Chronic heart disease poses high financial burden to low-income families

The financial burdens of long-term care for a family member with atherosclerotic cardiovascular disease (ASCVD) disproportionately affect low-income American families, even those who have insurance, found researchers at Yale University’s Center for Outcomes Research and Evaluation (CORE) and the University of Texas. The study appears in the July 3 issue of JAMA Cardiology.

Using the data from the cross-sectional Medical Expenditure Panel Survey from January 2006 through December 2015, researchers found that one in four low-income families with a member with ASCVD experience a high financial burden from the out-of-pocket healthcare costs associated with treating the chronic condition. Low-income families were also three times as likely to experience this high financial burden than middle- or high-income families with a member with ASCVD.

Additionally, 1 in 10 low-income families in the survey experienced a “catastrophic” financial burden (defined as 40% of their annual post-subsistence income), which was nine times more frequent for low-income than middle- and high-income families. For families of someone with ASCVD of any income level, the two categories of greatest healthcare spending were insurance premiums and prescription medications.

“It’s sobering to realize that the way we finance medical care places nearly one in four low-income families and millions of Americans with cardiovascular disease in a position of significant financial burden,” said Khurram Nasir, M.D., senior author, a faculty member in the Section of Cardiovascular Medicine and at Yale CORE.

“Unfortunately, private insurance—which one would expect to cushion from financial risk—actually further exacerbated the out-of-pocket costs, including medical premiums, copayments, deductibles, and essential medications,” said Nasir. “This was especially true for self-purchased private insurance, which may provide less comprehensive and equitable coverage than that afforded by most employer-based group healthcare insurance. In comparison, those covered via public insurances, especially among low-income families, were the least likely to suffer from financial hardships at the family level.”

Nasir said that these findings will certainly influence the way he approaches the “difficult conversations about the management costs of cardiovascular disease” with his own patients, but that he hopes “the provision of appropriate support services for the neediest members of our society becomes an integral component of our cardiovascular disease management programs.”

“There are many people who are not only suffering from the disruption, pain, and suffering associated with an acute illness or chronic condition but also dealing with the financial toxicity of the associated healthcare costs to them and their families,” explained Harlan Krumholz, director of Yale CORE. “We’re doing this research to put some numbers to this issue so that it can’t be ignored. These numbers will influence the policy debates about healthcare, for when people say ‘We’re doing well enough,’ or ‘Things have gotten better,’ we can show with these numbers that, no, we’re not nearly where we need to be.”

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Cardiac hybrid imaging an effective tool for predicting heart attacks

Cardiac hybrid imaging with CT and nuclear stress testing is an excellent long-term predictor of adverse cardiac events like heart attacks in patients being evaluated for coronary artery disease, according to a study published in the journal Radiology.

Coronary artery disease is a leading cause of death and disability worldwide. Invasive coronary angiography (ICA) is considered the gold standard for determining the percent of stenosis, or narrowing, due to plaque in a coronary artery. However, the degree of stenosis on ICA is not always an accurate predictor of heart attack risk because it gives no information on perfusion, or the flow of blood into the heart muscle. Inadequate perfusion, also known as ischemia, is a potential danger to the patient.

“In lesions with less than 50 percent narrowing, one in five lesions still produce an ischemia,” said study coauthor Philipp A. Kaufmann, M.D., professor and chair of nuclear medicine, and director of cardiac imaging at University Hospital Zurich in Switzerland.

Cardiac hybrid imaging combines coronary computed tomography angiography (CCTA) and myocardial perfusion imaging with single photon emission tomography (SPECT) to provide information on both stenosis and perfusion. The approach has shown promise in studies focusing on short-term observations, but information is lacking on long-term outcomes.

The research team looked at 428 patients who underwent hybrid imaging. During a median follow-up of 6.8 years, a total of 160 major adverse cardiac events, including 45 deaths, were observed in the final study population. Patients with matched findings—stenosis of 50 percent or more on CCTA with evidence of ischemia on SPECT in the area of the heart to which the blocked vessel was supplying blood—had more than five times the risk of adverse events than those with normal findings. Patients with unmatched findings, or evidence of ischemia but not in the area of the heart being fed by the stenotic artery, had three times the risk. Major adverse cardiac event rates were 21.8 percent for matched findings and 9.0 percent for unmatched—considerably higher than the 2.4 percent rate for normal findings.

The results show that cardiac hybrid imaging is an excellent long-term predictor of adverse cardiac events in patients evaluated for coronary artery disease. Dr. Kaufmann said that hybrid imaging findings could help guide treatment decisions, such as whether or not a patient should have a revascularization procedure such as bypass or angioplasty.

“In patients with multiple lesions or complex coronary anatomy, it is, in many cases, very difficult to correctly identify the culprit lesion,” he said. “In a previous multicenter trial, with hybrid imaging we were able to see that about one in five patients should be revascularized in another coronary artery than originally planned. The present study now documents the prognostic importance of the comprehensive assessment provided by hybrid imaging.”

The study supports CCTA use for an initial, noninvasive evaluation of patients with known or suspected stable coronary artery disease. No additional imaging would be necessary if the results were normal. If a lesion was evident, then clinicians could employ a nuclear scan to assess ischemia and take advantage of both modalities by fusing the results together to make a hybrid image.

“The strategy of direct referral to invasive coronary angiography without noninvasive imaging is obsolete,” Dr. Kaufmann said. “Even after documenting coronary artery disease with coronary CT angiography, we need further noninvasive evaluation before deciding upon revascularization versus medication.”

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Link to brain protein holds promise for new depression treatments

Scientists have long known that an imbalance in brain chemistry can lead to depression. University of Victoria researchers have taken this knowledge a step further, examining what happens inside the brain’s cells in order to better understand how depression occurs.

The results of that research raise the possibility of new treatments in the future for depression, which affects more than 300 million people worldwide. The health condition is a leading cause of disability worldwide and the highest risk factor for suicide.

UVic neuroscientist Lisa Kalynchuk and her team started out studying a large protein called reelin, responsible for many different cell-to-cell interactions in the brain. They found a correlation between decreased levels of reelin and increased levels of depressive symptoms, both in animals and humans.

“We know reelin is found in the brain, but it’s also found in the immune system, which is itself linked to depression,” said Kalynchuk, UVic’s associate vice-president of research, who worked on the research with doctoral student Josh Allen, post-doctoral fellow Raquel Romay-Tallon, and neuroscientist Hector Caruncho.

“We also know that certain immune factors are linked to the building blocks of cells, so we began thinking about how activities within individual cells might be implicated in depression.”

The team, based out of UVic’s Division of Medical Sciences, focused on a specific cell component, the mitochondria. These are a cell’s energy-producing machinery, providing the fuel for everything a cell does.

If mitochondria aren’t working properly, cells may not be able to produce enough reelin, which the team’s research had strongly correlated with depression.

The study’s initial outcomes are exciting, says Kalynchuk. In lab rats suffering from depressive symptoms, an infusion of reelin provided immediate relief.

“We’re trying to propose a new neurobiological theory for what causes depression, which can then be used to develop new treatments that will work more quickly, in more patients, and with fewer side-effects,” said Kalynchuk.

Kalynchuk anticipates further studies will identify other cells and systems tied to depression. These studies could lead to novel treatments, such as repairing mitochondria and other cell functions, and could eventually result in alternatives to anti-depressant drugs, which are effective in only half of patients experiencing depression.

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Prostate cancer diagnosis later for Kiwi men

New Zealand men are being diagnosed with prostate cancer later in life at a higher prostate-specific antigen (PSA) level and higher disease grade compared to men in the United States according to University of Auckland research.

Dr. Nishi Karunasinghe and colleagues at the Auckland Cancer Society Research Centre at the University’s Faculty of Medical and Health Sciences compared prostate cancer data from New Zealand and US.

The study, in conjunction with clinicians from the Auckland City Hospital and academics from the Laboratory of Human Carcinogenesis, National Cancer Institute in Maryland, has just been published in PLOS One.

In New Zealand, 408 men were recruited for the study from Auckland DHBs between 2006 and 2013. In the US, 976 men recruited and were either African American or European American.

In the US, 31-36 per cent of men have been PSA screened between 2000 and 2010. In New Zealand there was no dedicated prostate screening system in place and PSA testing or digital rectal examination or both were undertaken at varying levels (7-41 per cent) by primary care physicians

The current study shows that New Zealand men are diagnosed at a mean age of 66 years, compared to 62 years for the African Americans, and 64 years for European Americans. Even our median PSA and median grade at cancer detection are higher than that of both African and European Americans.

“The cumulative high-risk prostate cancer detection variation with increasing PSA levels shows that our high-risk prostate cancers are detected at higher PSA levels compared to the US men,” says Dr. Karunasinghe.

She says the figures are even worse among patients that smoke, either currently or in the past as smoking could impact delayed diagnosis particularly among those with certain genotypes that are more common in Māori and Pacific men. Dr. Karunasinghe says the results are also more concerning for Māori and Pacific men as more of them tend to smoke compared to European New Zealand men.

“Several factors including lower levels of PSA screening, delayed referral to specialist care and lower subsequent biopsies on those with elevated PSA levels compared to that of US could be underlying reasons for this discrepancy that require attention from the New Zealand health authorities.”

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Drugs that block structural changes to collagen could prevent lung fibrosis

Scientists have found that it is the structure of collagen, rather than the amount, that leads to the devastating condition of lung fibrosis, according to a report in the journal eLife.

The study provides the first evidence in humans that altered collagen structure affects tissue stiffness during progression of lung fibrosis and identifies a potential new target for drugs to prevent the condition.

It is widely thought that fibrosis occurs when components that hold together a tissue’s architecture (called the extracellular matrix (ECM)) build up in the tissue and lead to tissue stiffness. But recently evidence has suggested that this increased stiffness causes the build-up of yet more ECM components, resulting in a cycle that causes more scar tissue.

“We knew that stiffness is an important factor in the build-up of scar tissue in the lung,” explains lead author Mark Jones, NIHR Clinical Lecturer in Respiratory Medicine at the NIHR Southampton Biomedical Research Centre and University of Southampton, UK. “But we didn’t understand what specifically causes increased stiffness in diseased human tissue. Given that excessive build-up of collagen is considered a hallmark of fibrosis, we wanted to see whether this molecule has a role in tissue stiffness.”

They started by looking at the biological and mechanical features of lung tissue from people with lung fibrosis and compared this to healthy lung tissue. They found that the lung fibrosis samples were much stiffer than those from healthy people but, surprisingly, had similar levels of collagen.

However, when they looked at enzymes that give collagen its unique ‘cross-linked’ structure within the ECM, they found that a family of these enzymes (the LOXL family) was more abundant in the fibrosis samples. This led them to further investigate the types of collagen structures found in the fibrosis samples—which are broadly grouped into immature and mature collagen cross-links. They found that increased lung tissue stiffness only occurred where there were higher amounts of the mature cross-linked collagen and that, in these samples, the structure of each collagen building block—or fibril—was altered. This suggested that it is collagen structure, controlled by the LOXL family, that determines tissue stiffness.

Having made this discovery, the team tested whether they could alter the structure of collagen by blocking the LOXL enzymes, with a view to preventing lung fibrosis. They tested a compound called PXS-S2A that blocks LOXL-2 and LOXL-3 in lung tissue cells isolated from people with fibrosis. They found that the number of cross-linked collagen molecules declined with an increasing dose of PXS-S2A.The compound also reduced tissue stiffness, even at low concentrations, suggesting that blocking LOXL-2/LOXL-3 could be an effective way to reduce tissue stiffness.

Finally, they tested the LOXL-2/3 inhibitor in rats with lung fibrosis and found that although there was no effect on total collagen content in the lungs, the treated rats had reduced fibrosis and improved lung function, with no adverse effects.

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Economic burden of fatty liver disease in US is $32 billion annually, new study finds

Nonalcoholic fatty liver disease, or NAFLD, which affects roughly 100 million Americans, costs the United States healthcare system $32 billion annually, according to a first-of-its-kind study by Intermountain Healthcare researchers on the economic impact of the disease.

The prevalence of nonalcoholic fatty liver disease mirrors the rising trend of obesity in the United States. Globally, one in four people are living with the disease, which results when there is buildup of extra fat in liver cells that is not caused by alcohol. Nonalcoholic fatty liver disease is now the most common form of chronic liver disease.

For comparison purposes, stroke costs the United States about $34 million annually, roughly the same amount as NAFLD, according to the Centers for Disease Control and Prevention. Results of the research were presented during the Digestive Disease Week annual conference in Washington, D.C.

Identifying the economic burden of nonalcoholic fatty liver disease brings attention to the real need for readily-available treatments that will save money and lives, according to researchers.

For the study, researchers at Intermountain Medical Center in Salt Lake City examined medical records during a 10-year period (2005-2015) and identified 4,569 patients diagnosed with nonalcoholic fatty liver disease. A control group of 12,486 patients with no diagnosis of the disease was identified for comparison purposes.

Using integrated data from SelectHealth, the health insurance arm of Intermountain Healthcare, researchers analyzed the healthcare costs per patient and overall costs per year in both groups. The costs were then extrapolated to a national scale, which indicated an economic burden of $32 billion annually for the U.S.

Costs of the disease include:

  • Inpatient hospitalization and outpatient appointments
  • Emergency room visits
  • Organ transplantation
  • Mortality
  • Medical procedures or new diagnoses
  • New medications or changes to existing medications

“Our research is the first real-world estimate on actual healthcare utilization associated with nonalcoholic fatty liver disease in the United States,” said Richard Gilroy, MD, medical director of the hepatology and liver transplant program at Intermountain Medical Center. “The results highlight the major problem we face today and the potential tsunami we will encounter if we choose to not address the causes of NAFLD now.”

Nonalcoholic fatty liver disease occurs when fat is stored in liver cells. As the amount of fat in the liver increases, the disease progresses to nonalcoholic steatohepatitis, and is marked by liver inflammation and scarring that may cause irreversible damage. Left unaddressed, it can lead to liver failure. People who are overweight, have diabetes or who have a family member with liver disease should consider getting screened for nonalcoholic fatty liver disease.

“We are already in an era of escalating healthcare costs and we see what was an unrecognized and infrequent disease in the 1980s, is now a major epidemic that will further drive costs in years to come,” said Dr. Gilroy.

“Looking at the financial implications specifically, the results of the study also highlight the potential reduction in healthcare costs if treatments do become available,” added Michael Charlton, MD, with the Intermountain Medical Center transplant program and author of the new research study. “We currently have validated a predictive risk score that uses basic lab values and a patient’s medical history to allow us to predict which patients are at a higher risk of developing liver damage due to the disease.”

Researchers plan to use the prediction tool to get upstream of the problem at a population level by intervening with nutritional and therapeutic options, which may include clinical trials, before the patient reaches end-stage liver disease.

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Expecting a stressful day may lower cognitive abilities throughout the day

There may be some truth to the saying “getting up on the wrong side of the bed,” according to Penn State researchers who say starting your morning by focusing on how stressful your day will be may be harmful to your mindset throughout the day.

The researchers found that when participants woke up feeling like the day ahead would be stressful, their working memory—which helps people learn and retain information even when they’re distracted—was lower later in the day. Anticipating something stressful had a great effect on working memory regardless of actual stressful events.

Jinshil Hyun, a doctoral student in human development and family studies, said the findings suggest that the stress process begins long before a stressful event occurs.

“Humans can think about and anticipate things before they happen, which can help us prepare for and even prevent certain events,” Hyun said. “But this study suggests that this ability can also be harmful to your daily memory function, independent of whether the stressful events actually happen or not.”

Martin Sliwinski, director of Penn State’s Center for Healthy Aging, said working memory can affect many aspects of a person’s day, and lower working memory can have a negative impact on individuals’ daily lives, especially among older adults who already experience cognitive decline.

“A reduced working memory can make you more likely to make a mistake at work or maybe less able to focus,” Sliwinski said. “Also, looking at this research in the context of healthy aging, there are certain high stakes cognitive errors that older adults can make. Taking the wrong pill or making a mistake while driving can all have catastrophic impacts.”

While previous research has examined how stressful events can affect emotion, cognition and physiology, not as much has been done on the effects of anticipating stressful events that haven’t yet happened in the context of everyday life.

The researchers recruited 240 racially and economically diverse adults to participate in the study. For two weeks, the participants responded seven times a day to questions prompted from a smartphone app: once in the morning about whether they expected their day to be stressful, five times throughout the day about current stress levels, and once at night about whether they expected the following day to be stressful. The participants also completed a working memory task five times a day.

Hyun said that while laboratory studies have the benefit of controlling the participants’ experience during the study, the use of smartphones to collect data as the participants went about their daily lives had benefits, as well.

“Having the participants log their stress and cognition as they went about their day let us get a snapshot of how these processes work in the context of real, everyday life,” Hyun said. “We were able to gather data throughout the day over a longer period of time, instead of just a few points in time in a lab.”

The researchers found that more stress anticipation in the morning was associated with poorer working memory later in the day. Stress anticipation from the previous evening was not associated with poorer working memory.

Sliwinski said the findings—recently published in the Journals of Gerontology: Psychological Sciences—show the importance of a person’s mindset first thing in the morning, before anything stressful has happened yet.

“When you wake up in the morning with a certain outlook for the day, in some sense the die is already cast,” Sliwinski said. “If you think your day is going to be stressful, you’re going to feel those effects even if nothing stressful ends up happening. That hadn’t really been shown in the research until now, and it shows the impact of how we think about the world.”

The researchers said the results open the door for possible interventions that can help people predict when their cognition may not be optimal.

“If you wake up and feel like the day is going to be stressful, maybe your phone can remind you to do some deep breathing relaxation before you start your day,” Sliwinski said. “Or if your cognition is at a place where you might make a mistake, maybe you can get a message that says now might not be the best time to go for a drive.”

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Conservative management up for low-risk prostate CA in veterans

(HealthDay)—Among U.S. veterans with low-risk prostate cancer, use of conservative management increased from 2005 to 2015, according to a research letter published online June 5 in the Journal of the American Medical Association.

Stacy Loeb, M.D., from Manhattan Veterans Affairs Medical Center in New York City, and colleagues examined treatment patterns for veterans diagnosed with low-risk prostate cancer from January 2005 through November 2015. The use of conservative management was explored over time, stratified by age. Data were included for 125,083 veterans with low-risk prostate cancer.

The researchers found that of the 59,941 veterans (48 percent) who received conservative management, 37,717 and 22,224 (30 and 18 percent), respectively, received watchful waiting and active surveillance. From 2005 to 2015, there was an increase in utilization of conservative management among men aged younger than 65 years (27 to 72 percent) and among those aged 65 years or older (35 to 79 percent). The increase was mainly due to more use of active surveillance from 2005 to 2015 (4 to 39 percent in men aged <65 years and 3 to 41 percent in men aged ≥65 years).

“Utilization of conservative management has increased significantly among U.S. veterans with low-risk prostate cancer, suggesting a substantial reduction in overtreatment during the past decade,” the authors write.

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What To Do If Your Workplace Is Impacting Your Mental Health

Whether we like it or not, most of us spend the majority of our lives at work.

What happens within that cubicle or behind that counter can impact us in many ways, particularly when it comes to our mental health. In fact, a new study has found that high job strain is associated with an increased risk of developing common mental illnesses like depression and anxiety. And it’s a vicious circle – mental illness has now become the leading cause of absence in the workplace, with research finding that 25 per cent of workers have taken days off due to stress. So what can we do to better our mental wellbeing in the workplace? We turned to psychologist Breanna Jayne Sada, from online psychologist network Lsyn, to find out. 

The signs you might be struggling 

“For employees, self satisfaction is often found through accomplishments and success at work, and if you are burdened by poor mental health which impacts on your productivity and performance, you in turn may see a reduction in your self esteem further impacting on your mental health,” Breanna explains.  

According to Breanna, the signs that something is not quite right at work include:

Next steps

If you’re feeling this way, there are are a number things you can do. First of all, set clear boundaries between your work and the rest of your life. 

“Switching off when you leave work is really important, make time to do things you love outside of work, and spend quality time with friends and family,” Breanna says.

Leaving on time and ensuring you take a lunch break are also important.

“If you are spending extra time in an already unhealthy environment, spending more time there will only further increase your feelings of distress,” Breanna adds. 

Methods that improve your physical health, will also have a significant impact on your mental wellbeing. 

“We know how great exercise is for our mental health and scheduling a session before or after work will not only help your mind, but a session with a punching bag may also ensure you don’t knock out someone in the office,” Breanna says. 

She also recommends asking for help when you need it.

“Those around you might not realise you are in need of help, so don’t be afraid to speak up.”

What if a boss or colleague is to blame?

If work-related stress is more than just the workload and you’re dealing with a problem colleague or a bad boss, it can be a lot harder to remain positive each day. 

“Very few of us get through our careers without having a difficult boss or colleague… research has shown that most people leave a job because of their managers, not workplace stress,” Breanna explains.

So what can we do about it? Breanna advises to deal with the problem person head on.

“Appeal to their motives, figure out what motivates them… and use language and behaviour that appeals to their objectives.”

As hard as it might be, don’t let their negativity bring you down.

“You will not gain anything from being on their bad side or exposing their shortcomings, this will only tarnish your own reputation,” she says. Try to celebrate their success and always remain pleasant when dealing with them.

“Always take the high road, and don’t be intimidated by a bully”.

And if you’re the one in charge?

Whilst most companies aim to foster positive, inclusive work environments, stress is contagious and may spread throughout the workplace if not properly addressed. For employers, Breanna says it’s important to consider the mental health of your employees.

“If they are mentally unwell, they are not as productive. Do not assume a mental illness is something that develops outside of the workplace – an unhealthy work environment, poor colleague relationships, and workplace incidents can all contribute to poor mental health and mental illness.”

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Cell ‘chatter’ discovery could open clinical trial opportunity for fatal childhood brain tumour

Brain tumours are hard to treat. But even this is a harrowing understatement for some forms of the disease.

Diffuse intrinsic pontine glioma (DIPG) is one such example. These rare brain tumours almost exclusively affect children, and they’re invariably fatal.

“Almost all children with DIPG sadly die within a couple of years of diagnosis,” says Professor Chris Jones from the Institute of Cancer Research, London, a Cancer Research UK-funded expert on the disease.

“There aren’t any effective treatments.”

One of the main reasons that the outlook for DIPG is so poor is down to where it grows in the brain. These tumours start in the brainstem, which lies at the base of the brain and hooks up the spinal cord with deeper brain regions. This crucial piece of machinery controls many of the body’s vital processes, such as breathing and our heart beat.

That means surgery – a cornerstone treatment for many cancers – is out of the question. Drugs are also notoriously ineffective for brain tumours, because most are shut out by the protective blood brain barrier. DIPG is no exception, and Jones says that no chemotherapies have convincingly shown a beneficial effect, despite many different clinical trials testing a variety of drugs. This leaves radiotherapy as the only option, but it isn’t a cure.

“Radiotherapy is the only treatment that’s been shown to have any effect on DIPG,” he says.

“Usually patients will be given a drug as well in an attempt to find something that works, but the cancer usually comes back within 6-9 months.”

Difficult by name and by nature

This situation leaves a pressing need for new treatments. Behind every cancer treatment is research, but that’s where the nature of DIPG presents scientists with yet another challenge.

Studying samples of patients’ tumours in the lab helps scientists understand the biology of the disease and leads them towards new treatments. But for many years biopsy samples weren’t taken from children with DIPG, because the procedure was too dangerous due to the tumours’ delicate position. That left scientists with a shortage of tissue to work with and learn from.

“DIPG is diagnosed by imaging, so questions were raised over the need for invasive and risky biopsies. That set back the collection of tissue for study,” Jones says.

But the field was reawakened in 2012 when a new way of taking biopsy samples with a thin needle was shown to be safe. Using this brain tissue, and also samples taken from children who have died from the diseases, scientists can now grow DIPG cells in the lab and in mice, boosting research efforts and uncovering the genes and molecules that may fuel the disease.

And Jones’ latest research, published in Nature Medicine, is testament to how important these samples are.

More than meets the eye

Scientists already knew that DIPG doesn’t grow as a uniform bundle of cells. Instead, these tumours resemble a diverse patchwork of cells with distinct genetic and molecular fingerprints.

“Down the microscope it looks like adult glioblastoma,” says Jones. “So, a variety of drugs designed against the biology of this tumour type have been tried in DIPG patients, but none of them have worked.”

The tumour isn’t limited to the brainstem either; it spreads throughout the brain, seeding new patchworks of cancer cells in distant regions.

Armed with this knowledge, Jones and his team studied the brains of children who had died of DIPG, comparing the genetic features of different populations of cells. By creating a map of their DNA faults, the scientists showed that spreading cells move early in the tumour’s development, although they tended to grow slower than those in the original tumour.

Next, they grew up samples taken from the brains of children with DIPG into balls of cells in the lab, observing their behaviour and characteristics.

“We found that they were very different; some grew very fast while others didn’t, and some could spread extensively when others couldn’t,” Jones says.

But when they mixed cells together, those that previously had weaker characteristics became more aggressive. “We think these different populations are cooperating, helping one another to grow or spread,” he adds.

This helping hand seems to come from molecular signals that the cancer cells send out, since bathing cells in the liquid that more aggressive cells had been grown in also boosted their ability to divide and spread.

Trials and tribulations

Alongside revealing the intricacies of the disease, Jones hopes that his research brings new, smarter ways to treat DIPG.

“This work opens up a new way of thinking about how we may treat tumours,” he says. “If we can better understand what these different populations of cells are doing, and how they’re interacting, maybe we can identify which ones are the key to go after with drugs.”

With support from Cancer Research UK, the next stage of this research aims to find out precisely that. Hopefully, discoveries that emerge could make their way towards patients sooner, as Jones is also part of a Cancer Research UK-funded clinical trial that’s treating children with DIPG based on the biology of their disease. Because the study is designed to be adaptive, meaning the treatment a child receives on the trial isn’t set in stone, promising new treatments being developed could be added in and tested out in the trial as it progresses.

Supporting this type of research is exactly why we’ve made brain tumours a top priority, and why we’re committing an extra £25 million over the next 5 years specifically for research in this area.

“New, targeted drugs are now starting to make their way into clinical trials for DIPG,” says Jones.

“We don’t yet know whether they’ll work, but ultimately we want to combine targeted drugs with other treatments, such as radiotherapy or immunotherapy.

“For the first time, these kinds of trials are now opening for DIPG.”

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