his Nobel Prize award

Sir Gregory Winter

Sir Greg Winter

Born in 1951 in Leicester, Greg studied Natural Sciences at Trinity College, ��Ī, and completed a PhD in 1977 at the Laboratory of Molecular Biology (LMB), ��Ī, where he worked on the amino acid sequence of tryptophanyl tRNA synthetase from the bacterium Bacillus stearothemophilus. Greg continued to specialise in protein and nucleic acid sequencing through post-doctoral research at the LMB and became a Group Leader in 1981.

In the 1980s, Greg became interested in the idea that all antibodies have the same basic structure, with only small changes making them specific for one target. Previously, Georges Köhler and César Milstein had won the Nobel Prize for their work at the LMB in discovering a method to isolate and reproduce individual, or monoclonal, antibodies from among the multitude of antibody proteins the immune system makes to seek and destroy foreign invaders attacking the body. However, these monoclonal antibodies had limited application in human medicine, because mouse monoclonal antibodies are rapidly inactivated by the human immune response, which prevents them from providing long-term benefits.

Greg Winter then pioneered a technique to “humanise” mouse monoclonal antibodies – a technique that was used in the development of Campath-1H by ��Ī scientists. This antibody now looks promising for the treatment of multiple sclerosis. Humanised monoclonal antibodies form the majority of antibody-based drugs on the market today and include several blockbuster antibodies, such as Keytruda, which was developed by LifeArc, the Medical Research Council’s technology transfer organisation, and works with your immune system to help fight certain cancers.

Greg then went on to develop methods for making fully human antibodies. This technique was used in the development of Humira (also known as adalimumab) by ��Ī Antibody Technology, an MRC spin-out company founded by Greg. Humira, the first fully human monoclonal antibody drug, was launched in 2003 as a treatment for rheumatoid arthritis. Today, monoclonal antibodies account for a third of all new treatments. These include therapeutic products for breast cancer, leukaemia, asthma, psoriasis and transplant rejection, and dozens more that are in late-stage clinical trials.

Greg has been presented with many awards for his work, including the 2013 Gairdner Foundation International Award, the MRC’s 2013 Millennium Medal, and the Cancer Research Institute’s William B. Coley Award in 1999. He is a Fellow of the Royal Society and of the Academy of Medical Sciences, was Deputy Director of the LMB from 2006-2011, and acting Director 2007-2008. He has been Master of Trinity College, ��Ī since 2012, and received a Knighthood for services to Molecular Biology in 2004.

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Synthetic organs, nanobots and DNA ‘scissors’: the future of medicine

lw355 — Thu, 12 Oct 2017 08:00:43 +0000

In a new film to coincide with the recent launch of the ��Ī Academy of Therapeutic Sciences, researchers discuss some of the most exciting developments in medical research and set out their vision for the next 50 years.

Professor Jeremy Baumberg from the NanoPhotonics Centre discusses a future in which diagnoses do not have to rely on asking a patient how they are feeling, but rather are carried out by nanomachines that patrol our bodies, looking for and repairing problems. Professor Michelle Oyen from the Department of Engineering talks about using artificial scaffolds to create ‘off-the-shelf’ replacement organs that could help solve the shortage of donated organs. Dr Sanjay Sinha from the Wellcome Trust-MRC Stem Cell Institute sees us using stem cell ‘patches’ to repair damaged hearts and return their function back to normal.

Dr Alasdair Russell from the Cancer Research UK ��Ī Institute describes how recent breakthroughs in the use of CRISPR-Cas9 – a DNA editing tool – will enable us to snip out and replace defective regions of the genome, curing diseases in individual patients; and lawyer Dr Kathy Liddell, from the ��Ī Centre for Law, Medicine and Life Sciences, highlights how research around law and ethics will help to make gene editing safe.

Professor Gillian Griffiths, Director of the ��Ī Institute for Medical Research, envisages us weaponising ‘killer T cells’ – important immune system warriors – to hunt down and destroy even the most evasive of cancer cells.

All of these developments will help transform the field of medicine, says Professor Chris Lowe, Director of the ��Ī Academy of Therapeutic Sciences, who sees this as an exciting time for medicine. New developments have the potential to transform healthcare “right the way from how you handle the patient to actually delivering the final therapeutic product - and that’s the exciting thing”.

Read more about research on future therapeutics in Research Horizons magazine.

Nanobots that patrol our bodies, killer immune cells hunting and destroying cancer cells, biological scissors that cut out defective genes: these are just some of technologies that ��Ī researchers are developing which are set to revolutionise medicine in the future.

The Future of Medicine

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The self-defence force awakens

cjb250 — Tue, 04 Jul 2017 16:50:17 +0000

An army of cells constantly patrols within us, attacking anything it recognises as foreign, keeping us safe from invading pathogens. But sometimes things go wrong: the soldiers mistake benign cells for invaders, turning their friendly fire on us and declaring war.

The consequences are diseases like multiple sclerosis (MS), asthma, inflammatory bowel disease, type 1 diabetes and rheumatoid arthritis – diseases that are increasing at an alarming rate in both the developed and developing worlds.

��Ī will be ramping up the fight against immune-mediated and inflammatory diseases with the opening next year of the ��Ī Institute of Therapeutic Immunology and Infectious Disease, headed by Professor Ken Smith. The Institute will work at the interface between immunity, infection and the microbiome (the microorganisms that live naturally within us). “We’re interested in discovering fundamental mechanisms that can turn the immune system on or off in different contexts, to modify, treat or prevent both inflammatory and infectious diseases,” says Smith.

But while diseases such as Crohn’s and asthma have long been understood to be a consequence of friendly fire, scientists are starting to see this phenomenon give rise to more surprising conditions, particularly in mental health.

In 2009, Professor Belinda Lennox, then at ��Ī and now at Oxford, led a study that showed that 7% of patients with psychoses tested positive for antibodies that attacked a particular receptor in the brain, the NMDA receptor. This blocked a key neurotransmitter, affecting communication between nerve cells and causing the symptoms.

Professor Alasdair Coles from ��Ī’s Department of Clinical Neurosciences is working with Lennox on a trial to identify patients with this particular antibody and reverse its effects. One of their treatments involves harnessing the immune system – weaponising it, one might say – to attack rogue warriors using rituximab, a monoclonal antibody therapy that kills off B-cells, the cells that generate antibodies.

“You can make monoclonal antibodies for experimental purposes against anything you like within a few days,” explains Coles. “In contrast, to come up with a small molecule – the alternative sort of drug – takes a long, long time.”

The first monoclonal antibody to be made into a drug, created here in ��Ī, is called alemtuzumab. It targets both B- and T-cells and has been used in a variety of autoimmune diseases and cancers. Its biggest use is in MS, where it eliminates the rogue T- and B-cells that attack the protective insulation (myelin sheath) around nerve fibres. Licensed in Europe in 2013 and approved by NICE in 2014, it has now been used in tens of thousands of MS patients.

As well as treating diseases caused by the immune system, antibody therapies are now widely used to treat cancer. And, as Professor Gillian Griffiths, Director of the ��Ī Institute for Medical Research, explains, antibody-producing cells are not the only immune cells that can be weaponised.

“T-cells are also showing great promise,” she says. “They are the body’s serial killers, patrolling, identifying and destroying infected and cancer cells with remarkable precision and efficiency.”

But cancer cells are able to trick T-cells by sending out a ‘don’t kill’ signal. Antibodies that block these signals, which have become known as ‘checkpoint inhibitors’, are proving remarkably successful in cancer therapies. “My lab focuses on what tells a T-cell to kill, and how you make it a really good killer, using imaging and genetic approaches to understand how these cells can be fine-tuned,” Griffiths explains. “This has revealed some novel mechanisms that play key roles in regulating killing.”

A second, more experimental, approach uses souped-up cells known as chimeric antigen receptor (CAR) T-cells programmed to recognise and attack a patient’s tumour.

Neither approach is perfect: antibody therapies can dampen down the entire immune system, causing secondary problems, while CAR T-cell therapies are prohibitively expensive as each CAR T-cell needs to be programmed to suit an individual. But, says Griffiths, “the results to date from both approaches are really rather remarkable”.

One of the problems that’s dogged immunotherapy trials is that T-cells only have a short lifespan. Most of the T-cells transplanted during immunotherapy are gone within three days, nowhere near long enough to defeat the tumour.

This is where Professor Randall Johnson comes in. He’s been working with a molecule (2-hydroxyglutarate), which he says has “become trendy of late”. It’s an ‘oncometabolite’, believed to be responsible for making cells cancerous, which is why pharmaceutical companies are trying to inhibit its action. Johnson has taken the opposite approach.

He’s shown that a slightly different form of the molecule plays a critical role in T-cell function: it can turn them into renewable cells that hang around for a long time and can reactivate to combat cancer. Increasing the levels of this molecule in T-cells makes them stay around longer and be much better at destroying tumours. “Rather than creating killer T-cells that are active from the start, but burn out very quickly, we’re creating an army of cells that can stay quiet for a long time, but will go into action when necessary.”

This counterintuitive approach caught the attention of Apollo Therapeutics, who recognised the enormous promise and has invested in Johnson’s work, which he carried out in mice, to see if it can be applied to humans.

But T-cells face other problems, particularly in pancreatic cancer, explains Professor Duncan Jodrell from the Cancer Research UK ��Ī Institute, which is why immunotherapy against these tumours has so far failed. The problem with pancreatic cancer is that ‘islands’ of tumour cells sit in a ‘sea’ of other material, known as stroma. As Jodrell and colleagues have shown, it’s possible for T-cells to get into the stroma, but they go no further. “You can rev up your T-cells, but they just can’t get at the tumour cells.” They are running a study that tries to overcome this immune privilege and allow the T-cells to get to the tumour cells and attack them.

Tim Eisen, Professor of Medical Oncology at ��Ī and Head of the Oncology Translational Medicine Unit at AstraZeneca, believes we can expect great advances in cancer treatment from optimising and, in some cases, combining existing checkpoint inhibitor approaches.

Eisen is working with the Medical Research Council to trial checkpoint inhibitor antibody therapies as a complement – ‘adjuvant’ – to surgery for kidney cancer. Once the kidney is removed, the drug is used to destroy stray tumour cells that have remained behind. But even antibody therapies, which are now widely used within the NHS, are not universally effective and can cause serious complications. “One of the most important things for us to focus on now is which immunotherapeutic drug or particular combination of drugs might be effective in destroying tumour cells and be well tolerated by the patient.”

T-cell therapies – and, in particular, CAR T-cell therapies – are “very exciting, futuristic and experimental,” he says, “but they’re going to take some years to come in as standard therapy.”

The problem is how to make them cost-effective. “It’s never going to be easier to engineer an individual person’s T-cells than it is to take a drug off the shelf and give it to them,” he says. “The key is going to be whether you can industrialise production. But I’m very optimistic about our ability to re-engineer processes and make it available for people in general.”

We may soon see an era, then, when our immune systems become an unstoppable force for good.

Our immune systems are meant to keep us healthy, but sometimes they turn their fire on us, with devastating results. Immunotherapies can help defend against this ‘friendly fire’ – and even weaponise it in our defence.

T-cells are the body’s serial killers, patrolling, identifying and destroying infected and cancer cells with remarkable precision and efficiency.

Gillian Griffiths

The moment when a T-cell kills

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Weight loss condition provides insight into failure of cancer immunotherapies

cjb250 — Tue, 08 Nov 2016 17:00:36 +0000

Cancer immunotherapies involve activating a patient’s immune cells to recognise and destroy cancer cells. They have shown great promise in some cancers, but so far have only been effective in a minority of patients with cancer. The reasons behind these limitations are not clear.

Now, researchers at the Cancer Research UK ��Ī Institute at the ��Ī have found evidence that the mechanism behind a weight loss condition that affects patients with cancer could also be making immunotherapies ineffective. The condition, known as cancer cachexia, causes loss of appetite, weight loss and wasting in most patients with cancer towards the end of their lives. However, cachexia often starts to affect patients with certain cancers, such as pancreatic cancer, much earlier in the course of their disease.

In research published today in the journal Cell Metabolism, the scientists have shown in mice that even at the early stages of cancer development, before cachexia is apparent, a protein released by the cancer changes the way the body, in particular the liver, processes its own nutrient stores.

“The consequences of this alteration are revealed at times of reduced food intake, where this messaging protein renders the liver incapable of generating sources of energy that the rest of the body can use,” explains Thomas Flint, an MB/PhD student from the ��Ī School of Clinical Medicine and co-first author of the study. “This inability to generate energy sources triggers a second messaging process in the body – a hormonal response – that suppresses the immune cell reaction to cancers, and causes failure of anti-cancer immunotherapies.”

“Cancer immunotherapy might completely transform how we treat cancer in the future – if we can make it work for more patients,” says Dr Tobias Janowitz, Medical Oncologist and Academic Lecturer at the Department of Oncology at the ��Ī and co-first author. “Our work suggests that a combination therapy that either involves correction of the metabolic abnormalities, or that targets the resulting hormonal response, may protect the patient’s immune system and help make effective immunotherapy a reality for more patients.”

The next step for the team is to see how this discovery might be translated for the benefit of patients with cancer.

“If the phenomenon that we’ve described helps us to divide patients into likely responders and non-responders to immunotherapy, then we can use those findings in early stage clinical trials to get better information on the use of new immunotherapies,” says Professor Duncan Jodrell, director of the Early Phase Trials Team at the ��Ī Cancer Centre and co-author of the study.

“We need to do much more work in order to transform these results into safe, effective therapies for patients, however,” adds Professor Douglas Fearon, Emeritus Sheila Joan Smith Professor of Immunology at the ��Ī and the senior author, who is now also working at Cold Spring Harbor Laboratory and Weill Cornell Medical College. “Even so, the results raise the distinct possibility of future cancer therapies that are designed to target how the patient’s own body responds to cancer, with simultaneous benefit for reducing weight loss and boosting immunotherapy.”

The research was largely funded by Cancer Research UK, the Lustgarten Foundation, the Wellcome Trust and the Rosetrees Trust.

Nell Barrie, senior science information manager at Cancer Research UK, said: "Understanding the complicated biological processes at the heart of cancer is crucial for tackling the disease - and this study sheds light on why many cancer patients suffer from both loss of weight and appetite, and how their immune systems are affected by this process. Although this research is in its early stages, it has the potential to help make a difference on both fronts - helping treat weight loss and also improving treatments that boost the power of the immune system to destroy cancer cells."

Reference
Flint, TR et al. Tumor-Induced IL-6 Reprograms Host Metabolism to Suppress Anti-tumor Immunity. Cell Metabolism; 8 Nov 2016; DOI: 10.1016/j.cmet.2016.10.010

A weight loss condition that affects patients with cancer has provided clues as to why cancer immunotherapy – a new approach to treating cancer by boosting a patient’s immune system – may fail in a substantial number of patients.

Cancer immunotherapy might completely transform how we treat cancer in the future – if we can make it work for more patients

Tobias Janowitz

Dialysis Technician Salary

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Self-renewable killer cells could be key to making cancer immunotherapy work

cjb250 — Wed, 26 Oct 2016 17:00:35 +0000

In order to protect us from invading viruses and bacteria, and from internal threats such as malignant tumour cells, our immune system employs an army of specialist immune cells. Just as a conventional army will be made up of different types of soldiers, each with a particular role, so each of these immune cells has a particular function.

Among these cells are cytotoxic T-cells – ‘killer T-cells’, whose primary function is to patrol our bodies, programmed to identify and destroy infected or cancerous cells. Scientists are now trying to harness these cells as a way to fight cancer, by growing T-cells programmed to recognise cancer cells in the laboratory in large numbers and then reintroducing them into the body to destroy the tumour – an approach known as adoptive T-cell immunotherapy.

However, this approach has been hindered by the fact that killer T-cells are short-lived – most killer T cells are gone within three days of transfer – so the army may have died out before it has managed to rid the body of the tumour.

Now, an international team led by researchers at the ��Ī has identified a way of increasing the life-span of these T-cells, a discovery that could help scientists overcome one of the key hurdles preventing progress in immunotherapy.

In a paper published today in the journal Nature, the researchers have identified a new role for a molecule known as 2-hydroxyglutarate, or 2-HG, which is known to trigger abnormal growth in tumour cells. In fact, the team has shown that a slightly different form of the molecule also plays a normal, but critical, role in T-cell function: it can influence T-cells to reside in a 'memory state’. This is a state where the cells can renew themselves, persist for a very long period of time, and re-activate to combat infection or cancer.

The researchers found that by increasing the levels of 2-HG in the T-cells, the researchers could generate cells that could much more effectively destroy tumours. Rather than expiring shortly after reintroduction, the memory state T-cells were able to persist for much longer, destroying tumour cells more effectively.

“In a sense, this means that rather than creating killer T-cells that are active from the start, but burn out very quickly, we are creating an army of ‘renewable cells’ that can stay quiet for a long time, but will go into action when necessary and fight tumour cells,” says Professor Randall Johnson, Wellcome Trust Principal Research Fellow at the Department of Physiology, Development & Neuroscience, ��Ī.

“So, with a fairly trivial treatment of T-cells, we’re able to change a moderate response to tumour growth to a much stronger response, potentially giving people a more permanent immunity to the tumours they are carrying. This could make immunotherapy for cancer much more effective.”

The research was largely funded by the Wellcome Trust.

Reference
Tyrakis, PA et al. The immunometabolite S-2-hydroxyglutarate regulates CD8+ T-lymphocyte fate; Nature; 26 Oct 2016; DOI: 10.1038/nature2016

A small molecule that can turn short-lived ‘killer T-cells’ into long-lived, renewable cells that can last in the body for a longer period of time, activating when necessary to destroy tumour cells, could help make cell-based immunotherapy a realistic prospect to treat cancer.

Rather than creating killer T-cells that are active from the start, but burn out very quickly, we are creating an army of ‘renewable cells’ that can stay quiet for a long time, but will go into action when necessary and fight tumour cells

Randall Johnson

NIAID

T lymphocyte

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Study of peanut allergy therapy shows 84 per cent success

fpjl2 — Thu, 30 Jan 2014 10:47:30 +0000

Allergy experts have found that 84 and 91 per cent of the two groups of children treated with a new form of immunotherapy could eat at least five peanuts a day.

The phase 2 trial - the largest of its kind worldwide - used oral immunotherapy (OIT), in which peanut protein is consumed in increasingly larger amounts on a regular basis to build up tolerance. The results are published today in The Lancet.

The research involved young people, aged between seven and sixteen, eating daily doses of peanut protein - starting with a tiny dose and slowly building up over four to six months.

After 6 months of OIT, 84–91% of the children could safely tolerate daily ingestion of 800 mg of peanut protein (roughly the equivalent of five peanuts), at least 25 times as much peanut protein as they could before the therapy.

Peanut allergy affects around half a million people in the UK and over 10 million people across the globe. It’s the most common cause of fatal food allergy reactions and, unlike other childhood food allergies such as cow’s milk, peanut allergy rarely goes away. People with peanut allergy risk anaphylactic shock or even death if they become accidentally exposed to peanut.

The ��Ī allergy research team, led by Dr Andrew Clark and Dr Pamela Ewan from the University’s Department of Medicine, have been leading allergy research for more than 20 years.

“Before treatment children and their parents would check every food label and avoiding eating out in restaurants,” said Clark. “Now most of the patients in the trial can safely eat at least five whole peanuts. The families involved in this study say that it has changed their lives dramatically.”

“This large study is the first of its kind in the world to have had such a positive outcome, and is an important advance in peanut allergy research,” added Ewan.
“However, further studies in wider populations are needed. It is important to note that OIT is not a treatment people should try on their own and should only be done by medical professionals in specialist settings.”

In the first part of the trial, 99 children with varying severities of peanut allergy were randomly assigned to receive either 26 weeks of OIT or peanut avoidance (the present standard of care). All the children then participated in a double-blind placebo-controlled oral food challenge during which they gradually consumed increasing amounts of peanut protein under medical supervision to determine at what level they experienced allergic symptoms. In the second part, the control group was offered 26 weeks of OIT followed by a final food challenge.

After 6 months of therapy, 24 of 39 children (62%) who received OIT in the first phase passed the challenge and tolerated a daily dose of 1400 mg of peanut protein, roughly equivalent to 10 peanuts (an amount unlikely to be encountered accidentally), compared with none of those in the control group. After the second phase, 54% tolerated the challenge. Food-allergy specific quality of life scores also improved after OIT.

Although a fifth of those receiving OIT reported adverse events, most were mild with oral itching being the most common.

Lena Barden, 11, from Histon in ��Īshire, said: “I felt like I had won a prize after I found out I had been picked for the active group. It meant a trip to the hospital every two weeks. A year later I could eat 5 whole peanuts with no reaction at all. The trial has been an experience and adventure that has changed my life and I’ve had so much fun. But I still hate peanuts!”

Thomas Baragwanath, 16, from Holbeach, Lincolnshire, said: “The trial has helped me so much. I don’t have to worry when I go out with my friends about what I’m eating and where it’s come from ‘What’s in it? Where’s it been prepared?’ - I don’t have to worry at all.”

The trial was carried out over five and a half years in the NIHR Wellcome Trust Clinical Research Facility at Addenbrooke’s, part of ��Ī University Hospitals (CUH). It was funded by the MRC-NIHR partnership through the Efficacy and Mechanism Evaluation (EME) Programme. Initial pilot work was funded by the Evelyn Trust, ��Ī.

The next step is to make peanut immunotherapy widely available to patients. Further investigation and a licensing review will be required to obtain a product licence from the regulatory authorities, which will take several years. In the meantime, ��Ī University Hospitals is planning to open a peanut allergy clinic that would make a range of services, including immunotherapy on a named patient basis, available to patients.

For further information about the development of peanut immunotherapy and when it will become available in clinics, visit www.cambridgeallergytherapy.com.

For more information on this research, please contact Adrian Ient: adrian.ient@addenbrookes.nhs.uk

Inset image: Dr Clark in the allergy clinic at Addenbrooke's Hospital

A new therapy for peanut allergy has been successful in the majority of the 99 children who took part in a clinical trial.

The trial has been an experience and adventure that has changed my life and I’ve had so much fun. But I still hate peanuts!

Lena Barden, 11, from Histon in ��Īshire

Daniella Segura

Peanuts

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�������������Ī - immunotherapy

Supertroopers: CAR-T cell cancer therapy

Sir Greg Winter wins the 2018 Nobel Prize in Chemistry

Synthetic organs, nanobots and DNA ‘scissors’: the future of medicine

The Future of Medicine

The self-defence force awakens

Weight loss condition provides insight into failure of cancer immunotherapies

Self-renewable killer cells could be key to making cancer immunotherapy work

Study of peanut allergy therapy shows 84 per cent success

��Ī - immunotherapy