It’s possible that I shall make an ass of myself. But in that case one can always get out of it with a little dialectic. I have, of course, so worded my proposition as to be right either way (K.Marx, Letter to F.Engels on the Indian Mutiny)
A calculator that predicts risk of lung cancer underperforms in diverse populations
Research finds that a commonly used risk-prediction model for lung cancer does not accurately identify high-risk Black patients who could benefit from early screening
PHILADELPHIA - Lung cancer is the third most common cancer in the U.S. and the leading cause of cancer death, with about 80% of the total 154,000 deaths recorded each year caused by cigarette smoking. Black men are more likely to develop and die from lung cancer than persons of any other racial or ethnic group, pointing to severe racial disparities. For example, research has shown that Black patients are less likely to receive early diagnosis and life-saving treatments like surgery. Now researchers at Jefferson have found that a commonly used risk prediction model does not accurately identify high-risk Black patients who could gain life-saving benefit from early screening, and paves the way for improving screenings and guidelines. The research was published in JAMA Network Open on April 6.
"Black individuals develop lung cancer at younger ages and with less intense smoking histories compared to white individuals," explains Julia Barta, MD, Assistant Professor of Medicine in the Division of Pulmonary and Critical Care Medicine at Thomas Jefferson University, and researcher at the Jane and Leonard Korman Respiratory Institute. "Updated guidelines now recommend screening eligible patients beginning at age 50, but could still potentially exclude higher-risk Black patients. We are interested in finding methods that could help identify at-risk patients who are under-screened."
Screening for lung cancer is an annual CT scan to detect the presence of lung cancer in otherwise healthy people with a high risk of lung cancer. Current guidelines do not require a risk score for screening eligibility, but some researchers think that risk models could improve care. Risk prediction models are mathematical equations that take into account risk factors like smoking history and age to produce a risk score, which indicates the risk for developing lung cancer. Existing risk prediction models are derived from screening data that only include 5% or fewer African American individuals.
"What makes our study unique is that our screening cohort included more than 40% Black individuals," says senior author Dr. Barta, a member of Sidney Kimmel Cancer Center - Jefferson Health. "To our knowledge, our study is the first to examine lung cancer risk in a diverse screening program and aims to strengthen the argument for more inclusive guidelines for screening eligibility."
The most well-validated model used in screening research is the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial modified logistic regression model (PLCOm2012). "It uses 10-12 risk factors that include age, race, smoking history, as well as some socioeconomic factors like education to calculate a risk score," says Christine Shusted, MPH, first author of the study and research data analyst for Jefferson's Lung Cancer Screening Program through the Korman Respiratory Institute at Thomas Jefferson University. "The higher the score, the higher the risk of developing lung cancer. We wanted to see how well this model identifies patients with the highest risk of lung cancer in this diverse patient population."
The researchers conducted a cross-sectional, retrospective study in 1,276 Black and white patients (mean age, 64.25 years; 42.7% Black; 59.3% women) who enrolled in the Jefferson Lung Cancer Screening Program between January 2018 and September 2020. From this screening cohort, lung cancer was detected in 32 patients, 44% of whom were Black - these patients formed the cancer cohort. The researchers then calculated risk scores using the PLCOm2012 model. In the screening cohort, more Black patients than white patients were in high-risk groups, indicating that Black patients in this cohort had a higher risk of developing lung cancer.
As anticipated, white patients with screen-detected lung cancer generally had high lung cancer risk scores. "Among Black patients, we would have expected to see a similar trend," explains Dr. Barta. "However, we saw that despite having a lung cancer diagnosis through screening, Black patients were actually defined as lower risk. This indicates that the model is not accurately predicting risk of lung cancer in Black patients."
"These findings allowed us to identify weaknesses in this model for risk calculation for lung cancer," explains Shusted. "It indicates that we need to not only expand criteria for lung cancer screening so that more diverse populations are included, but that these prediction models need to include factors, like environmental contributors, access to health care, and other social determinants of health."
The researchers hope to continue building on these findings, with the ultimate goal of defining comprehensive risk factors and improving lung cancer screening uptake and adherence especially among vulnerable populations.
"This work is an important step to reducing disparities in the screening and early detection of lung cancer, and making sure we can trust our models to predict those individuals at the highest risk," says Dr. Barta.
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This work was supported in part by the Bristol Myers-Squibb Foundation's Specialty Care for Vulnerable Populations initiative. Dr. Barta reported receiving grants from the Genentech Health Equity Innovations Fund and the Prevent Cancer Foundation outside the submitted work. The authors report no other conflicts of interest.
Article Reference: Christine Shusted, Nathaniel Evans, Hee-Soon Juon, Gregory Kane, Julie Barta, "Association of Race With Lung Cancer Risk Among Adults Undergoing Lung Cancer Screening," JAMA Network Open, DOI: 10.1001/jamanetworkopen.2021.4509, 2021
Monday, February 08, 2021
AIR POLLUTION ENVIRONMENTAL TOXINS
‘But I never smoked’: A growing share of lung cancer cases is turning up in an unexpected population
Breast cancer wouldn’t have surprised her; being among the 1 in 8 women who develop it over their lifetime isn’t statistically improbable. Neither would have colorectal cancer; knowing the risk, Mandi Pike “definitely” planned to have colonoscopies as she grew older.
But when a PET scan in November 2019 revealed that Pike, a 33-year-old oil trader, wife, and mother of two in Edmond, Okla., had lung cancer — she had been coughing and was initially misdiagnosed with pneumonia — her first reaction was, “but I never smoked,” she said. “It all seemed so surreal.”
Join the club. Cigarette smoking is still the single greatest cause of lung cancer, which is why screening recommendations apply only to current and former smokers and why 84% of U.S. women and 90% of U.S. men with a new diagnosis of lung cancer have ever smoked, according to a study published in December in JAMA Oncology. Still, 12% of U.S. lung cancer patients are never-smokers.
Scientists disagree on whether the absolute number of such patients is increasing, but the proportion who are never-smokers clearly is. Doctors and public health experts have been slow to recognize this trend, however, and now there is growing pressure to understand how never-smokers’ disease differs from that of smokers, and to review whether screening guidelines need revision.
“Since the early 2000s, we have seen what I think is truly an epidemiological shift in lung cancer,” said surgeon Andrew Kaufman of Mount Sinai Hospital in New York, whose program for never-smokers has treated some 3,800 patients in 10 years. “If lung cancer in never-smokers were a separate entity, it would be in the top 10 cancers in the U.S.” for both incidence and mortality.
A 2017 study of 12,103 lung cancer patients in three representative U.S. hospitals found that never-smokers were 8% of the total from 1990 to 1995 but 14.9% from 2011 to 2013. The authors ruled out statistical anomalies and concluded that “the actual incidence of lung cancer in never smokers is increasing.” Another study that same year, of 2,170 patients in the U.K., found an even larger increase: The proportion of lung cancer patients who were never-smokers rose from 13% in 2008 to 28% in 2014.
“It is well-documented that approximately 20% of lung cancer cases that occur in women in the U.S. and 9% of cases in men, are diagnosed in never-smokers,” Kaufman said.
To a great extent, this is a function of straightforward math, said epidemiologist Ahmedin Jemal of the American Cancer Society. Fewer people smoke today than in previous decades — 15% in 2015, 25% in 1995, 30% in 1985, 42% in 1965. Simply because there are fewer smokers in the population, out of every 100 lung cancer patients, fewer will therefore be smokers. And that means more of them will be never-smokers.
There are also hints that the absolute incidence of lung cancer in never-smokers has been rising, said oncologist John Heymach of MD Anderson Cancer Center. Some data say it has, but other data say no. The stumbling block is that old datasets often don’t indicate a lung cancer patient’s smoking status, Heymach said, making it impossible to calculate what percent of never-smokers in past decades developed lung cancer.
Jemal, however, cautions that it is not the case that a never-smoker has a greater chance of developing lung cancer today than never-smokers did in the past.
Current cancer screening guidelines recommend a CT scan for anyone 50 to 80 years old who has smoked at least 20 pack years (the equivalent of one pack a day for 20 years, or two packs a day for 10 years, and so on) and who is still smoking or quit less than 15 years ago. Screening is not recommended for never-smokers because the costs of doing so are deemed greater than the benefits, Jemal said; thousands of never-smokers would have to be screened in any given year to find one lung cancer.
Still, low-dose CT can catch lung cancer in a significant number of never-smokers. A 2019 study in South Korea diagnosed lung cancer in 0.45% of never-smokers, compared to 0.86% of smokers. The researchers urged policymakers to “consider the value of using low-dose CT screening in the never-smoker population.”
“It used to be that the high-risk group” for whom CT screening is recommended “was the vast majority of lung cancer patients,” Heymach said. “But now that so many lung cancer cases are in nonsmokers, there is absolutely a need to reevaluate the screening criteria.”
Researchers are trying to improve screening by reducing the incidence of false positives — when CT finds lung nodules “or an old scar that you got 20 years ago,” he said. Those don’t pose a threat but have to be biopsied to ascertain that. Screening never-smokers would also be more efficient than it is today “if we could identify who, among nonsmokers, are at higher risk,” he said.
Cancer doctors already know part of the answer: women. Worldwide, 15% of male lung cancer patients are never-smokers. But fully half of female lung cancer patients never smoked. And women never-smokers are twice as likely to develop lung cancer as men who never put a cigarette to their lips.
Beyond sex, “nothing stands out as a single large risk factor that, if we only got rid of it, we would solve the problem” of lung cancer in never-smokers, said Josephine Feliciano, an oncologist at Johns Hopkins University School of Medicine. “But air pollution, radon, family history of lung cancer, [and] genetic predispositions” all play a role. Chronic lung infections and lung diseases such as chronic obstructive pulmonary disorder (COPD) also seem to increase risk.
None of those, with the possible exception of genetics and indoor pollution (cooking fires in some low-income countries), affect women more than men. So what’s going on?
At least one biotech believes that biological differences between lung cancer in never-smokers and smokers merits a new drug, and one that might be especially effective in women. “A different disease needs a different drug,” said co-founder and CEO Panna Sharma of Lantern Pharma. In fact Lantern, which is developing a drug for lung cancer in female never-smokers, believes that disease is so different it recently tried to convince the U.S. Food and Drug Administration to designate it an orphan disease, said Sharma.
Called LP-300, the Lantern drug increased overall survival from 13 months to more than 27, compared to chemotherapy alone, in female nonsmokers, in a small trial. It “targets molecular pathways that are more common in female nonsmokers than in any other group,” said Sharma, targeting the mutations EGFR, ALK, MET, and ROS1 (common in never-smokers) directly and boosting the efficacy of other drugs that attack them, such as erlotinib and crizotinib. Lantern plans a larger trial this year.
Smokers’ tumors tend to have more mutations overall, thanks to mutagen-packed cigarette smoke attacking their lungs, but scientists have developed more drugs for never-smokers’ lung tumors than for smokers’. For instance, EGFR and ALK mutations are more common in never-smokers. (Mandi Pike had the EGFR mutation, which was relatively fortunate: A drug targets it, and she has been cancer-free since November.)
The targeted drugs bollix up each mutation’s cancer-causing effects. KRAS mutations are more common in smokers’ lung tumors, and there are no KRAS drugs. (A KRAS drug for lung cancer is imminent, though, said thoracic oncologist Ben Creelan of Moffitt Cancer Center in Tampa, Fla.)
According to national guidelines, lung cancer in never-smokers should be treated the same as in smokers, said Creelan. “But I think we should reconsider this,” he said.
Because never-smokers have fewer tumor mutations, it’s harder to find them. So he said clinicians should be more aggressive about looking for actionable mutations in these patients. “I keep looking for a mutation until I find something important,” he said, adding that doctors might need better biopsy material or to use a different sequencing method in never-smokers.
In a cruel twist, the breakthrough drugs that take the brakes off immune cells, which then attack the tumor, are less effective in never-smokers’ lung cancer than in smokers’. The reason seems to be that smokers’ tumors have more mutations, said Mount Sinai’s Kaufman; the mutations often cause the tumor cells to have molecules on their surface that the immune system perceives as foreign and revs up to attack. Never-smokers’ tumors have few, if any, of those “come and get me” molecules. Immune cells therefore ignore them.
“In smokers, conversely, with more mutations, there is more for the immune system to recognize as bizarre and foreign, and so to provoke” an attack, Creelan said.
In contrast, never-smokers’ tumors are more likely to respond to targeted drugs, and as a result to be in remission for a long time or even cured. That’s because with fewer mutations, never-smokers’ tumors are more likely to have an “oncogene addiction,” Heymach explained: They are propelled by only one mutation. The plethora of mutations in smokers’ tumors means that there is usually a back-up cancer driver if a targeted drug eliminates cells with only one. “When a tumor has more and more mutations, blocking one is less likely to have an impact,” Heymach said. “But in nonsmokers, it can.”
Heymach called for more funding to study lung cancer in never-smokers. It “is an area that’s underserved and deserves more investment,” Heymach said. “It should be commensurate with the public health threat it represents.”
About the Author
Sharon Begley Senior Writer, Science and Discovery (1956-2021) Sharon covered science and discovery.
Particles linked to climate change also promote cancerous changes in airway cells
Cells with EGFR and KRAS gene mutations can turn cancerous when exposed to air pollutants
Late-breaking data pave way to new approaches to lung cancer prevention and treatment
Paris, France, 10 September 2022 - A new mechanism has been identified through which very small pollutant particles in the air may trigger lung cancer in people who have never smoked, paving the way to new prevention approaches and development of therapies, according to late-breaking data [to be] reported at the ESMO Congress 2022 by scientists of the Francis Crick Institute and University College London, funded by Cancer Research UK (1). The particles, which are typically found in vehicle exhaust and smoke from fossil fuels, are associated with non-small cell lung cancer (NSCLC) risk, accounting for over 250,000 lung cancer deaths globally per year (2,3).
“The same particles in the air that derive from the combustion of fossil fuels, exacerbating climate change, are directly impacting human health via an important and previously overlooked cancer-causing mechanism in lung cells. The risk of lung cancer from air pollution is lower than from smoking, but we have no control over what we all breathe. Globally, more people are exposed to unsafe levels of air pollution than to toxic chemicals in cigarette smoke, and these new data link the importance of addressing climate health to improving human health,” said Charles Swanton, the Francis Crick Institute and Cancer Research UK Chief Clinician, London, UK, who will present the research results at the ESMO 2022 Presidential Symposium on Saturday, 10 September.
The new findings are based on human and laboratory research on mutations in a gene called EGFR which are seen in about half of people with lung cancer who have never smoked. In a study of nearly half a million people living in England, South Korea and Taiwan, exposure to increasing concentrations of airborne particulate matter (PM) 2.5 micrometres (μm) in diameter was linked to increased risk of NSCLC with EGFR mutations.
In the laboratory studies, the Francis Crick Institute scientists showed that the same pollutant particles (PM2.5) promoted rapid changes in airway cells which had mutations in EGFR and in another gene linked to lung cancer called KRAS, driving them towards a cancer stem cell like state. They also found that air pollution drives the influx of macrophages which release the inflammatory mediator, interleukin-1β, driving the expansion of cells with the EGFR mutations in response to exposure to PM2.5, and that blockade of interleukin-1β inhibited lung cancer initiation. These findings were consistent with data from a previous large clinical trial showing a dose dependent reduction in lung cancer incidence when people were treated with the anti-IL1β antibody, canakinumab (4).
In a final series of experiments, the Francis Crick team used state-of-the-art, ultradeep mutational profiling of small samples of normal lung tissue and found EGFR and KRAS driver mutations in 18% and 33% of normal lung samples, respectively.
“We found that driver mutations in EGFR and KRAS genes, commonly found in lung cancers, are actually present in normal lung tissue and are a likely consequence of ageing. In our research, these mutations alone only weakly potentiated cancer in laboratory models. However, when lung cells with these mutations were exposed to air pollutants, we saw more cancers and these occurred more quickly than when lung cells with these mutations were not exposed to pollutants, suggesting that air pollution promotes the initiation of lung cancer in cells harbouring driver gene mutations. The next step is to discover why some lung cells with mutations become cancerous when exposed to pollutants while others don’t,” said Swanton.
Commenting on the results, Tony Mok, Chinese University of Hong Kong, not involved in the study, said: “This research is intriguing and exciting as it means that we can ask whether, in the future, it will be possible to use lung scans to look for pre-cancerous lesions in the lungs and try to reverse them with medicines such as interleukin-1β inhibitors. We don’t yet know whether it will be possible to use highly sensitive EGFR profiling on blood or other samples to find non-smokers who are predisposed to lung cancer and may benefit from lung scanning, so discussions are still very speculative.”
Like Swanton, he stresses the importance of reducing air pollution to lower the risk of lung diseases, including cancer. “We have known about the link between pollution and lung cancer for a long time, and we now have a possible explanation for it. As consumption of fossil fuels goes hand in hand with pollution and carbon emissions, we have a strong mandate for tackling these issues – for both environmental and health reasons,” Mok concluded.
-END-
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References
1 LBA1 ‘Mechanism of action and an actionable inflammatory axis for air pollution induced non-small cell lung cancer in never smokers’ will be presented by Charles Swanton during Presidential Symposium 1 on Saturday, 10 September, 16:30 to 18:00 CEST in Paris Auditorium. Annals of Oncology, Volume 33 Supplement 7, September 2022
2 Liu X, Mubarik S, Wang S. Lung Cancer Death Attributable to Long-Term Ambient Particulate Matter (PM2.5) Exposure in East Asian Countries During 1990–2019. Frontiers in Medicine 2021 Oct 15;8:742076
3 Turner MC, Andersen ZJ, Baccarelli A et al. Outdoor Air Pollution and Cancer: An Overview of the Current Evidence and Public Health Recommendations. CA: Cancer J Clin 2020; 70: 460-479
4 Ridker PM, MacFadyen JG, Thuren T et al. Effect of interleukin-1β inhibition with canakinumab on incident lung cancer in patients with atherosclerosis: exploratory results from a randomised, double-blind, placebo-controlled trial. Lancet 2017 Oct 21; 390 (10105): 1833-1842
ESMO is the leading professional organisation for medical oncology. With 25,000 members representing oncology professionals from over 160 countries worldwide, ESMO is the society of reference for oncology education and information. Drawing on more than 45 years of experience, ESMO serves its members and the oncology community by providing networking and professional growth opportunities: oncologists can engage in projects, committees and working groups aiming to promote science and foster improvements in the oncology practice. With training, resources and tools, oncologists are enabled to stay up to date with the latest scientific advances and continue to deliver the best possible care to cancer patients. By representing and advocating for the oncology community at the highest political levels, ESMO ensures that the needs of both patients and doctors are properly taken care of. Driven by a shared determination to secure the best possible outcomes for patients, ESMO is committed to standing by those who care about cancer through addressing the diverse needs of #ONEoncologycommunity, offering #educationforLIFE, and advocating for #accessiblecancerCARE. www.esmo.org
The Francis Crick Institute is a biomedical discovery institute dedicated to understanding the fundamental biology underlying health and disease. Its work is helping to understand why disease develops and to translate discoveries into new ways to prevent, diagnose and treat illnesses such as cancer, heart disease, stroke, infections, and neurodegenerative diseases. An independent organisation, its founding partners are the Medical Research Council (MRC), Cancer Research UK, Wellcome, UCL (University College London), Imperial College London and King’s College London. The Crick was formed in 2015, and in 2016 it moved into a brand new state-of-the-art building in central London which brings together 1500 scientists and support staff working collaboratively across disciplines, making it the biggest biomedical research facility under a single roof in Europe. www.crick.ac.uk
Cancer Research UK is the world’s leading cancer charity dedicated to saving lives through research, influence and information. Cancer Research UK’s pioneering work into the prevention, diagnosis and treatment of cancer has helped save millions of lives. Cancer Research UK has been at the heart of the progress that has already seen survival in the UK double in the last 40 years. Today, 2 in 4 people survive their cancer for at least 10 years. Cancer Research UK wants to accelerate progress and see 3 in 4 people surviving their cancer by 2034. Cancer Research UK supports research into the prevention and treatment of cancer through the work of over 4,000 scientists, doctors and nurses. Together with its partners and supporters, Cancer Research UK is working towards a world where people can live longer, better lives, free from the fear of cancer. www.cancerresearchuk.org or +44(0) 300 123 1022
LBA1 - Mechanism of action and an actionable inflammatory axis for air pollution induced non-small cell lung cancer: towards molecular cancer prevention
C. Swanton1, W. Hill2, E. Lim3, C. Lee4, C.E. Weeden5, M. Augustine6, K. Chen7, F.-C. Kuan8, F. Marongiu9, F. Rodrigues10, H. Cha11, T. Jacks12, M. Luchtenborg13, I. Malanchi14, J. Downward15, C. Carlsten16, A. Hackshaw17, K.R. Litchfield18, J. DeGregori19, M. Jamal-Hanjani20
1Translational Cancer Therapeutics Department, Francis Crick Institute, London/United Kingdom, 2Cancer Evolution And Genome Instability Laboratory, Francis Crick Institute, London/United Kingdom, 3Cancer Evolution And Genome Instability Laboratory, The Francis Crick Institute, London/United Kingdom, 4Cegi, Francis Crick Institute, London/United Kingdom, 51 Midland Rd, The Francis Crick Institute, London/United Kingdom, 6Tumour Immunogenomics And Immunosurveillance, UCL - University College London, London/United Kingdom, 7Thoracic Surgery, Peking University People’s Hospital, Beijing/China, 8Hematology Oncology, Chang Gung Medical Foundation - Chiayi Chang Gung Memorial Hospital, Puzi City/Taiwan, 9Department Of Biochemistry & Molecular Genetics, UCHealth Cancer Care - Anschutz Medical Campus - University of Colorado Cancer Center, Aurora/United States of America, 10Tumour-host Interaction Laboratory, The Francis Crick Institute, London/United Kingdom, 11Division Of Hematology-oncology, Samsung Medical Center (SMC) - Sungkyunkwan University School of Medicine, Seoul/Korea, Republic of, 12The Jacks Lab, Koch Institute For Integrative Cancer Research at MIT, Cambridge/United States of America, 13National Cancer Registration And Analysis Service, Public Health England, London/United Kingdom, 14Tumour Host Interaction Lab, Francis Crick Institute, London/United Kingdom, 15Oncogene Biology Laboratory, The Francis Crick Institute, London/United Kingdom, 16Centre For Lung Health, UBC - The University of British Columbia, Vancouver/Canada, 17Clinical Trials, Cancer Research UK & University College London Cancer Trials Centre, London/United Kingdom, 18Tumour Immunogenomics And Immunosurveillance, UCL Cancer Institute - UCL - London's Global University, London/United Kingdom, 19Biochemistry And Molecular Genetics, UCHealth Cancer Care - Anschutz Medical Campus - University of Colorado Cancer Center, Aurora/United States of America, 20Medical Oncology Dept., UCL Cancer Institute - Paul O'Gorman Building, London/United Kingdom
Background: A mechanistic basis for non-small cell lung cancer (NSCLC) initiation in never smokers, a disease with a high frequency of EGFR mutations (EGFRm), is unknown. The air pollutant, particulate matter (PM), is known to be associated with the risk of NSCLC, however a direct cause and mechanism remain elusive.
Methods: We analysed 463,679 individuals to address the associations of increasing 2.5um PM (PM2.5) concentrations with cancer risk. We performed ultra-deep profiling of 247 normal lung tissue samples, analysed normal lung tissue from humans and mice following exposures to PM, and investigated the consequences of PM on tumour promotion in mouse lung cancer models.
Results: Increasing PM2.5 levels were associated with increased risk of EGFRm NSCLC in England, S.Korea and Taiwan and with increased risk of mesothelioma (HR=1.19), lung (HR=1.16), anal (HR=1.23), small intestine (HR=1.30), GBM (HR=1.19), lip, oral cavity and pharynx (HR: 1.15) and laryngeal carcinomas (HR=1.26) in UK Biobank; HR for each 1ug/m3 PM2.5 increment. 18-33% of normal lung tissue samples harbour driver mutations in EGFR and KRAS in the absence of malignancy. PM promotes a macrophage response and a progenitor-like state in lung epithelium harbouring mutant EGFR. Consistent with PM promoting NSCLC in at-risk epithelium harbouring driver mutations, PM increased tumour burden in three EGFR or KRAS driven lung cancer models in a dose-dependent manner. Finally, we uncover an actionable inflammatory axis driven by IL1B in response to PM, with anti-IL1B therapy preventing PM-induced mouse tumour formation, consistent with reductions in human lung cancer incidence with anti-IL1B therapy.
Conclusions: These results shed light on the aetiology of EGFRm lung cancer, particularly in never-smokers, and suggest that oncogenic mutations may be necessary but insufficient for tumour formation. These data reveal a mechanistic basis for PM driven lung cancer in the absence of classical carcinogen-driven mutagenesis, reminiscent of models of tumour initiation and promotion proposed 70 years ago, providing evidence to limit air pollution and opportunities for molecular targeted cancer prevention.
Clinical trial identification: TRAcking Non-small Cell Lung Cancer Evolution Through Therapy (Rx) (TRACERx) (NCT01888601) The PEACE (Posthumous Evaluation of Advanced Cancer Environment) Study (PEACE) (NCT03004755) Biomarkers and Dysplastic Respiratory Epithelium (NCT00900419)
Legal entity responsible for the study: Francis Crick Institute and UCL Hospitals NHS Trust
Funding: Foundation or academic group WITHOUT funding from a pharma, biotech, or other commercial company - This work has been supported by the Mark Foundation ASPIRE I Award (Grant 21-029-ASP), Lung Cancer Research Foundation Grant on Disparities in Lung Cancer, Advanced Grant (PROTEUS, Grant Agreement no. 835297), CRUK EDD (EDDPMA-Nov21100034), and Rosetrees Out-of-round Award (OoR2020100009). E.L.L. receives funding from NovoNordisk Foundation (ID 16584), The Mark Foundation (Grant 21-029-ASP) and has been supported by Rosetrees. W.H is funded by an ERC Advanced Grant (PROTEUS, Grant Agreement no. 835297), CRUK EDD (EDDPMA-Nov21100034), The Mark Foundation (Grant 21-029-ASP) and has been supported by Rosetrees. K.C. is supported by Research Unit of Intelligence Diagnosis and Treatment in Early Non-small Cell Lung Cancer, Chinese Academy of Medical Sciences (2021RU002), National Natural Science Foundation of China (No.82072566) and Peking University People's Hospital Research and Development Funds (RS2019-01). T.K. receives grant support from JSPS Overseas Research Fellowships Program (202060447). S.H.L is supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (No. 2020R1A2C3006535), the National Cancer Center Grant (NCC1911269-3), and a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (grant number : HR20C0025). N.M. is a Sir Henry Dale Fellow, jointly funded by the Wellcome Trust and the Royal Society (Grant Number 211179/Z/18/Z) and also receives funding from Cancer Research UK, Rosetrees and the NIHR BRC at University College London Hospitals and the CRUK University College London Experimental Cancer Medicine Centre. J.D., M.G., Y.E.M. D.T.M. and R.L.K receive funding from American Association for Cancer Research/Johnson&Johnson (18-90-52-DEGR), and J.D. is supported by the Courtenay C. and Lucy Patten Davis Endowed Chair in Lung Cancer Research. M.G., Y.E.M. D.T.M. and R.L.K. were supported by National Cancer Institute (NCI) RO1 CA219893. E.J.E. was supported by NCI Ruth L. Kirschstein National Research Service Award T32-CA190216. The work at the University of Colorado was also supported by NCI Cancer Center Support Grant P30CA046934. M.J.-H. has received funding from Cancer Research UK, National Institute for Health Research, Rosetrees Trust, UKI NETs and NIHR University College London Hospitals Biomedical Research Centre. C.S. is Royal Society Napier Research Professor. He is supported by the Francis Crick Institute, which receives its core funding from Cancer Research UK (FC001169), the UK Medical Research Council (FC001169), and the Wellcome Trust (FC001169). C.S. is funded by Cancer Research UK (TRACERx, PEACE and CRUK Cancer Immunotherapy Catalyst Network), Cancer Research UK Lung Cancer Centre of Excellence, the Rosetrees Trust, Butterfield and Stoneygate Trusts, NovoNordisk Foundation (ID16584), Royal Society Research Professorships Enhancement Award (RP/EA/180007), the NIHR BRC at University College London Hospitals, the CRUK-UCL Centre, Experimental Cancer Medicine Centre and the Breast Cancer Research Foundation (BCRF). This research is supported by a Stand Up To Cancer-LUNGevity-American Lung Association Lung Cancer Interception Dream Team Translational Research Grant (SU2C-AACR-DT23-17). Stand Up To Cancer is a program of the Entertainment Industry Foundation. Research grants are administered by the American Association for Cancer Research, the Scientific Partner of SU2C. C.S. also receives funding from the European Research Council (ERC) under the European Union’s Seventh Framework Programme (FP7/2007-2013) Consolidator Grant (FP7-THESEUS-617844), European Commission ITN (FP7-PloidyNet 607722), an ERC Advanced Grant (PROTEUS) from the European Research Council under the European Union’s Horizon 2020 research and innovation programme (835297) and Chromavision from the European Union’s Horizon 2020 research and innovation programme (665233). This work was supported by the Francis Crick Institute, which receives its core funding from Cancer Research UK (grant no. FC001112), the UK Medical Research Council (grant no. FC001112), and the Wellcome Trust (grant no. FC001112) and the European Research Council (grant no. ERC CoG-H2020-725492).
Disclosure:C. Swanton: Financial Interests, Personal, Invited Speaker, Activity took place in 2016.: Pfizer; Financial Interests, Personal, Invited Speaker, October 26th 2020: Novartis; Financial Interests, Personal, Invited Speaker: Roche/Ventana; Financial Interests, Personal, Invited Speaker: BMS; Financial Interests, Personal, Invited Speaker, Activity took place in 2016.: Celgene; Financial Interests, Personal, Invited Speaker: AstraZeneca; Financial Interests, Personal, Invited Speaker: MSD; Financial Interests, Personal, Invited Speaker: Illumina; Financial Interests, Personal, Advisory Board, AdBoard - November 12th, 2020: Amgen; Financial Interests, Personal, Advisory Board: Genentech; Financial Interests, Personal, Advisory Board: Sarah Canon Research Institute; Financial Interests, Personal, Advisory Board, Joined October 2020. Also have stock options: Bicycle Therapeutics; Financial Interests, Personal, Advisory Board: Medicxi; Financial Interests, Personal, Invited Speaker: GlaxoSmithKline; Financial Interests, Personal, Advisory Board, Member of the Science Management Committee. Also have stock options: GRAIL; Financial Interests, Personal, Other, Consultancy agreement: Roche Innovation Centre Shanghai; Financial Interests, Personal, Full or part-time Employment, Chief Clinician since October 2017: Cancer Research UK; Financial Interests, Personal, Ownership Interest, Co-Founder of Achilles Therapeutics. Also, have stock options in this company.: Achilles Therapeutics; Financial Interests, Personal, Stocks/Shares, Stocks owned until June 2021: GRAIL; Financial Interests, Personal, Stocks/Shares, Stocks owned until June 2021: Apogen Biotechnologies; Financial Interests, Personal, Stocks/Shares: Epic Biosciences; Financial Interests, Personal, Stocks/Shares: Bicycle Therapeutics; Financial Interests, Institutional, Research Grant, Funded RUBICON grant - October 2018 - April 2021.: Bristol Myers Squibb; Financial Interests, Institutional, Research Grant, Collaboration in minimal residual disease sequencing technologies.: Archer Dx Inc; Financial Interests, Institutional, Research Grant: Pfizer; Financial Interests, Institutional, Invited Speaker, Chief Investigator for the MeRmaiD1 clinical trial and chair of the steering committee.: AstraZeneca; Financial Interests, Institutional, Research Grant: Ono Pharmaceutical; Financial Interests, Institutional, Research Grant: Boehringer Ingelheim; Financial Interests, Institutional, Research Grant, Research Grants from 2015-2019.: Roche-Ventana; Financial Interests, Personal, Other, Co-chief investigator: NHS-Galleri Clinical Trial; Non-Financial Interests, , Principal Investigator, Chief Investigator for MeRmaiD1 clinical trial: AstraZeneca; Non-Financial Interests, , Invited Speaker, From 2019: AACR; Non-Financial Interests, , Other, Board of Directors: AACR; Non-Financial Interests, , Advisory Role, EACR Advisory Council member: EACR. T. Jacks: Financial Interests, Personal, Member of the Board of Directors: Amgen; Financial Interests, Personal, Member of the Board of Directors: Thermo Fisher Scientific; Financial Interests, Personal, Advisory Board, co-Founder: Dragonfly Therapeutics; Financial Interests, Personal, Other, co-Founder: T2 Biosystems; Financial Interests, Personal, Advisory Board: SQZ Biotech; Financial Interests, Personal, Advisory Board: Skyhawk Therapeutics; Financial Interests, Personal, Leadership Role: Break Through Cancer; Financial Interests, Institutional, Funding: Johnson & Johnson. J. Downward: Financial Interests, Personal, Other, consultant: AstraZeneca; Financial Interests, Personal, Other, consultant: Bayer; Financial Interests, Personal, Other, consultant: Jubilant; Financial Interests, Personal, Other, consultant: Theras; Financial Interests, Personal, Other, consultant: Vividion; Financial Interests, Personal, Other, consultant: Novartis; Financial Interests, Institutional, Research Grant: BMS; Financial Interests, Institutional, Research Grant: Revolution Medicines; Financial Interests, Institutional, Research Grant: Boehringer Ingelheim. K.R. Litchfield: Financial Interests, Personal, Invited Speaker: Roche Tissue Diagnostics; Financial Interests, Personal, Other, Consulting work: Monopteros Therapeutics; Financial Interests, Institutional, Research Grant: Ono/LifeArc; Financial Interests, Institutional, Research Grant, Research funding: Genesis Therapeutics; Non-Financial Interests, Institutional, Proprietary Information, Collaboration on data analysis: Bms. M. Jamal-Hanjani: Financial Interests, Personal, Invited Speaker, Invited speaker honorarium: Oslo Cancer Cluster; Financial Interests, Personal, Invited Speaker, Invited speaker honorarium: Astex Pharmaceutical; Non-Financial Interests, , Advisory Role, Scientific Advisory Board and Steering Committee member: Achilles Therapeutics; Other, , Other, I am named as co-inventor on patent PCT/US2017/028013 relating to methods for lung cancer detection.: Patent. All other authors have declared no conflicts of interest.
Late-breaking results presented at the ESMO Congress 2022 elucidate the link between air pollution and lung cancer
ESMO partners with EONS to launch the Cancer Prevention across Europe (PrEvCan) campaign
Study confirms accuracy of multi-cancer early detection blood testing, paving the way for a new era in cancer screening
Paris, France, 9 September 2022 – Sustainability will be at the heart of many discussions at the ESMO Congress 2022, as illustrated by the new results and initiatives spanning cancer prevention, early detection and treatment that were announced today during the opening press conference to the annual meeting of the international oncology community taking place 9-13 September in Paris, France.
“By definition, sustainability is about being able to maintain important, high-quality processes over time. In oncology, seeing the rise in cancer cases, we need to ask ourselves how we can make sure the essential process of caring for patients can be maintained,” said ESMO President Prof. Solange Peters. “Sustainability encompasses the notion of avoiding degradation, meaning that we also have to look at maintaining the quality – which, in cancer, includes the availability of and access to anticancer drugs. It also includes quality of life, which is still dependent on the environment, and as ESMO we need to start looking at the environmental sustainability of everything we do.”
Underscoring the multifaceted nature of sustainability as a societal goal, late-breaking results to be presented at the ESMO Congress 2022 offer a deeper understanding of the long-established link between air pollution and non-small cell lung cancer (NSCLC) arising in people who have never smoked, and make clear the link between climate change and human health. “Pollution has a known association with lung cancer, but we didn’t know if and how it directly causes the disease,” said study author and ESMO 2022 Scientific Co-Chair Prof. Charles Swanton, the Francis Crick Institute and Cancer Research UK Chief Clinician, London, UK, explaining the background to this work. (1)
The research, based on human and laboratory studies, showed for a population of nearly half a million people living in England, South Korea and Taiwan that exposure to increasing concentrations of airborne particulate matter (PM) 2.5 micrometres (μm) in diameter was linked to increased risk of NSCLC with mutations in the EGFR gene, which are known to be present in about half of people with lung cancer who have never smoked. In laboratory mouse models, the same pollutant particles (PM2.5) were seen to directly cause lung cancer by acting through lung tissue inflammation, driving the release of a molecule known as interleukin-1β that causes epithelial cells to transdifferentiate into cancer stem-like cells. In the presence of mutations in EGFR and in another gene linked to lung cancer called KRAS, these cells can then bloom into a tumour.
“These mutations can be found in over half of normal lung tissue biopsies and are a natural process of ageing. They are necessary, but not sufficient to drive cancer: it is in combination with pollution that the cancer stem cells can expand and initiate a tumour. This begins to explain how environmental carcinogens that don’t induce DNA mutations can drive cancer,” said Swanton, deriving from this discovery a public health mandate to lower the levels of these pollutants, which are produced by the combustion of fossil fuels. “We have to achieve a 50% reduction in greenhouse gas emissions by 2030, and by doing so we will naturally reduce levels of PM2.5. We can all play a part here: we need to cycle more, walk more. It’s worth bearing in mind that PM2.5 cause 8 million deaths a year, not just due to cancer but also to other diseases like cardiovascular disease, strokes, dementia – that is more than the deaths caused by tobacco globally.”
In light of the fact that his research confirmed the blockade of interleukin-1β could inhibit lung cancer initiation by blocking the pollution-induced transformation of airway cells into cancer stem cells, Swanton also suggested that targeting interleukin-1β should be further explored in the future as a potential new approach to cancer prevention.
The findings come in a context where the global incidence of respiratory cancers is on the rise, with annual new cases expected to jump by about 70% over the next two decades. In Europe alone, similar trends observed for other malignancies could result in an increase in overall cancer mortality, from 2 million annual deaths in 2020, to as many as 3 million by 2040. (2) As up to half of all cancers are thought to be preventable, prevention is considered by the World Health Organisation to be the most cost-effective, and thus the most sustainable, long-term strategy for cancer control.
“The ESMO Vision 2025, made very clear that if we want to succeed in tackling cancer, we need to develop a clear plan for primary and secondary prevention, continue to offer the optimal care for cancers that cannot be prevented and adequately support cancer survivorship. Focusing on only one of these areas and neglecting the others would lead to failure,” said ESMO Director of Public Policy Dr. Rosa Giuliani.
In line with the Society’s commitment to promoting research-based cancer prevention, the ESMO representatives joined European Oncology Nursing Society (EONS) Executive Board member Dr. Lena Sharp, Regional Cancer Centre, Stockholm, Sweden, in announcing the launch today of the Cancer Prevention across Europe Campaign (PrEvCan).
Led by EONS with ESMO as key partner alongside other international organisations, the campaign will over a one-year period dedicate each month to promoting and explaining the scientific evidence for each one of the 12 recommendations of the European Code Against Cancer (ECAC) to prevent the disease, starting in October with smoking as one of the most important cancer risk factors.
“What is new here is that it is the cancer care workforce leading the way,” said Sharp, the PrEvCan project leader. “We are the ones who meet patients and their families, so we could intervene on a daily basis supporting and advising people to adopt healthier lifestyles to reduce the risk of new cancers but also to reduce negative effects on the current disease.”
The campaign will target the general public, including the most vulnerable groups who can be difficult to reach with health promotion and lifestyle advice, but equally healthcare professionals, who according to Sharp can also take a more prominent role in supporting vaccination and screening programmes.
The ESMO President added: “We thought for a while that prevention should be in the hands of family doctors, but then we started to learn that preventing the disease must be at least partly in the hands of the specialists of a specific disease, in order to convince people about its importance. Particularly after COVID, a certain degree of suspicion can happen in medicine. You need to make sure that everything you propose has a basis – and one of these bases for cancer prevention is the burden of cancer, what it represents not only in terms of lost years of life but also in terms of the sustainability of our societies and healthcare systems.” Peters further highlighted that oncologists should view prevention as an integral part of oncology care, also because the science of prevention still requires more data.
For cancers that are not currently avoidable, screening and early detection has the potential to both maximise individuals’ chances of survival, and alleviate the burden on health systems by reducing the proportion of patients with advanced disease who require costly, chronic therapies and care.
A study to be presented at this year’s Congress could lead to a major paradigm shift in this field, having confirmed the feasibility of multi-cancer early detection (MCED) blood testing as a method of screening for up to 50 different cancer types simultaneously. (3)
“This is one of the very first studies where the detection of cancer DNA in the blood has allowed us to detect cancer at an early stage,” said ESMO 2022 Scientific Co-Chair Prof. Fabrice André, Institute Gustave Roussy, Villejuif, France. “If this test works, in the future, it will be good news for patients, but most cancer centres are not equipped to scale up surgeries for hundreds more patients with, say, early-stage pancreatic cancer. With this landmark study comes a need for a wake-up call for hospitals to see what will happen in 10 years and start now to train fellows and change their infrastructures accordingly.”
Highlighting the time and patience required to turn promising research results into meaningful innovation for patients, Swanton observed: “ESMO 2022 is a celebration of the collaboration between basic scientists and healthcare professionals to advance care for our patients. Some of the breakthroughs that will be discussed over the next four days have come from biological studies of worms, yeast, bacteria and plants – but they took 30 or 40 years of painstaking science from the bench to the bedside. We need our funders to recognise that and to sustain investment in discovery research to generate the medicines of the future.”
Among other highly anticipated results to be presented at the ESMO Congress 2022 , André drew attention to several examples of novel approaches which could soon become a reality in the clinic: from the phase III trial of gamma secretase inhibitor (GSI) nirogacestat, a first-in-class drug targeting a new molecular alteration in a rare category of cancers known as desmoid tumours, through a landmark trial of cell therapy using tumour-infiltrating lymphocytes (TILs) to improve the outcomes of patients with advanced melanoma, all the way to several late-phase trials of immunotherapy, including for non-small cell lunger cancer patients not eligible to standard platinum chemotherapy. André welcomed the presence of studies for underrepresented patient populations in the Congress’s scientific programme, concluding: “We cannot exclude patients from clinical trials.”
In closing, ESMO 2022 Press Officer Dr. Antonio Passaro called for a wide and wise dissemination of the data to be presented: “We have here a community of about 25,000 people, with more than 1,900 abstracts and 76 LBAs that will be presented in the coming days. We need to pass these messages to all of our colleagues and the public in order to dramatically improve the future of our patients, which risks being worse than it is today considering current cancer incidence trends.”
-END-
Notes to Editors
Please make sure to use the official name of the meeting in your reports: ESMO Congress 2022
3 Abstract 903O ‘A prospective study of a multi-cancer early detection blood test’ will be presented by Deb Schrag during the proffered paper
session “Basic science and translational research” on Sunday, 11 September, 16:30 to 18:00 CEST in Orléans Auditorium. Annals of Oncology,
Volume 33 Supplement 7, September 2022
4 The ESMO ANMS 2.0 survey about access to cancer medicines will be discussed during the educational session “The Universal Health Coverage (UHC) dilemma: Can we afford to pay for what we want?” on Saturday, 10 September, 8:30 to 10:00 CEST in Marseille Auditorium.
ESMO is the leading professional organisation for medical oncology. With 25,000 members representing oncology professionals from over 160 countries worldwide, ESMO is the society of reference for oncology education and information. Driven by a shared determination to secure the best possible outcomes for patients, ESMO is committed to standing by those who care about cancer through addressing the diverse needs of #ONEoncologycommunity, offering #educationforLIFE, and advocating for #accessiblecancerCARE. www.esmo.org
Friday, September 10, 2021
NOT SMOKING
Balkan countries and Poland rank highest in lung cancer risk for ages 50 to 69, attributable to air pollution
INTERNATIONAL ASSOCIATION FOR THE STUDY OF LUNG CANCER
(Denver Sept. 9, 2021 9 a.m. GMT/10 a.m. CDT/11 a.m. EDT)—Five European countries rank highest for lung cancer risk among those aged 50 to 69 years attributable to air pollution, according to research presented in today’s Presidential Symposium Plenary Session at the IASLC 2021 World Conference on Lung Cancer.
Although tobacco smoke is clearly a major cause of lung cancer, a recent analysis determined that worldwide, air pollution accounts for 14% of lung cancers, according to data reported by Christine Berg.
The causal evidence of a link between air pollution and lung cancer has been building for decades, but the risk varies widely in different regions of the world, depending on the age of the population, the amount of tobacco smoking over time, and the amount of air pollution in the country. Berg and co-researcher Dr. Joan Schiller, an adjunct professor at the University of Virginia and a Board Member of the Lung Cancer Research Foundation, sought to better understand the worldwide variability in air pollution attributable to lung cancer.
Berg conducted a review of the literature on the burden of indoor and outdoor air pollution. She assessed the burden of lung cancer by country from air pollution by querying The Global Burden of Disease Compare publicly accessible database. Lung cancer mortality was chosen as the endpoint in an age-standardized population of 100,000. Because the incidence of lung cancer increases with age, two age groups were selected: ages 50-69 and 70 and older. Both genders were combined in the analysis. Berg ranked the top 15 countries in each age group and compared changes in relative country ranking by age group.
According to her analysis, Serbia (36.88 per 100,000), Montenegro (34.61 per 100,000), North Macedonia (30.67 per 100,000), Bosnia/Herzegovina (30.64 per 100,000), and Poland (27.97 per 100,000) ranked highest for risk of lung cancer attributable to air pollution among ages 50-69.
Among the 70 and older group, China (98.55 per 100,000), Mongolia (71.11 per 100,000), North Korea (63.45 per 100,000), Laos (62.07 per 100,000), and Montenegro (61.80 per 100,000) ranked highest.
“For comparison, in the United States the number of lung cancer deaths per 100,000 attributed to air pollution in ages 50 to 69 is 3.91 and is 13.62 for 70 and older,” Berg said. The Balkans, Poland, Turkey, China, and some southeast Asian countries have the highest attributable risks. Serbia had the highest number of attributable deaths in the 50-69 age group, whereas China had the highest in the 70 and older age group.
“Patterns of cigarette smoking and amounts of pollution from fossil fuel energy sources are most likely the primary drivers of the variability in risk attributable to lung cancer,” said Berg. “As the tobacco epidemic is addressed, we also need to address other preventable causes of lung cancer.”
About the IASLC:
The International Association for the Study of Lung Cancer (IASLC) is the only global organization dedicated solely to the study of lung cancer and other thoracic malignancies. Founded in 1974, the association's membership includes nearly 7,500 lung cancer specialists across all disciplines in over 100 countries, forming a global network working together to conquer lung and thoracic cancers worldwide. The association also publishes the Journal of Thoracic Oncology, the primary educational and informational publication for topics relevant to the prevention, detection, diagnosis, and treatment of all thoracic malignancies. Visit www.iaslc.org for more information.
About the WCLC:
The WCLC is the world’s largest meeting dedicated to lung cancer and other thoracic malignancies, attracting more than 7,000 researchers, physicians and specialists from more than 100 countries. The goal is to increase awareness, collaboration and understanding of lung cancer, and to help participants implement the latest developments across the globe. The conference will cover a wide range of disciplines and unveil several research studies and clinical trial results. For more information, visit https://wclc2021.iaslc.org/.
SUBJECT OF RESEARCH
People
Tuesday, March 07, 2023
Death rates from lung cancer will fall overall in the EU and UK in 2023, but rise among women in France, Italy and Spain
A total of 1,261,990 people will die from cancer in 2023 in the EU (EU-27). A further 172,314 people will die from the disease in the UK, according to new research published in the leading cancer journal Annals of Oncology [1] today (Monday).
Researchers led by Carlo La Vecchia (MD), a professor at the University of Milan (Italy), estimate there will be a 6.5% fall in cancer death rates in men and a 3.7% fall in women between 2018 and 2023.
They predict that death rates from the ten most common cancers will continue to fall in most European countries in 2023, although the numbers of people dying will go up due to aging populations. A greater proportion of elderly people in the population means there is a greater number at the age where they are more likely to develop and die from cancer.
Compared to a peak in cancer death rates in 1988, the researchers calculate that nearly 5.9 million deaths will have been avoided in the 35 years between 1989 and 2023 in the EU-27. In the UK, 1.24 million deaths will have been avoided.
Prof. La Vecchia said: “If the current trajectory of declining cancer death rates continues, then it is possible there could be a further 35% reduction by 2035. More smokers quitting contribute to these favourable trends. In addition, greater efforts need to be made to control the growing epidemic in overweight, obesity and diabetes, alcohol consumption and infections, together with improvements in screening, early diagnosis and treatments.
“The advances in tobacco control are reflected in the favourable lung cancer trends but more could be done in this respect, particularly among women, as lung cancer death rates continue to rise among them. No deaths from lung cancer have been avoided in women, both in the EU-27 and the UK, during the period between 1989 and 2023.
“Pancreatic cancer is also a cause for concern, as death rates from this disease will not fall among men and will rise by 3.4% in women in the EU and 3.2% in women in the UK. Smoking can explain between about a quarter to a third of these deaths, and women, particularly in the middle and older age groups, did not give up smoking as early as men.”
The researchers analysed cancer death rates in the EU 27 Member States [2] as a whole and separately in the UK. They also looked at the five most populous EU countries (France, Germany, Italy, Poland and Spain) and, individually, for stomach, intestines, pancreas, lung, breast, uterus (including cervix), ovary, prostate, bladder and leukaemias for men and women [3]. Prof La Vecchia and his colleagues collected data on deaths from the World Health Organization and Eurostat databases from 1970 to 2018 for most of the EU-27 and the UK. This is the thirteenth consecutive year the researchers have published these predictions.
In the EU-27 countries the researchers predict that will be an age standardised rate (ASR) [4] of 123.8 deaths per 100,000 men by the end of 2023. In women, the age standardised death rate will be 79.3 per 100,000. In the UK, the death rates will be 106.5 and 83.5 per 100,000 for men and women, respectively.
Cancer death rates will fall for all cancers in men in the EU-27 and the UK. They will also fall for women in the UK. Among EU women, death rates will rise by 3.4% to nearly six per 100,000 for pancreatic cancer, and to just over 1% to 13.6 per 100,00 for lung cancer. Although there will be a 13.8% drop in lung cancer death rates among women in the UK, the death rate of 16.2 per 100,000 is still higher than among EU women because more UK women started smoking earlier than those in the EU. Lung cancer now kills more women in the UK than breast cancer, which has a death rate of 13.5 per 100,000.
When the researchers looked specifically at lung cancer death rates in five EU countries as well as the UK, they found that, although death rates are predicted to fall in men for all six countries, for women they will rise by nearly 14% in France, 5.6% in Italy and 5% in Spain. Among women in different age groups, the researchers found a decrease in predicted death rates from lung cancer among those aged 25 to 64, but an increase in those aged 65 to over 75 years, and consequently an increase overall.
“This is because women now aged 45 to 65, born in the 1960s and 1970s, have smoked less and stopped earlier than those born in the 1950s, who were in their twenties in the 1970s when smoking among young women was most prevalent,” said Prof. Eva Negri from the University of Bologna (Italy), co-leader of the research.
Colorectal (bowel) cancer will be the third biggest killer for women in both the EU and the UK: eight and ten per 100,000, respectively. Prostate cancer will be the third biggest killer for men: 9.5 and 11.2 per 100,000 in the EU and UK, respectively.
The researchers say that organised screening programmes using low dose computed tomography (CT scans) could reduce deaths from lung cancer by up to 20%. However, there are no such organised programmes in Europe, and it is too early to evaluate the impact of screening in the UK, following the Lung Cancer Screening trial.
The researchers highlight the role that overweight and obesity plays in cancers such as post-menopausal breast, endometrial (womb) cancer, stomach and colorectal cancer. Although death rates from stomach cancer are falling overall, mainly because of improved methods of food preservation, healthier diets and a decline in Helicobacter pylori infection, approximately a third of stomach cancers now occur in the cardia, the entrance to the stomach, and are associated with overweight and obesity and, hence, reflux, which is a risk factor for the development of cancer at this site. For colorectal cancer, death rates are falling in the EU but the decline has slowed in the UK.
“This is concerning as increases in both incidence and mortality from colorectal cancer in young women have been recorded in the UK. This can be partly explained by the prevalence of overweight and obesity, and alcohol and tobacco consumption,” said Prof. Negri.
The researchers caution that their estimates do not take account of the COVID pandemic, which occurred after the dates when data were available on cancer deaths. “The COVID-19 pandemic may have an effect on cancer mortality in 2023 as a result of delayed visits and procedures, influencing both secondary prevention and treatment, and disease management for cancer,” they write.
(ends)
Notes:
[1] “European cancer mortality predictions for the year 2023 with focus on lung cancer”, by M. Malvezzi et al. Annals of Oncology, doi: 10.1016/j.annonc.2023.01.010
[2] At the time of this analysis, the EU had 27 member states, with the UK leaving in 2020. Cyprus was excluded from the analysis due to excessive missing data.
[3] The paper contains individual tables of cancer death rates for each of the six countries.
[4] Age-standardised rates per 100,000 of the population reflect the annual probability of dying adjusted to reflect the age distribution of a population.
