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Uninterrupted Sedentary Time Linked to Increased Cancer Risk

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Data from more than 91 000 participants in the UK Biobank who wore activity monitors for seven days revealed an association between prolonged sedentary behaviour and the risk of cancer death

Each additional hour of prolonged, uninterrupted sedentary behaviour in a person’s day is associated with a 9% higher risk of cancer death, according to a study published July 2nd in the open access journal PLOS Medicine by Frederick Ho of the University of Glasgow, UK, and colleagues.

Previous studies have shown that spending more total time on sedentary behaviour, such as sitting, reclining or lying down while awake, is linked to poorer health outcomes. However, most sedentary behaviour guidelines focus on total time spent sedentary, rather than whether that time is accumulated in many short intervals or fewer prolonged intervals.

In the new study, researchers analysed data from 91 292 UK Biobank participants who had worn activity monitors for 7 days and were followed for a median of 12.38 years afterward. Activity was categorised as either prolonged sedentary (bouts of at least 30 minutes with at least 90% of time sedentary), interrupted sedentary behaviour (which lasted less than 30 minutes or was broken up with more than 10% non-sedentary time), or varying degrees of physical activity.

Prolonged sedentary behaviour was associated with a higher risk of cancer mortality (HR 1.09; 95% CI 1.06, 1.11), overall cancer incidence, obesity-related cancers (such as oesophageal, liver, kidney, pancreatic, colorectal, breast, ovarian, and thyroid cancers), and type 2 diabetes-related cancers. Interrupted sedentary behaviour showed the opposite pattern, associated with lower risk across all outcomes. Replacing one hour per day of prolonged sedentary behaviour with light physical activity was associated with a 12% lower risk of cancer death (HR 0.88; 95% CI 0.79, 0.99).

As a single-cohort study of UK Biobank volunteers, who have known health volunteer bias and higher physical activity levels than the general UK population, the findings may not be generalisable and do not prove causality. The researchers also had no data on the context of sedentary behaviour, such as whether it was during work or driving.

“Our findings suggest that the health effects of sedentary behaviour may depend not only on total sedentary time, but also on whether that time is accumulated in prolonged bouts or interrupted by activity,” the authors say. “This pattern is biologically plausible: experimental studies have shown that interrupting prolonged sitting with short bouts of activity can improve metabolic responses compared with uninterrupted sitting.”

The authors add, “Current health guidelines focus heavily on moderate or vigorous exercise, but our findings show that light movement shouldn’t be ignored. Moving forward, clinical trials will help us move beyond blanket advice and develop personalised strategies for breaking up sitting time.”

Provided by PLOS

Categories : CancerTags :

Early-onset Colorectal Cancer Risks Also Linked to Parental Characteristics

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Photo by LOGAN WEAVER | @LGNWVR on Unsplash

A recent study found that factors such as a person’s birthweight, sex, ethnicity, and father’s age may affect the risk of being diagnosed with colorectal cancer at a young age. The findings are published by Wiley online in CANCER, a peer-reviewed journal of the American Cancer Society.

In the study of 1,221 people born and diagnosed with early-onset colorectal cancer – defined as being diagnosed before age 50 – in California in 1988–2021 and 61 050 matched individuals without cancer, men had a 34% higher risk of early-onset colorectal cancer compared with women. Also, Hispanic ethnicity was linked with a 43% higher risk compared with white ethnicity. Having a foreign-born mother was associated with a 15% lower risk of early-onset colorectal cancer. Among females, every 500g increase in birthweight was associated with a 10% increase in early-onset colorectal cancer risk and having a father aged 35 years or older was associated with a 56% higher risk. Investigators did not observe any links between early-onset colorectal cancer risk and other demographic, birth, and parental characteristics.

Additional research is needed to uncover potential mechanisms behind these associations.

“Evaluating demographic, birth, and parental characteristics is important in understanding what’s causing the rising incidence of early-onset colorectal cancer,” said lead author Sunny Siddique, MPH, PhD, of the Yale School of Public Health. “Our findings warrant future studies aimed to understand the mechanisms through which factors such as male sex, Hispanic ethnicity, birthweight, maternal birthplace, and paternal age may influence risk of early onset colorectal cancer.”

Source: Wiley

Categories : CancerTags :

Which Genes Contribute to Early-onset Breast Cancer in Black Women?

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Photo by National Cancer Institute

Black women experience disproportionately elevated risks of developing and dying from early-onset breast cancer. New research published by Wiley online in CANCER, a peer-reviewed journal of the American Cancer Society, reveals the genes that are most likely to be mutated to contribute to these increased risks.

In the study of 686 young Black women diagnosed in Florida and Tennessee with invasive breast cancer at age 50 or younger in 2005–2018, genetic testing showed that 15.3% of the women carried a gene variant with a suspected link to breast and/or ovarian cancer, with most occurring in the BRCA1 and BRCA2 genes and fewer in PALB2, ATM, and other genes. A family history of breast cancer was common in women with mutations in BRCA1, BRCA2, and PALB2. Triple-negative breast cancers (one of the most aggressive forms) were most often seen in women with BRCA1 mutations. Also, most of the women with BRCA1 mutations were diagnosed at or below age 40, whereas the age at diagnosis was more evenly distributed up to age 50 for women with variants in the other genes.

The study’s findings point to the importance of breast cancer genetic testing for young Black women, a group that is less likely to receive such screening compared with other racial and ethnic groups. Such tests could identify women most likely to benefit from more frequent screening and preventive measures to safeguard their health.

“We must test at-risk women across all populations – testing is essential to personalise treatment strategies and enable life-saving prevention for future cancers, and it may empower at-risk family members to get tested so they too can benefit from this information,” said senior author Tuya Pal, MD, of Vanderbilt University Medical Center. “Equitable access to inherited cancer testing ensures that all women, regardless of race, can benefit from precision medicine and take control of their genetic health.”

Source: Wiley

Categories : Substance UseTags :

Even Low Alcohol Consumption Linked to Cancer and Heart Risks

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Study provides much-needed benchmark with finding that alcohol consumption is associated with increased risk above one drink per day for both men and women

Photo by Pavel Danilyuk on Pexels

Even what many consider to be moderate drinking is linked to an increased risk of death, disability, and chronic diseases such as cancer and heart disease, according to a new study published in the Journal of Studies on Alcohol and Drugs.

“This study provides the most comprehensive US estimates to date of lifetime risks of alcohol-attributable mortality and morbidity, showing that even moderate levels of consumption increase the risk of premature death and disability,” said study co-author Katherine M. Keyes, PhD, professor of Epidemiology at Columbia University Mailman School of Public Health. “No protective effect of drinking was observed even at low levels,” noted Keyes, whose research focuses on alcohol use and other substances epidemiology across the life course.

The findings show mortality risk from alcohol of 1 in 25 for people who consumed an average of 14 drinks per week. In contrast, drinking up to 7 drinks per week was associated with only minimally elevated risks for most conditions.

“Even low levels of alcohol use come with health risks,” says first study author Kevin Shield, PhD, an associate professor at the University of Toronto and a senior scientist who leads the World Health Organization (WHO)/Pan American Health Organization (PAHO) Collaborating Centre in Addiction and Mental Health. “And that risk continues to increase the more someone drinks.”

The researchers, from the United States and Canada, aimed to estimate how lifetime drinking habits affect Americans’ risk of illness and death related to alcohol. After medical experts reviewed more than 7200 scientific articles on alcohol-related diseases and injuries to determine the level of risk for each condition, the researchers applied those risks to large national health data sets. They then used statistical modelling to estimate how different drinking levels influence long-term health outcomes.

The study offers more concrete guidance than the new US Dietary Guidelines, which currently advise Americans to “limit alcoholic beverages” without specifying how much alcohol is safe to drink. Previous guidelines recommended a daily limit of two alcoholic drinks for men and one for women. The definition of a ‘drink’ varies by beverage type, typically 12 ounces (340mL) for beer, 5 ounces (140mL) for wine, and 1.5 ounces (40mL)for spirits, although that too can vary by alcohol concentration.

While the new US Dietary Guidelines contain a useful ‘less-is-best’ message, they provide no quantitative framework, according to the authors. This study was designed to do just that across the drinking spectrum. 

It turns out that an average of two drinks per day, which might be considered ‘moderate’ from a social standpoint, is associated with a substantially elevated risk of a premature death caused by alcohol, they explain.

In addition to mortality risk, researchers examined how drinking patterns influence chronic and acute alcohol-related conditions such as cancer – including oesophageal, oral, and breast – cardiovascular disease, liver disease, and injury. 

The study overturns a common misconception that alcohol can protect health. The researchers did not observe a significant protective effect of alcohol on overall health at any level of consumption. They noted that at low levels, alcohol may be associated with a reduced risk of ischemic heart disease and stroke. But when you look across the full range of health outcomes, including cancer and other chronic diseases, those potential benefits are outweighed by the risks even at 7 drinks per week.

Statistical modelling used in the study to determine health risks was based on “the best possible data,” according to the team. But they caution one should not assume that means one person’s individual health risk is the same as what is reported here – that depends on other factors like lifestyle, genetics, drinking patterns, and other choices that differ person to person.

The researchers estimated risk for all health conditions known to be causally related to alcohol and then aggregated these estimates to determine the total health risk. Yet, new research continues to emerge that links alcohol with additional health conditions, such as pancreatic cancer. “Understanding those relationships, and how much alcohol contributes to those risks, is an area that still needs further work,” says Keyes and Shield.

By finding that alcohol consumption is associated with increased risk above one drink per day for both men and women, the study offers a much-needed benchmark.

“Having a clearer threshold helps people better understand what level of drinking is associated with increased risk and make more informed decisions when drinking.”

In an accompanying editorial, Robert M. Vincent, a former associate administrator for the US Substance Abuse and Mental Health Services Administration, discusses his view of the behind-the-scenes environment in which the study was produced. “The Alcohol Intake and Health report was explicitly invited to inform alcohol guidance during development of the Dietary Guidelines for Americans, 2025–2030,” he writes. “Despite the study’s adherence to its mandate, its findings were sidelined.”

See the paper for a full list of co-authors and their institutions.

Source: Columbia University Mailman School of Public Health

Categories : CancerTags :

Study of North Korean Defectors Reveals Cancer Risk Changes

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North Korean defectors who resettled in South Korea share genetics but markedly contrasting early-life exposures with South Korean residents. Research published in the Journal of Internal Medicine compared overall and site-specific cancer incidence rates between North Korean defectors and native South Koreans.

Breast cancer cells. Image by National Cancer Institute

Using the Korean National Health Insurance database, researchers matched 25 798 North Korean defectors and 1 276 601 South Korean residents. Defectors had higher risks of infection-related cancers (such as liver and cervical cancers) and lower risks of breast, colon, and prostate cancers (which are more prevalent in developed countries). Over time, though, their cancer profile changed, suggesting adaptation to South Korean society.

“The study provides a model for understanding how cancer epidemiology evolves in such transitions, offering lessons that may help guide prevention and health planning for other vulnerable groups in transition worldwide,” said corresponding author Sin Gon Kim, MD, PhD, of the Korea University College of Medicine.

Source: Wiley

Categories : Cancer Diet and NutritionTags :

More Preservatives in Diet Linked to Increased Cancer Risk

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Findings may have important public health implications given the ubiquitous use of these additives, say researchers

Photo by Erik Mclean

Higher intake of food preservatives, widely used in industrially processed foods and beverages to extend shelf-life, is associated with a modestly increased risk of cancer, finds a study from France published by The BMJ.

While further research is needed to better understand these links, the researchers say these new data call for the re-evaluation of regulations governing the use of these additives by the food industry to improve consumer protection.

Preservatives are substances added to packaged foods to extend shelf life. Some experimental studies have shown that certain preservatives can damage cells and DNA, but firm evidence linking preservatives to cancer risk remains scarce.

To address this, researchers set out to examine the association between exposure to preservative food additives and risk of cancer in adults, using detailed dietary and health data from 2009 to 2023.

Their findings are based on 105,260 participants aged 15 years and older (average age 42 years; 79% women) enrolled in the NutriNet-Santé cohort study who were free of cancer and completed regular 24 hour brand-specific dietary records over an average 7.5 year period. Health questionnaires and official medical and death records were then used to track cancer cases up to 31 December 2023.

A total of 17 individual preservatives were analysed including citric acid, lecithins, total sulfites, ascorbic acid, sodium nitrite, potassium sorbate, sodium erythorbate, sodium ascorbate, potassium metabisulfite, and potassium nitrate.

Preservatives were grouped into non-antioxidants (which inhibit microbial growth or slow chemical changes that lead to spoilage) and antioxidants (which delay or prevent food deteriorating by removing or limiting oxygen levels in packaging).

During the follow-up period, 4,226 participants received a diagnosis of cancer, comprising 1,208 breast, 508 prostate, 352 colorectal, and 2,158 other cancers.

Of the 17 individually studied preservatives, 11 were not associated with cancer incidence, and no link was found between total preservatives and cancer incidence.

However, higher intakes of several preservatives (mostly non-antioxidants including potassium sorbate, potassium metabisulfite, sodium nitrite, potassium nitrate, and acetic acid) were associated with higher risk of cancers compared with non-consumers or lower consumers.

For example, total sorbates, specifically potassium sorbate, was associated with a 14% increased risk of overall cancer and a 26% increased risk of breast cancer, while total sulfites were associated with a 12% increased risk of overall cancer.

Sodium nitrite was associated with a 32% increased risk of prostate cancer, while potassium nitrate was associated with an increased risk of overall cancer (13%) and breast cancer (22%).

Total acetates were associated with an increased risk of overall cancer (15%) and breast cancer (25%), while acetic acid was associated with a 12% increased risk of overall cancer.

Among antioxidant preservatives, only total erythorbates and specific sodium erythorbate were found to be associated with higher incidence of cancer.

While more studies are needed to better understand these potential risks, the researchers note that several of these compounds can alter immune and inflammatory pathways, possibly triggering the development of cancer.

This is an observational study, so no firm conclusions can be drawn about cause and effect, and the researchers can’t rule out the possibility that other unmeasured factors may have influenced their results.

However, they say this was a large study based on detailed dietary records linked to food databases over 14 years and results are consistent with existing experimental data suggesting adverse cancer related effects of several of these compounds.

As such, they conclude: “This study brings new insights for the future re-evaluation of the safety of these food additives by health agencies, considering the balance between benefit and risk for food preservation and cancer.”

In the meantime, they call on manufacturers to limit the use of unnecessary preservatives, and support recommendations for consumers to favour freshly made, minimally processed foods.

From a policy perspective, preservatives offer clear benefits by extending shelf life and lowering food costs, which can be particularly important for populations with lower incomes, point out US researchers in a linked editorial.

However, they say the widespread and often insufficiently monitored use of these additives, with uncertainties of their long term health effects, call for a more balanced approach.

Findings from NutriNet-Santé may prompt regulatory agencies to revisit existing policies, such as setting stricter limits on use, requiring clearer labeling, and mandating disclosure of additive contents, while collaborative global monitoring initiatives, similar to those implemented for trans fatty acids and sodium, could also support evidence based risk assessments and guide reformulation by the food industry, they write.

“At the individual level, public health guidance is already more definitive about the reduction of processed meat and alcohol intake, offering actionable steps even as evidence on the carcinogenic effects of preservatives is evolving,” they conclude.

Source: BMJ Group

Categories : Cancer Environmental EffectsTags :

No Increased Childhood Cancer Risk near UK Nuclear Sites, Study Finds

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Photo by Vladyslav Cherkasenko on Unsplash

Children living near nuclear power stations in the UK are not at increased risk of childhood cancers, according to a new analysis.

The research was led by scientists at Imperial College London and University of Bristol and commissioned by the UK Committee on the Medical Aspects of Radiation in the Environment (COMARE). The results, published in International Journal of Epidemiology, found no evidence of increased risk of childhood cancers among children living near 28 nuclear installations between 1995 and 2016.

Researchers analysed cancer incidence data for nearly 50 000 cases of childhood leukaemia, non-Hodgkin’s lymphoma (LNHL), central nervous system (CNS) tumours, and other solid tumours in children aged 0–14 years.

They looked at data for communities living within 25 kilometres of installations, including those which have been linked to historical concerns about potential health impacts – such as Sellafield in Cumbria and Dounreay in northern Scotland.

The analysis found no evidence of increased risk of childhood cancers among children living near 28 nuclear installations between 1995 and 2016.
(Credit: Davies, B. et al. Int J Epidemiol, 2025)

Using these data and advanced statistical modelling, they found no increased incidence of childhood cancers in these areas compared to national averages.[1] They also found no evidence that cancer risk increased the closer children lived to the nuclear sites.

Dr Bethan Davies, from Imperial’s School of Public Health and lead author of the study, said: “For many years there have been public concerns about the potential health impacts of living near nuclear installations. Our analysis suggests that children living near these sites today are not at increased risk.”

The latest study builds on decades of research following reports in the 1980s of clusters of cancer cases near nuclear facilities in England, Scotland and Germany[2] – following which, the UK Government set up COMARE to advise on the health effects of radiation.

Early investigations confirmed clusters of cases of some cancers near nuclear installations, particularly LNHL.

However, subsequent studies failed to show any direct link between these cases and radiation exposure from nuclear facilities.

In 2016, a COMARE report[3] suggested other potential explanations for these case clusters, including infections introduced due to population mixing in the areas.

The new findings come at a time of renewed interest in nuclear energy as part of the UK’s strategy to meet net-zero carbon targets and the government committing £14.2bn to build a new nuclear power station in Suffolk and develop small modular reactors.

The researchers say that while their study offers reassurance, they support COMARE’s recommendations for ongoing surveillance of cancer incidence near nuclear sites.

The authors acknowledge a number of limitations with their study, including the use of residential address at diagnosis as a proxy for exposure.

They were also unable to account for individual-level risk factors – such as genetic or medical conditions. However, they emphasise that the study’s design and comprehensive data make it one of the most detailed assessments to date.

Dr Davies added: “As the UK government announces a multibillion-pound investment for new nuclear energy infrastructure, our findings should provide reassurance that the historical clusters of childhood cancers reported near sites such as Sellafield and Dounreay are no longer evident.”

Professor Mireille Toledano, Mohn Chair in Population Child Health in Imperial’s School of Public Health, said: “These findings are both timely and important. As the UK and other countries expand their nuclear energy capacity, it’s vital that public health remains a central consideration. It’s reassuring that our study found that the historic case clusters have resolved, but it remains important we continue to monitor public health data around such sites across the UK for any emerging trends of concern.”

The full study, published today in the International Journal of Epidemiology, was supported by funding from the National Institute for Health and Care Research (NIHR), Health Data Research UK (HDRUK) and the UK Medical Research Council (UK Research and Innovation (UKRI)).

The work was carried out through the NIHR Health Protection Research Unit in Chemical and Radiation Threats and Hazards – a partnership between the UK Health Security Agency (UKHSA) and Imperial College London.

The work was also supported by the NIHR Imperial Biomedical Research Centre, a translational research partnership between Imperial College Healthcare NHS Trust and Imperial College London.

–

[1] Researchers obtained national incident cases of cancer diagnosed between 1995 and 2016 in children under 15 years of age from NHS England (formerly Public Health England), Welsh Cancer Intelligence and Surveillance Unit and Health Protection Scotland.

[2] A cluster of cases of leukaemia in children living close to the Sellafield nuclear plant was reported in 1983. An Independent Advisory Group confirmed the cluster and the UK government established COMARE to advise on the health effects of radiation. Subsequent studies identified increased risks of cancers in children and young adults living near Sellafield, Dounreay (Scotland), and Hamburg (Germany) nuclear installations.

[3] Committee on Medical Aspects of Radiation in the Environment (COMARE) – Seventh report (2016) https://assets.publishing.service.gov.uk/media/5a7f70ed40f0b6230268f83c/COMARE_17th_Report.pdf

Source: Imperial College London

Categories : Cancer Diet and NutritionTags :

Animal Protein Not Linked to Higher Mortality Risk, Study Finds

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Photo by Jose Ignacio Pompe on Unsplash

Eating animal-sourced protein foods is not linked to a higher risk of death and may even offer protective benefits against cancer-related mortality, new research finds.   

The study, published in Applied Physiology, Nutrition, and Metabolism, analysed data from nearly 16 000 adults aged 19 and older using the National Health and Nutrition Examination Survey (NHAMES III). 

Researchers examined how much animal and plant protein people typically consume and whether those patterns were associated with their risk of dying from heart disease, cancer or any cause.  

They found no increased risk of death associated with higher intake of animal protein. In fact, the data showed a modest but significant reduction in cancer-related mortality among those who ate more animal protein.  

“There’s a lot of confusion around protein – how much to eat, what kind and what it means for long-term health. This study adds clarity, which is important for anyone trying to make informed, evidence-based decisions about what they eat,” explains Stuart Phillips, Professor and Chair of the Department of Kinesiology at McMaster University, who supervised the research.  

To ensure reliable results, the team employed advanced statistical methods, including the National Cancer Institute (NCI) method and multivariate Markov Chain Monte Carlo (MCMC) modelling, to estimate long-term dietary intake and minimize measurement error.   

“It was imperative that our analysis used the most rigorous, gold standard methods to assess usual intake and mortality risk. These methods allowed us to account for fluctuations in daily protein intake and provide a more accurate picture of long-term eating habits,” says Phillips.   

The researchers found no associations between total protein, animal protein or plant protein and risk of death from any cause, cardiovascular disease, or cancer. When both plant and animal protein were included in the analysis, the results remained consistent, suggesting that plant protein has a minimal impact on cancer mortality, while animal protein may offer a small protective effect. 

Observational studies like this one cannot prove cause and effect; however, they are valuable for identifying patterns and associations in large populations. Combined with decades of clinical trial evidence, the findings support the inclusion of animal proteins as part of a healthy dietary pattern.  

“When both observational data like this and clinical research are considered, it’s clear both animal and plant protein foods promote health and longevity,” says lead researcher Yanni Papanikolaou, MPH, president, Nutritional Strategies. 

This research was funded by the National Cattlemen’s Beef Association (NCBA), a contractor to the Beef Checkoff. NCBA was not involved in the study design, data collection and analysis or publication of the findings.  

This article was first published on Brighter World. Read the original article.

Categories : Cancer GeneticsTags :

Women of African Ancestry May Be Biologically Predisposed to Early-onset or Aggressive Breast Cancers

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Photo by National Cancer Institute

While the incidence of breast cancer is highest for white women, Black women are more likely to have early-onset or more aggressive subtypes of breast cancer, such as triple-negative breast cancer. Among women under 50, the disparity is even greater: young Black women have double the mortality rate of young white women.

Now, research from the University of Notre Dame is shedding light on biological factors that may play a role in this disparity. The study published in iScience found that a population of cells in breast tissues, dubbed PZP cells, send cues that prompt behavioural changes that could promote breast cancer growth.

Funded by the National Cancer Institute at the National Institutes of Health, the study set out to explore what biological differences in breast tissue could be related to early onset or aggressive breast cancers. Most breast cancers are carcinomas, or a type of cancer that develops from epithelial cells. In healthy tissue, epithelial cells form linings in the body and typically have strong adhesive properties and do not move.

The researchers focused on PZP cells as previous studies had shown that these cells are naturally and significantly higher in healthy breast tissues of women of African ancestry than in healthy breast tissues of women of European ancestry. While PZP cell levels are known to be elevated in breast cancer patients in general, their higher numbers in healthy, African ancestry tissues could hold clues to why early-onset or aggressive breast cancers are more likely to occur in Black women.

“The disparity in breast cancer mortality rates, particularly among women of African descent, is multifaceted. While socioeconomic factors and delayed diagnosis may be contributing factors, substantial emerging evidence suggests that biological and genetic differences between racial groups can also play a role,” said Crislyn D’Souza-Schorey, the Morris Pollard Professor of Biological Sciences at Notre Dame and corresponding author of the study.

The study showed how PZP cells produce factors that activate epithelial cells to become invasive, where they detach from their primary site and invade the surrounding tissue.

For example, a particular biological signaling protein known as AKT is often overactive in breast cancers. This study showed that PZP cells can activate the AKT protein in breast epithelial cells, which in part allows them to invade the surrounding environment. PZP cells also secrete and deposit certain proteins outside the cell that guide the movement of breast epithelial cells as they invade.

Overall, the results of the study emphasize multiple mechanisms by which PZP cells may influence the early stages of breast cancer progression and their potential contribution to disease burden.

The researchers also looked at how a targeted breast cancer drug, capivasertib, which inhibits the AKT protein, impacted PZP cells and found it markedly reduced the effects of the PZP cells on breast epithelial cells.

“It’s important to understand the biological and genetic differences within normal tissue as well as tumours among racial groups, as these variations could potentially influence treatment options and survival rates. And consequently, in planning biomarker studies, cancer screenings or clinical trials, inclusivity is important,” said D’Souza-Schorey, also an affiliate of Notre Dame’s Berthiaume Institute for Precision Health and Harper Cancer Research Institute.

Source: University of Notre Dame

Categories : CancerTags :

Why Humans Are More Susceptible to Cancers than Other Primates

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Photo by Andre Mouton on Unsplash

New research from UC Davis Comprehensive Cancer Center has uncovered an evolutionary change that may explain why certain immune cells in humans are less effective at fighting solid tumours compared to non-human primates. The findings, published in Nature Communications, could lead to more powerful cancer treatments.

The study revealed a tiny genetic difference in an immune protein called Fas Ligand (FasL) between humans and non-human primates. This genetic mutation makes the FasL protein vulnerable to being disabled by plasmin, a tumour-associated enzyme. This vulnerability seems unique to humans and is not found in non-human primates, such as chimpanzees.

“The evolutionary mutation in FasL may have contributed to the larger brain size in humans,” said Jogender Tushir-Singh, senior author for the study and an associate professor in the Department of Medical Microbiology and Immunology. “But in the context of cancer, it was an unfavourable tradeoff because the mutation gives certain tumours a way to disarm parts of our immune system.”

Tumour environment neutralises key immune protein

FasL is an immune cell membrane protein that triggers apoptosis, which activated immune cells, including CAR-T cells, make use of to kill cancer cells.

The UC Davis team discovered that in human genes, a single evolutionary amino acid change — serine instead of proline at position 153 — makes FasL more susceptible to being cut and inactivated by plasmin.

Plasmin is a protease enzyme that is often elevated in aggressive solid tumours like triple negative breast cancer, colon cancer and ovarian cancer.

This means that even when human immune cells are activated and ready to attack the tumour cells, one of their key apoptosis tools, FasL, can be neutralised by the tumour environment, reducing the effectiveness of immunotherapies.

The findings may help explain why CAR-T and T-cell-based therapies can be effective in blood cancers but often fall short in solid tumours. Blood cancers often do not rely on plasmin to metastasise, whereas tumours like ovarian cancer rely heavily on plasmin to spread the cancer.

Plasmin inhibitors may enhance immunotherapy

Significantly, the study also showed that blocking plasmin or shielding FasL from cleavage can restore its cancer-killing power. That finding may open new doors for improving cancer immunotherapy.

By combining current treatments with plasmin inhibitors or specially designed antibodies that protect FasL, scientists may be able to boost immune responses in patients with solid tumours.

“Humans have a significantly higher rate of cancer than chimpanzees and other primates. There is a lot that we do not know and can still learn from primates and apply to improve human cancer immunotherapies,” said Tushir-Singh. “Regardless, this is a major step toward personalising and enhancing immunotherapy for the plasmin-positive cancers that have been difficult to treat.”

Source: UC Davis Cancer Center