Early identification of stroke type could be key to harnessing the benefits of very early in-ambulance blood pressure lowering treatment in patients with suspected acute stroke, according to new research.
The findings were presented at the 10th European Stroke Organisation Conference in Basel, Switzerland and simultaneously published in the New England Journal of Medicine.1
Professor Craig Anderson, Director of Global Brain Health at The George Institute for Global Health and lead investigator on the study, said that although more research was needed, the results provided a potential pathway to improving outcomes in patients with the most deadly type of stroke.
“Our study shows clear benefits from administering early blood pressure lowering treatment to patients with intracerebral haemorrhage in the ambulance, although overall there was no difference in outcome from this early intervention for all patients with suspected stroke.
“In fact, in patients with a final diagnosis of ischaemic stroke, it actually worsened their outcome, so the ability to make a reliable diagnosis at this early stage is key to harnessing the benefits of very early blood pressure treatment.”
The Intensive ambulance-delivered blood pressure reduction in hyper-acute stroke trial (INTERACT4) was a multicentre, randomised, open-label, blinded-outcome study conducted across dozens of ambulance services in China.
2404 ambulance-assessed patients with suspected acute stroke causing a motor deficit within two hours of onset and elevated systolic blood pressure (≥150mmHg) were randomly assigned to immediate blood pressure-lowering (target 130-140mmHg) or usual blood pressure (BP) management in hospital.

The pre-hospital ambulance-initiated BP reduction group with haemorrhagic stroke had a 30% lower likelihood of a poor functional outcome whereas the group with cerebral ischaemia had an equivalent 30% higher likelihood of a poor functional outcome, when compared to patients with these stroke types who received usual care BP management upon arrival at the hospital.
Overall, the effects of pre-hospital BP reduction had a balanced benefit and harm effect so that there was no overall difference in the functional outcome between those who received the usual care in all the stroke patients. Between-group rates of serious adverse events were similar.
Around 80 percent of strokes worldwide are ischaemic, caused by the loss of blood flow to an area of the brain due to a blockage in a blood vessel, leading to a loss of neurological function.1
Intracerebral haemorrhage (ICH) represents over a quarter of all cases of stroke and occurs when blood leaks out of a blood vessel into the brain tissue. ICH is the most deadly type of stroke, with up to one third of patients dying in 30 days, and it is more common in China where the study was conducted.2
“All treatments for acute stroke are highly time dependent — brain cells die rapidly when deprived of oxygen. But knowing the best treatment approach to take before being able to identify the type of stroke a patient has experienced, is difficult without brain imaging,” Professor Anderson said.
“The results do not support in-ambulance administration of blood pressure lowering treatment in patients with suspected acute stroke — that is clear.

“But in the last few years, we’ve seen the introduction of mobile stroke ambulances equipped with a CT scanner and other diagnostic tools that aim to identify cases of ischaemic stroke for early administration of clot-busting treatment.
“But our results do support the case for in-ambulance treatment to be administered to patients with haemorrhagic stroke as well.
“In the meantime, while acute stroke treatment happens in the hospital, quicker diagnosis and swift action as soon as the patient arrives at the emergency department is critical to preserving brain function.”
References GBD 2019 Stroke Collaborators. Global, regional, and national burden of stroke and its risk factors, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019. The Lancet Neurology 2021;20:795-820 Wu S, et al. Stroke in China: advances and challenges in epidemiology, prevention and management. The Lancet Neurology 2019;18:394-405

Disc-related back pain may one day meet its therapeutic match: gene therapy delivered by naturally derived nanocarriers that, a new study shows, repairs damaged discs in the spine and lowers pain symptoms in mice.
Scientists engineered nanocarriers using mouse connective-tissue cells called fibroblasts as a model of skin cells and loaded them with genetic material for a protein key to tissue development. The team injected a solution containing the carriers into damaged discs in mice at the same time the back injury occurred.
Assessing outcomes over 12 weeks, researchers found through imaging, tissue analysis, and mechanical and behavioral tests that the gene therapy restored structural integrity and function to degenerated discs and reduced signs of back pain in the animals.
“We have this unique strategy that’s able to both regenerate tissue and inhibit some symptoms of pain,” said co-senior author Devina Purmessur Walter, associate professor of biomedical engineering at The Ohio State University.
Though there is more to learn, the findings suggest gene therapy could offer an effective and long-lasting alternative to opioids for the management of debilitating back pain.
“This can be used at the same time as surgery to actually boost healing of the disc itself,” said co-senior author Natalia Higuita-Castro, associate professor of biomedical engineering and neurological surgery at Ohio State. “Your own cells are actually doing the work and going back to a healthy state.”
The study was published online recently in the journal Biomaterials.

An estimated 40% of low-back pain cases are attributed to degeneration of the cushiony intervertebral discs that absorb shocks and provide flexibility to the spine, previous research suggests. And while trimming away bulging tissue from a herniated disc during surgery typically reduces pain, it does not repair the disc itself — which continues to degenerate with the passage of time.
“Once you take a piece away, the tissue decompresses like a flat tire,” Purmessur Walter said. “The disease process continues, and impacts the other discs on either side because you’re losing that pressure that is critical for spinal function. Clinicians don’t have a good way of addressing that.”
This new study builds upon previous work in Higuita-Castro’s lab, which reported a year ago that nanocarriers called extracellular vesicles loaded with anti-inflammatory cargo curbed tissue injury in damaged mouse lungs. The engineered carriers are replicas of the natural extracellular vesicles that circulate in humans’ bloodstream and biological fluids, carrying messages between cells.
To create the vesicles, scientists apply an electrical charge to a donor cell to transiently open holes in its membrane, and deliver externally obtained DNA inside that converts to a specific protein, as well as molecules that prompt the manufacture of even more of a functional protein.
In this study, the cargo consisted of material to produce a “pioneer” transcription factor protein called FOXF1, which is important in the development and growth of tissues.
“Our concept is recapitulating development: FOXF1 is expressed during development and in healthy tissue, but it decreases with age,” Purmessur Walter said. “We’re basically trying to trick the cells and give them a boost back to their developmental state when they’re growing and at their healthiest.”
In experiments, mice with injured discs treated with FOXF1 nanocarriers were compared to injured mice given saline or mock nanocarriers and uninjured mice.

Compared to controls, the discs in mice receiving gene therapy showed a host of improvements: The tissue plumped back up and became more stable through production of a protein that holds water and other matrix proteins, all helping promote range of motion, load bearing and flexibility in the spine. Behavioral tests showed the therapy decreased symptoms of pain in mice, though these responses differed by sex — males and females showed varying levels of susceptibility to pain based on the types of movement being assessed.
The findings speak to the value of using universal adult donor cells to create these extracellular vesicle therapies, the researchers said, because they don’t carry the risk of generating an immune response. The gene therapy also, ideally, would function as a one-time treatment — a therapeutic gift that keeps on giving.
“The idea of cell reprogramming is that you express this transcription factor and the cell is then going to convert to this healthier state and stays committed to that healthier phenotype — and that conversion is not normally transient,” Higuita-Castro said. “So in theory, you would not expect to have to re-dose significantly.”
There are more experiments to come, testing the effects of other transcription factors that contribute to intervertebral disc development. And because this first study used young adult mice, the team also plans to test the therapy’s effects in older animals that model age-related degeneration and, eventually, in clinical trials for larger animals known to develop back problems.
Higuita-Castro, director of advanced therapeutics and engineering in the College of Medicine Davis Heart and Lung Research Institute and a core faculty member of Ohio State’s Gene Therapy Institute, and Purmessur Walter, an investigator in Ohio State’s Spine Research Institute and director of the Spinal Therapeutics Laboratory in the College of Engineering, are co-principal investigators on National Institutes of Health grants funding this research.
Additional co-authors include co-first authors Shirley Tang and Ana Salazar-Puerta, Mary Heimann, Kyle Kuchynsky, María Rincon-Benavides, Mia Kordowski, Gilian Gunsch, Lucy Bodine, Khady Diop, Connor Gantt, Safdar Khan, Anna Bratasz, Olga Kokiko-Cochran, Julie Fitzgerald and Benjamin Walter, all of Ohio State; Damien Laudier of Icahn School of Medicine at Mount Sinai; and Judith Hoyland of the University of Manchester.
Ohio State has filed a patent application on nonviral gene therapy for minimally invasively treating painful musculoskeletal disorders.

If you tend to do other things or get distracted while eating dinner, you may be running the risk of over-consuming everyday pleasures later, possibly because the distraction caused you to enjoy yourself less, according to research published by the American Psychological Association.
The study looked at how distraction affects “hedonic consumption,” or buying and using products and experiences because they make us feel good and not necessarily because we need them.
“On any given day, a person may take great pleasure from one or more of these activities, yet people often consume more hedonic goods than they want or than is good for them,” said lead author Stephen Lee Murphy, PhD, of Ghent University.
One reason for this overconsumption may be distraction, according to Murphy. When people are distracted while engaged in a hedonic activity, research suggests they are likely to experience less enjoyment from it than if they were fully focused. That may lead to feelings of dissatisfaction and drive more consumption to compensate for that shortfall.
The research was published in the Journal of Personality and Social Psychology.
To better understand the role of distraction in overconsumption, the researchers first conducted an experiment involving 122 participants (mostly female and mostly between the ages of 18 and 24) who reported on how much they expected to enjoy their lunch before eating it. They were then asked to eat their lunch under one of three conditions: no distraction, moderate distraction (watching a video), and high distraction (playing Tetris). After lunch, participants reported on their actual enjoyment, satisfaction, desire for further gratification and amount consumed. They also reported on their snacking later in the day.
Participants who ate while distracted reported lower enjoyment and satisfaction, which was associated with increased snacking afterward and a more general desire for further gratification.

The researchers believe that this proposed effect, which they called “hedonic compensation,” likely applies to other activities beyond eating. For example, people who are distracted while watching a movie or playing a game may be more likely to engage in additional consumption (e.g., checking social media) to compensate for a diminished enjoyment of the original activity.
The researchers also followed 220 participants aged 18 to 71 (again mostly female) for a week to investigate this broader effect, beyond food. Participants filled out seven brief surveys per day via their smartphones regarding their hedonic consumption, distraction and satisfaction. As with the food-based experiment, researchers found that when people were distracted during consumption, they were likely to enjoy a product less than they hoped, felt less satisfied, and experienced an elevated need for further gratification.
“Overconsumption often results due to a lack of self-control,” said Murphy. “However, our findings suggest overconsumption may also often be driven by the simple human desire to reach a certain level of enjoyment from an activity. When distraction gets in the way, it’s likely we may try to compensate by consuming more.”
Murphy and his colleagues plan to conduct further research to replicate and confirm the existence of a hedonic compensation effect. If additional research confirms the effect, they have plans to apply interventions that could help people pay more attention to their consumption experiences in an effort to lower the likelihood of overconsumption.
“By understanding the key drivers of hedonic overconsumption, we can develop strategies to help prevent its occurrence,” said Murphy.

If spiders use their webs like a large external eardrum, researchers reasoned, perhaps spider silk could be the basis for a powerful listening device.Engineers and scientists have an enduring fascination with spider silk. Similar to typical worm silk that makes for comfy bedsheets, but much tougher, the material has inspired the invention of lighter and more breathable body armor and materials that could make airplane components stronger without adding weight. Researchers are even using examples drawn from spider webs to design sensitive microphones that can one day be used to treat hearing loss and deafness and to improve other listening devices.Spiders use their webs like enormous external eardrums. A team of scientists from Binghamton University and Cornell University reported in 2022 that webs allow arachnids to detect sound from 10 feet away.When you hear a sound through your ear, what you’re really experiencing are changes in air pressure that cause your eardrum to vibrate. This is how microphones work: by mimicking the human ear and vibrating in response to pressure.Spider webs serve a similar purpose but use a different mechanism.A spider moves its body in response to sounds moving through particular parts of its web.Zhou et al.Instead of vibrating when hit by a wave of pressure like a stick hitting a drumhead, they move with the flow of the air being displaced. Air is a fluid medium “like honey,” said Ronald Miles, a professor of mechanical engineering at Binghamton. Humans navigate this environment without noticing much resistance, but silk fibers are buffeted about by the velocity of the viscous forces in air.Dr. Miles couldn’t help but wonder if this principle could lead to a new kind of microphone.“Humans are kind of arrogant animals,” he said. “They make devices that work like they do.” But he wondered about building a device to be more like a spider and sense “sound with the motion of the air.”We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Published41 minutes agoShareclose panelShare pageCopy linkAbout sharingThe daily fear of running out of attention deficit hyperactivity disorder (ADHD) medication feels like a “doomsday clock”, according to one man.Ryan Hendry, 30, has been affected by medication shortages and told the BBC he has about two weeks’ supply left.The Department of Health (DoH) said the UK-wide disruption should be resolved by September.But consultant paediatrician Dr Matthew McConkey said the shortages are having a “profound effect” on patients. Ryan said that every morning when he takes his medication it is like a “doomsday clock” is counting down the days until he will run out.”You go seven days left, six days left, five days left, this is time to panic. “Four days left, franticness. Two days left, every panic button has been pressed.”Ryan has been dealing with the shortages for around seven months. He works full time and said he and his partner “can’t just pause our lives running about” trying to get medication. ‘Isolating and frustrating’Ryan said that pharmacies he has spoken to don’t know when they will get the medication in.”It’s scary because I don’t know what happens if I go over that cliff edge,” he said.”It’s incredibly isolating and frustrating.”ADHD isn’t taken seriously, Ryan believes, and “there’s an attitude of ‘it’s just naughty children, it can be managed, these tablets aren’t really needed'”. However he has been on stimulants to deal with his ADHD for almost 20 years and stressed that once you find the right medication “it’s important that supply is maintained”. ‘Dire’ warning for adults waiting for ADHD diagnosisNumber of people seeking ADHD assessments risesWomen tell of their ADHD diagnosis struggles‘I ration my ADHD medication to save money'”On days I haven’t taken them I feel extremely agitated, panicky and it’s almost short-term memory loss,” he said.”I go to make myself a cup of tea and come back a few hours later in the kitchen there will be a cup with teabag and a boiled kettle but I won’t have made a cup of tea.”Other effects of stopping medication include mental fatigue and migraines, with symptoms worsening as time passes.”Hospitalisation would be a real possibility – my dosage is quite high and NHS guidelines says sudden withdrawal is to be avoided.”What is ADHD?ADHD is a neurodevelopmental condition that can cause memory issues, problems concentrating, focusing or sitting still.According to the NHS, people with ADHD can seem restless, may have trouble concentrating and may be impulsive. Most cases are diagnosed in childhood, but the UK-wide ADHD Foundation said it has seen a 400% rise in adults going to them compared to before the Covid-19 pandemic.What medication is available for ADHD?There are four different ADHD medications available which fall into two categories – stimulants and non-stimulants – with most people taking stimulants. Reasons for the shortages, according to Dr McConkey, include an increase in global demand for the medication and manufacturing issues.Image source, Getty ImagesWhile Dr McConkey works with children, he said he is also aware of the impact of the shortages on adults.”I’ve heard of some adults asking their bosses to make reasonable adaptations because of the fact they aren’t having access to medication and in some cases those people have lost their jobs,” he said. “So it has very profound effects on people who don’t have access to medication that was doing them a huge benefit.”For Dr McConkey’s patients, who are predominantly under 18, not taking medication affects their schooling, exam preparation, exam performance and mental health. “It can cause anxiety, it can cause low self-esteem, and more flashpoints with family, friends and schools, colleagues,” he said.Dr McConkey added that mortality for people with ADHD is twice that of the general population.”If you are a young driver there is an increased risk of accidents without medication. There is a risk of substantial mood disorder. “I am contacted daily by parents at their wits’ end trying to source medication for their child.”‘Light at the end of the tunnel’However Dr McConkey said he had conversations with some pharmacists last week who said that at least one medication shortage has ended – so he feels there is now “light at the end of the tunnel”. The DoH said that while supply disruptions of some ADHD treatments have now been resolved, there are “some ongoing disruptions across the UK affecting various preparations and strengths of these medicines”.The video game prescribed by doctors to treat ADHDThe spokesperson added: “Currently, the anticipated resupply dates of products affected by these disruptions are expected to resolve between May and September 2024, depending on the strength and preparation affected.”Guidance, which has been agreed by the UK administrations, has been issued to healthcare professionals in Northern Ireland addressing the medicines affected by these disruptions.”More on this story’Dire’ warning for adults waiting for ADHD diagnosisPublished2 April 2023‘I ration my ADHD medication to save money’Published23 May 2022The video game prescribed by doctors to treat ADHDPublished11 July 2022

Giving teenagers the HPV vaccine is cutting cases of cervical cancer by 90%, figures for England show.

“I consider the drugs available on the marked today as the first generation of weight-loss drugs. Now we have developed a new type of weight-loss drug that affects the plasticity of the brain and appears to be highly effective.”
So says Associate Professor and Group Leader Christoffer Clemmensen, from the Novo Nordisk Foundation Center for Basic Metabolic Research at the University of Copenhagen, who is senior author of the new study, which has been published in the scientific journal Nature.
In the study, Christoffer Clemmensen and colleagues demonstrate a new use of the weight loss hormone GLP-1. GLP-1 can be used as a ‘Trojan Horse’ to smuggle a specific molecule into the brain of mice, where it successfully affects the plasticity of the brain and results in weight loss.
“The effect of GLP-1 combined with these molecules is very strong. In some cases, the mice lose twice as much weight as mice treated with GLP-1 only,” Christoffer Clemmensen explains.
This means that future patients can potentially achieve the same effect with a lower dosage. Moreover, the new drug may be an alternative to those who do not respond well to existing weight-loss drugs.
“Our studies in mice show side effects similar to those experienced by patients treated with the weight loss drugs available on the market today, including nausea. But because the drug is so effective, we may be able to lower the dosage and thus mitigate some of the side effects in the future — though we still don’t know how humans respond to the drug,” he says.
Testing of the new weight loss drug is still in the so-called preclinical phase, which is based on studies with cells and on experimental animals. The next step is clinical trials with human participants.

“We already know that GLP-1-based drugs can lead to weight loss. The molecule that we have attached to GLP-1 affects the so-called glutamatergic neurotransmitter system, and in fact, other studies with human participants suggest that this family of compounds has significant weight loss potential. What is interesting here is the effect we get when we combine these two compounds into a single drug,” Christoffer Clemmensen stresses.
The drug must undergo three phases of clinical trials on human participants. According to Christoffer Clemmensen, it can therefore take eight years before the drug could be available on the market.
The brain defends excessive body weight
Christoffer Clemmensen and colleagues developed an interest in molecules that are used to treat chronic depression and Alzheimer’s disease.
The molecules block a receptor protein called the NMDA receptor, which play a key role in long-term changes in brain connections and have received scientific attention within fields of learning and memory. Drugs targeting these receptors will strengthen and/or weaken specific nerve connections.
“This family of molecules can have a permanent effect on the brain. Studies have demonstrated that even a relative infrequent treatment can lead to persistent changes to the brain pathologies. We also see molecular signatures of neuroplasticity in our work, but in this case in the context of weight loss,” he explains.

The human body has evolved to protect a certain body weight and fat mass. From an evolutionary perspective, this has probably been to our advantage, as it means that we have been able to survive periods of food scarcity. Today, food scarcity is not a problem in large parts of the world, where an increasing part of the population suffers from obesity.
“Today, more than one billion people worldwide have a BMI of 30 or more. This makes it increasingly relevant to develop drugs to aid this disease, and which can help the organism to sustain a lower weight. This topic is something we invest a lot of energy in researching,” says Christoffer Clemmensen.
A Trojan Horse smuggles small molecule modulators of neuroplasticity into appetite-regulating neurons
We know that drugs based on the intestinal hormone GLP-1 effectively target the part of the brain that is key to weight loss, namely the appetite control centre.
“What is spectacular — on a cellular level — about this new drug is the fact that it combines GLP-1 and molecules that block the NMDA receptor. It exploits GLP-1 as a Trojan Horse to smuggle these small molecules exclusively into the neurons that affect appetite control. Without GLP-1, the molecules that target the NMDA receptor would affect the entire brain and thus be non-specific,” says Postdoc Jonas Petersen from the Clemmensen Group, who is the first author on the study and the chemist who synthesized the molecules.
Non-specific drugs are often associated with severe side effects, which has previously been seen in drugs for treating different neurobiological conditions.
“A lot of brain disorders are difficult to treat, because the drugs need to cross the so-called blood-brain barrier. Whereas large molecules like peptides and proteins generally have difficulties accessing the brain, many small molecules have unlimited access to the entire brain. We have used the GLP-1 peptide’s specific access to the appetite control centre in the brain to deliver one of these otherwise non-specific substances to this region only,” Christoffer Clemmensen says and adds:
“In this study, we have focused on obesity and weight loss, but in fact this is a completely new approach for delivering drugs to specific parts of the brain. So, I hope our research can pave the way for a whole new class of drugs for treating conditions like neurodegenerative diseases or psychiatric disorders.”
What is neuroplasticity?
The plasticity of the brain, also known as neuroplasticity, is the brain’s ability to restructure itself by forming new neural connections. This ability allows the brain to adjust to new experiences, learn new skills, absorb new information and recover from injuries.
Neuroplasticity is found in several levels of the nervous system and can be anything from microscopic changes in the structure and function of individual neurons to major changes such as the formation of new neural connections or reorganisation of areas of the brain.
Christoffer Clemmensen, along with postdoc Jonas Petersen and a former scientist from the University of Copenhagen (Anders Klein), have co-founded of the biotech company Ousia Pharma, which is a spinout company from the University of Copenhagen. The company is continuing to develop the medical concept presented in this study for the treatment of severe obesity.

Records from nearly 30,000 nursing home residents indicate that blood pressure medications more than double the risk of life-threatening bone fractures, according to Rutgers Health research.
The authors of the study, which appears in JAMA Internal Medicine, said the increased risk stems from the medications’ tendency to impair balance, particularly when patients first stand up and temporarily experience low blood pressure that deprives the brain of oxygen. Interactions with other drugs and low baseline balance in many nursing home patients compound the problem.
“Bone fractures often start nursing home patients on a downward spiral,” said Chintan Dave, academic director of the Rutgers Center for Health Outcomes, Policy and Economics and lead author of the study. “Roughly 40 percent of those who fracture a hip die within the next year, so it’s truly alarming to find that a class of medications used by 70 percent of all nursing home residents more than doubles the bone-fracture risk.”
While many patients have high enough blood pressure that the benefits of treatment outweigh these dangers, “Such patients require careful observation, particularly when treatment begins, and that’s not happening,” Dave said. “Caregivers think of blood pressure medication as very low risk, and that’s not true in this patient population.”
Dave’s team analyzed Veterans Health Administration data from 29,648 elderly patients in long-term care facilities from 2006 to 2019. Researchers compared the 30-day risk of fractures to the hip, pelvis, humerus (upper arm) radius or ulna (forearm) for patients who began using blood pressure medications with similar patients who didn’t. To maximize the chance that medication use — and not some other factor — drove the different outcomes, they adjusted for more than 50 baseline covariates, such as patient demographics and clinical history.
The 30-day fracture risk for residents who began blood pressure medication was 5.4 per 100 people per year and 2.2 per 100 people per year for patients who took no blood pressure medication.
Further analysis showed drug usage predicted particularly elevated fracture risk in certain subgroups. Patients with dementia, systolic blood pressure above 139 (the first number in the blood pressure reading), diastolic blood pressure above 79 (the second number) or no recent use of blood pressure medication all experienced at least triple the fracture risk of unmedicated patients.
About 2.5 million Americans live in nursing homes or assisted living facilities. Up to 50 percent suffer falls in any given year, and up to 25 percent of those falls result in serious injury.
The Rutgers Health study indicates that blood pressure medication causes many of those falls and that a combination of less medication and better support could significantly reduce the problem.
“Caregivers can’t strike this right balance of risk and reward if they don’t have accurate data about the risks,” Dave said. “I hope this study gives them information that helps them serve their patients better.”

Compared with pre-surgical (neoadjuvant) chemotherapy alone, adding perioperative immunotherapy — given before and after surgery — significantly improved event-free survival (EFS) in patients with resectable early-stage non-small cell lung cancer(NSCLC), according to researchers from The University of Texas MD Anderson Cancer Center.
Results from the Phase III CheckMate 77T study were published today in the New England Journal of Medicine. At a median follow-up of 25.4 months, the median EFS with chemotherapy alone was 18.4 months, while the median had not yet been reached for patients receiving perioperative nivolumab, meaning EFS was prolonged significantly over the control group. These results correspond to a 42% reduction in risk of disease progression, recurrence, or death for those receiving the perioperative combination.
This data was first presented at the 2023 European Society for Medical Oncology (ESMO) Congress.
Patients who received the perioperative nivolumab-based regimen also saw significantly higher rates of pathological complete response (pCR), defined as no tumor remaining at surgery, compared with those who received chemotherapy alone (25.3% vs. 4.7%). Rates of major pathological response (MPR), less than or equal to 10% of viable tumor cells remaining at time of surgery, were also higher in patients who received perioperative immunotherapy (35.4% vs. 12.1%).
“This study builds on the standard-of-care neoadjuvant chemoimmunotherapy treatment and supports perioperative nivolumab as an effective approach that reduces the risk of lung cancer relapse,” said principal investigator Tina Cascone, M.D., Ph.D., associate professor of Thoracic/Head & Neck Medical Oncology. “These findings add to evidence that the perioperative immunotherapy path gives patients with operable lung cancer an opportunity to live longer without their cancer returning.”
Roughly 30% of patients diagnosed with NSCLC have operable disease, meaning their tumor can be removed by a surgical operation. While many of these patients can be potentially cured by surgery, more than half will experience cancer recurrence without additional therapy. Chemotherapy given either before or after surgery provides only a minimal survival benefit.
The randomized, double-blind CheckMate 77T trial, which began in 2019, included more than 450 NSCLC patients over the age of 18 from around the globe. Participants were randomized to treatment with either neoadjuvant nivolumab with chemotherapy followed by surgery and adjuvant nivolumab, or neoadjuvant chemotherapy and placebo followed by surgery and adjuvant placebo
The data showed no new safety signals with the perioperative nivolumab regimen and is consistent with the known safety profiles of individual agents. Grade 3-4 treatment-related side effects were observed in 32% and 25% of patients receiving the perioperative combination or control therapy, respectively. Surgery-related adverse events occurred in 12% of patients in both treatment arms.

These findings add to recent success seen with neoadjuvant nivolumab plus chemotherapy in NSCLC. In March 2022, the Phase III CheckMate 816 study led to FDA approval of nivolumab combined with platinum-based chemotherapy.
“I am enthusiastic about the initial findings of the study,” Cascone said. “Looking ahead, it will be critical to identify patient and disease characteristics that will tell us who can potentially be cured with neoadjuvant chemoimmunotherapy only and who will benefit from more intensified treatment strategies.”
The CheckMate 77T study was sponsored by Bristol Myers Squibb.

6 days agoHugh Pym