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Study finds lack of racial diversity in cancer drug clinical trials

Study finds lack of racial diversity in cancer drug clinical trials

New research published this week in JAMA Oncology has found a lack of racial and ethnic diversity in clinical trials for cancer drugs.

The study—conducted by researchers from UBC, the University of Texas MD Anderson Cancer Center, the Fred Hutchinson Cancer Center in Seattle and Baylor University in Texas—raises concerns about the effectiveness of cancer drugs in some patients, especially since genetic differences may affect how well a patient responds to a drug.

The researchers found that fewer than eight per cent of cancer drug trials reported participation from the four major races in the United States — white, Asian, black and Hispanic — between 2008 and 2018. Black and Hispanic patients were particularly underrepresented at 22 per cent and 44 per cent, respectively, considering their populations’ incidence of cancer.

“Our findings show that the science might not be applicable to the population that’s going to receive the medications,” said the study’s lead author, Dr. Jonathan Loree, assistant professor in the department of medicine, division of medical oncology. “If patients are going to be receiving the drug, we need to know that it’s going to work for them with the same effectiveness that’s seen in the trial.”

Loree cited an example of a medication used to treat lung cancer that showed mediocre trial results in the global population, but exhibited incredible success with young women who had never smoked in a study in Asia due to a genetic mutation that’s common in this population.

The researchers found that both reporting about race in trials and enrolment rates had changed minimally over the decade.

For this study, Loree and colleagues reviewed all reported trials supporting U.S. Food and Drug Administration (FDA) oncology drug approvals granted between July 2008 and June 2018. They scrutinized 230 trials with a total of 112,293 participants. They calculated the U.S. population-based cancer estimates by race using National Cancer Institute and U.S. Census data.

Although the researchers used U.S. data, Loree said the findings are relevant in Canada, as well. Pharmaceutical companies typically apply for drug approvals through the FDA first, because it serves the largest market, and then submit to the European Medicines Agency and Health Canada. The trials considered in the approvals are usually the same.

“One thing particularly relevant to the Canadian context is that we weren’t able to analyze the participation of Native Americans in trials because there were only 13 patients reported out of a total of 112,000 participants,” Loree said. “That’s shocking and definitely shows an area where improvement is needed.”

The researchers are now looking at whether clinical trials represent the same gender ratio as the general population to ensure the drugs are effective in all people.

Materials provided by University of British Columbia

Pancreatic Cancer

High insulin production may contribute to pancreatic cancer

UBC scientists have demonstrated for the first time a causal link between high insulin levels and pancreatic cancer.

In a study published today in Cell Metabolism, researchers lowered insulin levels in mice predisposed to developing pancreatic cancer and found that these lower levels protected the mice against developing the disease.

The findings hold promise for early detection and prevention of pancreatic cancer in humans.

“Pancreatic cancer can be tricky to detect and is too often diagnosed at a late stage, making it one of the deadliest cancers,” said James Johnson, senior co-author of the study, a professor and member of the Diabetes Research Group in the Life Sciences Centre at UBC. “The five-year-survival rate is less than five per cent, and incidences of the disease are increasing alongside obesity.”

Hyperinsulinemia, a condition in which the body produces more insulin than it needs to control blood sugar levels, is increasingly common, found in more than one-third of obese adults, and can be modulated by diet and lifestyle factors.

“The link between hyperinsulinemia has actually been found across multiple cancers, including breast cancer, but pancreatic cancer has the strongest link,” said Janel Kopp, senior co-author and associate professor in the department of cellular and physiological sciences. “Our experiment is the first to directly test that hypothesis, in any cancer, in any animal model.”

For the study, lead author and PhD student Anni Zhang crossed a strain of mice that is genetically incapable of developing a rise in insulin with a strain of mice predisposed to developing pancreatic cancer. These and the control mice were fed a diet for a year that was known to increase insulin levels and promote pancreatic cancer. At the end of the yearlong study, the mice with slightly reduced insulin levels were shown to be protected from the start of pancreatic cancer.

“No matter whether you look at the entire pancreas, lesions or tumours, less insulin meant reduced beginnings of cancer in the pancreas,” Johnson said.

“We don’t see a reason why this wouldn’t be generalizable to other cancers,” added Kopp, noting they used the same mutation as 90 per cent of pancreatic cancers in people. “Our mouse models are extremely relevant to people.”

In addition to examining the relationship between insulin levels and other cancers, the scientists would like to investigate whether decreasing excess insulin produced by the body could positively influence later stages of pancreatic cancer. They plan to work with colleagues at BC Cancer on human clinical trials.

Journal Reference: Cell Metabolism

Materials provided by the University of British Columbia

smartphone lock revelas age

How you lock your smartphone can reveal your age: UBC study

Older smartphone users tend to rely more on their phones’ auto lock feature compared to younger users, a new UBC study has found. They also prefer using PINs over fingerprints to unlock their phones.

Researchers also found that older users are more likely to unlock their phones when they’re stationary, such as when working at a desk or sitting at home.

Konstantin Beznosov

Konstantin Beznosov

The study is the first to explore the link between age and smartphone use, says Konstantin Beznosov, an electrical and computer engineering professor at UBC who supervised the research.

“As researchers working to protect smartphones from unauthorized access, we need to first understand how users use their devices,” said Beznosov. “By tracking actual users during their daily interactions with their device, we now have real-world insights that can be used to inform future smartphone designs.”

The analysis also showed that older users used their phone less frequently than younger users. For every 10-year interval in age, there was a corresponding 25 percent decrease in the number of user sessions. In other words, a 25-year-old might use their phone 20 times a day, but a 35-year-old might use it only 15 times.

The study tracked 134 volunteers, ranging from 19 to 63 years of age, through a custom app installed on their Android phones. For two consecutive months, the app collected data on lock and unlock events, choice of auto or manual lock and whether the phone was locked or unlocked while in motion. The app also recorded the duration of user sessions.

The study also found gender differences in authentication choices. As they age, men are much more likely to rely on auto locks, as opposed to manually locking their devices, compared to women. In terms of overall use, women on average use their phone longer than men, with women in their 20s using their smartphones significantly longer than their male peers. However, the balance shifts with age, with men in their 50s logging longer usage sessions than women of the same age.

While the study didn’t look at the reasons for these behaviours, Beznosov says the findings can help smartphone companies design better products.

“Factors such as age should be considered when designing new smartphone authentication systems, and devices should allow users to pick the locking method that suits their needs and usage patterns,” he said, adding that future research should look into other demographic factors and groups of participants, and explore the factors involved in authentication decisions.

The study was presented at last month’s CHI Conference on Human Factors in Computing Systems in Glasgow, Scotland.

Materials provided by the University of British Columbia

Testing Blood Sugar Levels or Diabetes

UBC study holds promise for novel and safe treatment for Type 2 diabetes

Reducing a specific protein in the fat cells of mice not only prevents onset of Type 2 diabetes but also appears to reverse the disease in the animals, researchers at the University of British Columbia and Sweden’s Karolinska Institute have found.

Researchers also found that levels of the protein, called CD248, were higher in the fat cells of people with diabetes, no matter their shape or size. When obesity-associated diabetes was reversed through weight loss, CD248 levels decreased to normal range, they found. 

The findings, published today in EBioMedicine, a journal of The Lancet, hold promise for the development of a new and safe treatment for Type 2 diabetes.

Type 2 diabetes is a chronic inflammatory condition that affects how the body metabolizes sugar. Obesity, smoking and a lack of physical activity are major risk factors for developing Type 2 diabetes, in which the body either resists the effects of insulin—a hormone that regulates the movement of sugar into cells—or doesn’t produce enough insulin to maintain normal glucose levels. Complications of Type 2 diabetes are common and include heart and blood vessel disease, stroke, kidney damage, poor skin wound healing, increased risk of infections and a higher incidence of some types of cancer.“It’s early days but modifying the amount or function of CD248, in fat cells seems to be a promising new treatment strategy, an approach that may be eventually used by itself or with other drugs,” said co-senior author Dr. Edward Conway, professor in the faculty of medicine at UBC, director of the Centre for Blood Research and recipient of a Canada Research Chair in Endothelial Cell Biology. “With more than 60 million adults diagnosed in North America and Europe and many more with pre-diabetes, the number of people with Type 2 diabetes is staggering. And as the incidence of obesity increases, more effective treatments for Type 2 diabetes are urgently needed.”

For the study, UBC researchers collaborated with a renowned diabetes research group at the Karolinska Institute, led by the co-senior investigator Dr. Mikael Rydén, a professor and senior consultant, unit of endocrinology and lipid laboratory. Rydén and his PhD student, Paul Petrus, used human genetic approaches to study fat biopsies of patients who were thin, obese, diabetic and not diabetic.

Their findings showed that CD248 protein levels in the fat might provide a better marker compared to current measures of how sensitive a person is to insulin, which may be used to better predict those who are at risk of developing Type 2 diabetes and to measure the effectiveness of treatments.

“The levels of CD248 in human fat are strongly associated with clinical measures of Type 2 diabetes risk. This, together with experiments in which we reduced the CD248 gene in human fat cells, suggested that this approach improved fat tissue function, which could be relevant in future treatments of Type 2 diabetes,” said Rydén. “We then contacted Dr. Conway, who had studied the effects of CD248 gene knock-out in mice, focusing on its role in tissues other than fat.”

To gain a better understanding of how CD248 works, the UBC researchers used genetically modified mice that lack CD248 only in the fat cells. They found that the lack of this protein in those cells protected the animals from developing Type 2 diabetes, even when fed high-fat diets that made them obese. Having no CD248 in their fat cells did not appear to be associated with negative health outcomes, suggesting that therapies that reduce CD248 to treat diabetes are likely to be safe.

“A most interesting finding was that the insulin sensitivity of mice that already have diabetes can be improved by reducing CD248 levels in the fat cells, even while they remain obese,” said Conway. “While these discoveries are exciting, we are still some distance from a new treatment. To reach that goal, our immediate goals are to understand how CD248 works so that safe and effective drugs that reduce the protein’s levels or that interfere with its function can be designed.”

The study was co-authored by scientists from the University of Turku in Finland, the Université de Sherbrooke in Quebec and members of the diabetes research group at UBC. It was supported by grants from the Canadian Institutes of Health Research, the Natural Sciences and Engineering Research Council of Canada, a Killam Scholarship, Morphotek Inc., along with funding from the Swedish Research Council, Novo Nordisk Foundation, Swedish Diabetes Foundation and the Diabetes Research Program at the Karolinska Institute.

Materials provided by the University of British Columbia

inhaler copd

Steroids can reduce lung cancer risk in COPD patients

For many people with chronic obstructive pulmonary disease or COPD, a steroid inhaler is a daily necessity to keep their airways open and help them to breathe. Now, a new UBC analysis shows that these medicated devices may also reduce patients’ risk of lung cancer by as much as 30 per cent.

The researchers evaluated 10 years’ worth of medical and pharmacy data for 39,676 adults in British Columbia who were diagnosed with COPD, including 994 people who were later diagnosed with lung cancer. They compared outcomes for people who took inhaled steroids versus those who used beta agonists, another class of drugs used to treat COPD.

Beta agonists, which work by relaxing muscles in the lungs to widen the airways, are the first choice of treatment for COPD. But doctors will often prescribe steroids, which reduce the number of inflammatory cells called eosinophils in the lungs, for more severe cases.

“Results showed that if you had COPD and consistently used a steroid inhaler, your chances of getting lung cancer were between 25 per cent and 30 per cent lower compared to people who took other treatments,” said study author Larry Lynd, a professor who leads the Collaboration for Outcomes Research and Evaluation project at UBC’s faculty of pharmaceutical sciences and an associate member of the faculty of medicine.

COPD is a group of diseases, including emphysema and chronic bronchitis, that hamper airflow to the lungs and cause serious long-term disability and early death. Although there is no cure, treatments can help manage the disease.

“In Canada alone, more than 700,000 people have been diagnosed with COPD,” said study co-author Don Sin, a professor of medicine at UBC and the Canada Research Chair in COPD. “These results highlight the importance of identifying which of those patients may be at the highest risk for lung cancer and may benefit from therapy with inhaled steroids.”

The study, recently published in European Respiratory Journal, is limited by its reliance on administrative data, which limits the scope of data available for analysis, and the fact that COPD diagnosis was based solely on prescription records. For the next stage in this research, the researchers plan to do studies to understand how steroids reduce lung cancer risk in COPD patients.

“More work is clearly needed to understand the exact nature of the relationship between lung cancer risks and steroid use,” said Lynd. “Over the next few months, we will find out which COPD patients would benefit the most from inhaled steroids.”

Materials provided by University of British Columbia

A calorimeter designed by UBC researchers that is capable of detecting anomalous heat at high temperatures and high pressures. Photo credit: Phil Schauer

Scientists revisit the cold case of cold fusion

Four academic laboratories partner with Google to explore how materials science can help make fusion more accessible

Scientists from the University of British Columbia, the Massachusetts Institute of Technology, the University of Maryland, the Lawrence Berkeley National Laboratory, and Google are conducting a multi-year investigation into cold fusion, a type of benign nuclear reaction hypothesized to occur in benchtop apparatus at room temperature.

A progress report published today in Nature publicly discloses the group’s collaboration for the first time.

The group, which included about 30 graduate students, postdoctoral researchers and staff scientists, has not yet found any evidence of the phenomenon, but they did find important new insights into metal-hydrogen interactions that could impact low-energy nuclear reactions. The team remains excited about investigating this area of science and hopes their ongoing journey will inspire others in the scientific community to contribute data to this intriguing field.

Operating as a “peer group” with a stringent internal review process, the team started out by vetting previous claims of cold fusion, which have not been pursued in mainstream academic research for the past 30 years. If cold fusion could be realized, the heat released by this process might offer an attractive option for decarbonizing the global energy system.

The collaborative effort has produced nine peer reviewed publications and three arXiv posts. The team continues to search for a reproducible reference experiment for cold fusion.

Read the full perspective in Nature“Revisiting the cold case of cold fusion,” Curtis P. Berlinguette (UBC), Yet-Ming Chiang (MIT), Jeremy N. Munday (UMD), Thomas Schenkel (Berkeley Lab), David K. Fork, Ross Koningstein and Matthew D. Trevithick (Google).

Quotes

“We need a fundamentally new energy technology that can be scaled within the span of a human lifetime. Achieving this goal requires scientists to be afforded the opportunity to do daring work. This program provided us with a safe environment to take the long shot – given the profound impact this could have on society, we should remain open to it even if there is an unknown probability of success.”

Curtis Berlinguette, principal investigator and professor of chemistry and chemical and biological engineering at the University of British Columbia (UBC).

“If any research project ever met the definition of high-risk, high-reward, this would be the one. Electrochemistry can create interesting states of matter. If those states of matter help us in the search for new clean energy sources, all the better.”

Yet-Ming Chiang, principal investigator and Kyocera professor of materials science and engineering at the Massachusetts Institute of Technology (MIT).

“This program explores several intriguing and overlooked problems with the potential for significant impact. Even if we do not find a better way to produce clean energy, our discoveries along the way will still shed new light onto a variety of areas in science and engineering.”

Jeremy Munday, principal investigator and associate professor of electrical and computer engineering at the University of Maryland (UMD).

“We shouldn’t shy away from looking into areas that may have been written off. Not frivolously – but with new ideas and a recognition that there are things we don’t know and that we should be curious about.”

Thomas Schenkel, principal investigator and interim director of the Accelerator Technology and Applied Physics Division at the Lawrence Berkeley National Laboratory (Berkeley Lab).

“Google cares deeply about data and sustainability. When we looked into the scientific record of cold fusion, we found some bold claims, but not a lot of current, credible data. Given the positive impact cold fusion could have if true, we saw an opportunity to help the situation. We are impressed with the research team that rose to this challenge, and are pleased with what has been accomplished so far.”

Matt Trevithick, senior program manager at Google Research.

Materials provided by University of British Columbia