Showing papers by "International Agency for Research on Cancer published in 2018"
TL;DR: A status report on the global burden of cancer worldwide using the GLOBOCAN 2018 estimates of cancer incidence and mortality produced by the International Agency for Research on Cancer, with a focus on geographic variability across 20 world regions.
Abstract: This article provides a status report on the global burden of cancer worldwide using the GLOBOCAN 2018 estimates of cancer incidence and mortality produced by the International Agency for Research on Cancer, with a focus on geographic variability across 20 world regions There will be an estimated 181 million new cancer cases (170 million excluding nonmelanoma skin cancer) and 96 million cancer deaths (95 million excluding nonmelanoma skin cancer) in 2018 In both sexes combined, lung cancer is the most commonly diagnosed cancer (116% of the total cases) and the leading cause of cancer death (184% of the total cancer deaths), closely followed by female breast cancer (116%), prostate cancer (71%), and colorectal cancer (61%) for incidence and colorectal cancer (92%), stomach cancer (82%), and liver cancer (82%) for mortality Lung cancer is the most frequent cancer and the leading cause of cancer death among males, followed by prostate and colorectal cancer (for incidence) and liver and stomach cancer (for mortality) Among females, breast cancer is the most commonly diagnosed cancer and the leading cause of cancer death, followed by colorectal and lung cancer (for incidence), and vice versa (for mortality); cervical cancer ranks fourth for both incidence and mortality The most frequently diagnosed cancer and the leading cause of cancer death, however, substantially vary across countries and within each country depending on the degree of economic development and associated social and life style factors It is noteworthy that high-quality cancer registry data, the basis for planning and implementing evidence-based cancer control programs, are not available in most low- and middle-income countries The Global Initiative for Cancer Registry Development is an international partnership that supports better estimation, as well as the collection and use of local data, to prioritize and evaluate national cancer control efforts CA: A Cancer Journal for Clinicians 2018;0:1-31 © 2018 American Cancer Society
58,675 citations
TL;DR: This year's update to the HMDB, HMDB 4.0, represents the most significant upgrade to the database in its history and should greatly enhance its ease of use and its potential applications in nutrition, biochemistry, clinical chemistry, clinical genetics, medicine, and metabolomics science.
Abstract: The Human Metabolome Database or HMDB (www.hmdb.ca) is a web-enabled metabolomic database containing comprehensive information about human metabolites along with their biological roles, physiological concentrations, disease associations, chemical reactions, metabolic pathways, and reference spectra. First described in 2007, the HMDB is now considered the standard metabolomic resource for human metabolic studies. Over the past decade the HMDB has continued to grow and evolve in response to emerging needs for metabolomics researchers and continuing changes in web standards. This year's update, HMDB 4.0, represents the most significant upgrade to the database in its history. For instance, the number of fully annotated metabolites has increased by nearly threefold, the number of experimental spectra has grown by almost fourfold and the number of illustrated metabolic pathways has grown by a factor of almost 60. Significant improvements have also been made to the HMDB's chemical taxonomy, chemical ontology, spectral viewing, and spectral/text searching tools. A great deal of brand new data has also been added to HMDB 4.0. This includes large quantities of predicted MS/MS and GC-MS reference spectral data as well as predicted (physiologically feasible) metabolite structures to facilitate novel metabolite identification. Additional information on metabolite-SNP interactions and the influence of drugs on metabolite levels (pharmacometabolomics) has also been added. Many other important improvements in the content, the interface, and the performance of the HMDB website have been made and these should greatly enhance its ease of use and its potential applications in nutrition, biochemistry, clinical chemistry, clinical genetics, medicine, and metabolomics science.
2,608 citations
TL;DR: The present estimates of the cancer burden in Europe alongside a description of the profiles of common cancers at the national and regional level provide a basis for establishing priorities for cancer control actions across Europe.
1,650 citations
TL;DR: These results may underestimate the overall proportion of cancers attributable to modifiable factors, because the impact of all established risk factors could not be quantified, and many likely modifiable risk factors are not yet firmly established as causal.
Abstract: Contemporary information on the fraction of cancers that potentially could be prevented is useful for priority setting in cancer prevention and control. Herein, the authors estimate the proportion and number of invasive cancer cases and deaths, overall (excluding nonmelanoma skin cancers) and for 26 cancer types, in adults aged 30 years and older in the United States in 2014, that were attributable to major, potentially modifiable exposures (cigarette smoking; secondhand smoke; excess body weight; alcohol intake; consumption of red and processed meat; low consumption of fruits/vegetables, dietary fiber, and dietary calcium; physical inactivity; ultraviolet radiation; and 6 cancer-associated infections). The numbers of cancer cases were obtained from the Centers for Disease Control and Prevention (CDC) and the National Cancer Institute; the numbers of deaths were obtained from the CDC; risk factor prevalence estimates were obtained from nationally representative surveys; and associated relative risks of cancer were obtained from published, large-scale pooled analyses or meta-analyses. In the United States in 2014, an estimated 42.0% of all incident cancers (659,640 of 1570,975 cancers, excluding nonmelanoma skin cancers) and 45.1% of cancer deaths (265,150 of 587,521 deaths) were attributable to evaluated risk factors. Cigarette smoking accounted for the highest proportion of cancer cases (19.0%; 298,970 cases) and deaths (28.8%; 169,180 deaths), followed by excess body weight (7.8% and 6.5%, respectively) and alcohol intake (5.6% and 4.0%, respectively). Lung cancer had the highest number of cancers (184,970 cases) and deaths (132,960 deaths) attributable to evaluated risk factors, followed by colorectal cancer (76,910 cases and 28,290 deaths). These results, however, may underestimate the overall proportion of cancers attributable to modifiable factors, because the impact of all established risk factors could not be quantified, and many likely modifiable risk factors are not yet firmly established as causal. Nevertheless, these findings underscore the vast potential for reducing cancer morbidity and mortality through broad and equitable implementation of known preventive measures. CA Cancer J Clin 2018;68:31-54. © 2017 American Cancer Society.
870 citations
Peking Union Medical College1, Duke University2, Peking University3, Centers for Disease Control and Prevention4, Hebei Medical University5, Fujian Medical University6, Cancer Council Queensland7, International Agency for Research on Cancer8, American Cancer Society9, Cancer Council New South Wales10
TL;DR: There was a marked overall increase in cancer survival from 2003 to 2015 in the population covered by these cancer registries in China, possibly reflecting advances in the quality of cancer care in these areas.
738 citations
University of Cambridge1, Australian National University2, Norwegian Institute of Public Health3, Utrecht University4, University of Tromsø5, Johns Hopkins University6, University of Oxford7, The George Institute for Global Health8, National Institutes of Health9, Copenhagen University Hospital10, University of Copenhagen11, Harry Perkins Institute of Medical Research12, University of Western Australia13, Fiona Stanley Hospital14, University of London15, Lund University16, University of Pittsburgh17, French Institute of Health and Medical Research18, University College London19, Technische Universität München20, University of Ulm21, University of Padua22, University of Southampton23, German Cancer Research Center24, Erasmus University Medical Center25, Umeå University26, Cardiff University27, Greifswald University Hospital28, Aarhus University29, Portland State University30, University of New South Wales31, Harvard University32, National and Kapodistrian University of Athens33, University of Hawaii34, Columbia University35, University of Iowa36, Duke University37, Yamagata University38, Tuskegee University39, University of Oulu40, University of Helsinki41, Medical University of South Carolina42, University of Washington43, Kaiser Permanente44, University of Groningen45, University of Granada46, Yale University47, Prevention Institute48, University of Edinburgh49, Uppsala University50, Basque Government51, Kyushu University52, Royal Prince Alfred Hospital53, Harokopio University54, University of California, San Diego55, VU University Medical Center56, Aalborg University57, University of Eastern Finland58, Laval University59, University of Vermont60, Wake Forest University61, Wake Forest Baptist Medical Center62, Kanazawa Medical University63, Baker IDI Heart and Diabetes Institute64, Heidelberg University65, Istituto Superiore di Sanità66, Pasteur Institute67, City College of New York68, Howard University69, University of Glasgow70, International Agency for Research on Cancer71, University of Bristol72, University of Auckland73
TL;DR: Current drinkers of alcohol in high-income countries, the threshold for lowest risk of all-cause mortality was about 100 g/week, and data support limits for alcohol consumption that are lower than those recommended in most current guidelines.
711 citations
Catholic University of the Sacred Heart1, Memorial Sloan Kettering Cancer Center2, International Agency for Research on Cancer3, University Health Network4, University of Lausanne5, Centre Hospitalier Universitaire de Grenoble6, Utrecht University7, Charité8, University of Texas MD Anderson Cancer Center9, Technische Universität München10, Belfast Health and Social Care Trust11, University of Zurich12, University of Nottingham13, Beatson West of Scotland Cancer Centre14, Tohoku University15, University of Verona16, Institut Gustave Roussy17, University of Bologna18, Radboud University Nijmegen19
TL;DR: This work believes this conceptual approach can form the basis for the next generation of NEN classifications and will allow more consistent taxonomy to understand how neoplasms from different organ systems inter-relate clinically and genetically.
688 citations
TL;DR: For the first time, specific loci that distinguish between BD and SCZ are discovered and polygenic components underlying multiple symptom dimensions are identified that point to the utility of genetics to inform symptomology and potential treatment.
569 citations
Princess Margaret Cancer Centre1, Wellcome Trust Sanger Institute2, University of Cambridge3, University of Toronto4, Weizmann Institute of Science5, Ontario Institute for Cancer Research6, International Agency for Research on Cancer7, European Bioinformatics Institute8, University Health Network9, Norwich University10, University of East Anglia11, National and Kapodistrian University of Athens12, University of Milan13, University of Granada14, Cancer Epidemiology Unit15, Prevention Institute16, University of Naples Federico II17, German Cancer Research Center18, Imperial College London19, Utrecht University20, Memorial Sloan Kettering Cancer Center21
TL;DR: Deep sequencing is used to analyse genes that are recurrently mutated in AML to distinguish between individuals who have a high risk of developing AML and those with benign ARCH, providing proof-of-concept that it is possible to discriminate ARCH from pre-AML many years before malignant transformation.
Abstract: The incidence of acute myeloid leukaemia (AML) increases with age and mortality exceeds 90% when diagnosed after age 65. Most cases arise without any detectable early symptoms and patients usually present with the acute complications of bone marrow failure1. The onset of such de novo AML cases is typically preceded by the accumulation of somatic mutations in preleukaemic haematopoietic stem and progenitor cells (HSPCs) that undergo clonal expansion2,3. However, recurrent AML mutations also accumulate in HSPCs during ageing of healthy individuals who do not develop AML, a phenomenon referred to as age-related clonal haematopoiesis (ARCH)4–8. Here we use deep sequencing to analyse genes that are recurrently mutated in AML to distinguish between individuals who have a high risk of developing AML and those with benign ARCH. We analysed peripheral blood cells from 95 individuals that were obtained on average 6.3 years before AML diagnosis (pre-AML group), together with 414 unselected age- and gender-matched individuals (control group). Pre-AML cases were distinct from controls and had more mutations per sample, higher variant allele frequencies, indicating greater clonal expansion, and showed enrichment of mutations in specific genes. Genetic parameters were used to derive a model that accurately predicted AML-free survival; this model was validated in an independent cohort of 29 pre-AML cases and 262 controls. Because AML is rare, we also developed an AML predictive model using a large electronic health record database that identified individuals at greater risk. Collectively our findings provide proof-of-concept that it is possible to discriminate ARCH from pre-AML many years before malignant transformation. This could in future enable earlier detection and monitoring, and may help to inform intervention.
567 citations
Aarhus University1, University of Erlangen-Nuremberg2, University of Bergen3, University of Rostock4, University of Picardie Jules Verne5, University of Natural Resources and Life Sciences, Vienna6, Austrian Academy of Sciences7, University of Turin8, University of Edinburgh9, Swiss Federal Institute for Forest, Snow and Landscape Research10, University of Lausanne11, University of Warsaw12, Polish Academy of Sciences13, University of Vienna14, University of Innsbruck15, Spanish National Research Council16, International Agency for Research on Cancer17, Norwegian University of Life Sciences18, Martin Luther University of Halle-Wittenberg19, University of Aberdeen20, Slovak Academy of Sciences21, Helmholtz Centre for Environmental Research - UFZ22, United States Environmental Protection Agency23, University College of Southeast Norway24, University of Geneva25, École Polytechnique Fédérale de Lausanne26
TL;DR: Analysis of changes in plant species richness on mountain summits over the past 145 years suggests that increased climatic warming has led to an acceleration in species richness increase, strikingly synchronized with accelerated global warming.
Abstract: Globally accelerating trends in societal development and human environmental impacts since the mid-twentieth century
1–7
are known as the Great Acceleration and have been discussed as a key indicator of the onset of the Anthropocene epoch
6
. While reports on ecological responses (for example, changes in species range or local extinctions) to the Great Acceleration are multiplying
8, 9
, it is unknown whether such biotic responses are undergoing a similar acceleration over time. This knowledge gap stems from the limited availability of time series data on biodiversity changes across large temporal and geographical extents. Here we use a dataset of repeated plant surveys from 302 mountain summits across Europe, spanning 145 years of observation, to assess the temporal trajectory of mountain biodiversity changes as a globally coherent imprint of the Anthropocene. We find a continent-wide acceleration in the rate of increase in plant species richness, with five times as much species enrichment between 2007 and 2016 as fifty years ago, between 1957 and 1966. This acceleration is strikingly synchronized with accelerated global warming and is not linked to alternative global change drivers. The accelerating increases in species richness on mountain summits across this broad spatial extent demonstrate that acceleration in climate-induced biotic change is occurring even in remote places on Earth, with potentially far-ranging consequences not only for biodiversity, but also for ecosystem functioning and services.
508 citations
TL;DR: Evidence is emerging regarding gene-environment interactions, particularly for tobacco and occupational exposures, and standardisation of reporting may help improve epidemiologic evaluation of risk.
TL;DR: Endometrial cancer incidence rates increased over time and in successive generations in several countries, especially in those countries with rapid socioeconomic transitions, with South Africa and several countries in Asia showing the largest increase.
Abstract: Background Cancers of the corpus uteri-primarily of the endometrium-rank as the sixth most common neoplasm in women worldwide. Analyses of the global patterns and trends of uterine cancer rates are needed in view of the ongoing obesity epidemic, a major risk factor for the disease. Methods Data on endometrial cancer (ICD-10 C54) incidence from population-based cancer registries in 43 populations, published in CI5plus or by registries, were extracted for 1978 to 2013. Age-standardized incidence rates were computed for all ages and for pre- (25-49 years) and postmenopausal ages (50 years and older). Temporal trends were assessed with Joinpoint analysis, and the effects of birth cohort and year of diagnosis on the overall trends were examined using age-period-cohort modeling. Results In 2006 to 2007, rates varied 10-fold across countries. The highest rates were in North America, Eastern and Northern Europe (19 cases per 100 000 among whites in the United States, 95% confidence interval [CI] = 18 to 20, and in Slovakia, 95% CI = 18 to 21), and the lowest rates were in middle-income countries (South Africa 1, 95% CI = 0 to 3, and India 3, 95% CI = 3 to 4). Rates during the most recent 10 data years increased in 26 of the 43 populations considered in this study, with South Africa and several countries in Asia showing the largest increase. The risk of endometrial cancer increased both in consecutive generations and over time in 11 of 23 populations, with the increases more pronounced in Japan, the Philippines, Belarus, Singapore, Costa Rica, and New Zealand. Conclusions Endometrial cancer incidence rates increased over time and in successive generations in several countries, especially in those countries with rapid socioeconomic transitions.
TL;DR: A global attainment analysis of the feasibility of attaining SDG targets on the basis of past trends and a estimates of health-related SDG index values in countries assessed at the subnational level varied substantially, particularly in China and India, although scores in Japan and the UK were more homogeneous.
University of Cologne1, Penn State Milton S. Hershey Medical Center2, University of North Carolina at Chapel Hill3, University of California, San Diego4, International Agency for Research on Cancer5, Max Planck Society6, French Institute of Health and Medical Research7, American Board of Legal Medicine8, University of Grenoble9, University of Zurich10, University of Oslo11, Oslo University Hospital12, University of Bonn13, Peter MacCallum Cancer Centre14, University of Milan15, University of Jena16, Memorial Sloan Kettering Cancer Center17, German Cancer Research Center18
TL;DR: It is shown LCNECs represent a distinct transcriptional subgroup among lung cancers and comprise two molecular subgroups, type I (TP53 and STK11/KEAP1 alterations) and type II ( TP53 and RB1 inactivation).
Abstract: Pulmonary large-cell neuroendocrine carcinomas (LCNECs) have similarities with other lung cancers, but their precise relationship has remained unclear. Here we perform a comprehensive genomic (n = 60) and transcriptomic (n = 69) analysis of 75 LCNECs and identify two molecular subgroups: “type I LCNECs” with bi-allelic TP53 and STK11/KEAP1 alterations (37%), and “type II LCNECs” enriched for bi-allelic inactivation of TP53 and RB1 (42%). Despite sharing genomic alterations with adenocarcinomas and squamous cell carcinomas, no transcriptional relationship was found; instead LCNECs form distinct transcriptional subgroups with closest similarity to SCLC. While type I LCNECs and SCLCs exhibit a neuroendocrine profile with ASCL1high/DLL3high/NOTCHlow, type II LCNECs bear TP53 and RB1 alterations and differ from most SCLC tumors with reduced neuroendocrine markers, a pattern of ASCL1low/DLL3low/NOTCHhigh, and an upregulation of immune-related pathways. In conclusion, LCNECs comprise two molecularly defined subgroups, and distinguishing them from SCLC may allow stratified targeted treatment of high-grade neuroendocrine lung tumors. The molecular nature of large-cell neuroendocrine lung carcinomas (LCNEC) has remained unclear. Here, the authors show LCNECs represent a distinct transcriptional subgroup among lung cancers and comprise two molecular subgroups, type I (TP53 and STK11/KEAP1 alterations) and type II (TP53 and RB1 inactivation).
German Cancer Research Center1, St. Jude Children's Research Hospital2, Heidelberg University3, Institut Gustave Roussy4, University Hospital Heidelberg5, University of Calgary6, University of Copenhagen7, University Health Network8, University of Utah9, Semmelweis University10, McGill University11, Asan Medical Center12, Masaryk University13, Stanford University14, The Chinese University of Hong Kong15, University of California, San Francisco16, Emory University17, Humboldt University of Berlin18, Children's Hospitals and Clinics of Minnesota19, University of Texas Southwestern Medical Center20, Children's Hospital at Westmead21, Boston Children's Hospital22, University of Duisburg-Essen23, University of Oslo24, Oslo University Hospital25, Karolinska Institutet26, University of Gothenburg27, International Agency for Research on Cancer28, Swiss Tropical and Public Health Institute29, University of Bern30, University of Zurich31, University of Würzburg32, Massachusetts Institute of Technology33, University Hospital of Basel34, Charles University in Prague35, Hannover Medical School36, BC Cancer Agency37, University of Hamburg38, University of Toronto39, University of Cambridge40
TL;DR: The prevalence of genetic predispositions differed between molecular subgroups in the retrospective cohort and was highest for patients in the MBSHH subgroup, and survival estimates differed significantly across patients with germline mutations in different medulloblastoma predisposition genes.
Abstract: Summary Background Medulloblastoma is associated with rare hereditary cancer predisposition syndromes; however, consensus medulloblastoma predisposition genes have not been defined and screening guidelines for genetic counselling and testing for paediatric patients are not available. We aimed to assess and define these genes to provide evidence for future screening guidelines. Methods In this international, multicentre study, we analysed patients with medulloblastoma from retrospective cohorts (International Cancer Genome Consortium [ICGC] PedBrain, Medulloblastoma Advanced Genomics International Consortium [MAGIC], and the CEFALO series) and from prospective cohorts from four clinical studies (SJMB03, SJMB12, SJYC07, and I-HIT-MED). Whole-genome sequences and exome sequences from blood and tumour samples were analysed for rare damaging germline mutations in cancer predisposition genes. DNA methylation profiling was done to determine consensus molecular subgroups: WNT (MB WNT ), SHH (MB SHH ), group 3 (MB Group3 ), and group 4 (MB Group4 ). Medulloblastoma predisposition genes were predicted on the basis of rare variant burden tests against controls without a cancer diagnosis from the Exome Aggregation Consortium (ExAC). Previously defined somatic mutational signatures were used to further classify medulloblastoma genomes into two groups, a clock-like group (signatures 1 and 5) and a homologous recombination repair deficiency-like group (signatures 3 and 8), and chromothripsis was investigated using previously established criteria. Progression-free survival and overall survival were modelled for patients with a genetic predisposition to medulloblastoma. Findings We included a total of 1022 patients with medulloblastoma from the retrospective cohorts (n=673) and the four prospective studies (n=349), from whom blood samples (n=1022) and tumour samples (n=800) were analysed for germline mutations in 110 cancer predisposition genes. In our rare variant burden analysis, we compared these against 53 105 sequenced controls from ExAC and identified APC, BRCA2, PALB2, PTCH1, SUFU , and TP53 as consensus medulloblastoma predisposition genes according to our rare variant burden analysis and estimated that germline mutations accounted for 6% of medulloblastoma diagnoses in the retrospective cohort. The prevalence of genetic predispositions differed between molecular subgroups in the retrospective cohort and was highest for patients in the MB SHH subgroup (20% in the retrospective cohort). These estimates were replicated in the prospective clinical cohort (germline mutations accounted for 5% of medulloblastoma diagnoses, with the highest prevalence [14%] in the MB SHH subgroup). Patients with germline APC mutations developed MB WNT and accounted for most (five [71%] of seven) cases of MB WNT that had no somatic CTNNB1 exon 3 mutations. Patients with germline mutations in SUFU and PTCH1 mostly developed infant MB SHH . Germline TP53 mutations presented only in childhood patients in the MB SHH subgroup and explained more than half (eight [57%] of 14) of all chromothripsis events in this subgroup. Germline mutations in PALB2 and BRCA2 were observed across the MB SHH , MB Group3 , and MB Group4 molecular subgroups and were associated with mutational signatures typical of homologous recombination repair deficiency. In patients with a genetic predisposition to medulloblastoma, 5-year progression-free survival was 52% (95% CI 40–69) and 5-year overall survival was 65% (95% CI 52–81); these survival estimates differed significantly across patients with germline mutations in different medulloblastoma predisposition genes. Interpretation Genetic counselling and testing should be used as a standard-of-care procedure in patients with MB WNT and MB SHH because these patients have the highest prevalence of damaging germline mutations in known cancer predisposition genes. We propose criteria for routine genetic screening for patients with medulloblastoma based on clinical and molecular tumour characteristics. Funding German Cancer Aid; German Federal Ministry of Education and Research; German Childhood Cancer Foundation (Deutsche Kinderkrebsstiftung); European Research Council; National Institutes of Health; Canadian Institutes for Health Research; German Cancer Research Center; St Jude Comprehensive Cancer Center; American Lebanese Syrian Associated Charities; Swiss National Science Foundation; European Molecular Biology Organization; Cancer Research UK; Hertie Foundation; Alexander and Margaret Stewart Trust; V Foundation for Cancer Research; Sontag Foundation; Musicians Against Childhood Cancer; BC Cancer Foundation; Swedish Council for Health, Working Life and Welfare; Swedish Research Council; Swedish Cancer Society; the Swedish Radiation Protection Authority; Danish Strategic Research Council; Swiss Federal Office of Public Health; Swiss Research Foundation on Mobile Communication; Masaryk University; Ministry of Health of the Czech Republic; Research Council of Norway; Genome Canada; Genome BC; Terry Fox Research Institute; Ontario Institute for Cancer Research; Pediatric Oncology Group of Ontario; The Family of Kathleen Lorette and the Clark H Smith Brain Tumour Centre; Montreal Children's Hospital Foundation; The Hospital for Sick Children: Sonia and Arthur Labatt Brain Tumour Research Centre, Chief of Research Fund, Cancer Genetics Program, Garron Family Cancer Centre, MDT's Garron Family Endowment; BC Childhood Cancer Parents Association; Cure Search Foundation; Pediatric Brain Tumor Foundation; Brainchild; and the Government of Ontario.
TL;DR: Estimates of the number of new cases of cancers attributable to hepatitis B virus (HBV) and hepatitis C virus (HCV) at a global, regional and country level, and by development status are calculated to help set priorities for liver cancer prevention.
Abstract: High-quality data on liver cancers by probable cause are scarce in many regions of the world. The United Nations recently set a goal of eliminating viral hepatitis as a major public health threat by 2030. We aimed to estimate the number of new cases of cancers attributable to hepatitis B virus (HBV) and hepatitis C virus (HCV) at a global, regional and country level, and by development status. We used data on the prevalence of HBV and HCV in hepatocellular carcinoma from a systematic review including 119,000 cases in 260 studies covering 50 countries. A statistical model was constructed to extrapolate empirical data to countries without prevalence data. Country-specific numbers of liver cancer cases attributable to HBV and HCV were calculated using data from GLOBOCAN 2012. Globally, 770,000 cases of liver cancer occurred worldwide in 2012, of which 56% (95% CI: 52-60) were attributable to HBV and 20% (95% CI: 18-22) to HCV. Currently, HBV causes approximately two out of three cases of liver cancer in less developed countries but one in four cases in more developed countries and shows a much higher degree of geographical aggregation in Eastern Asia and sub-Saharan Africa than HCV. These estimates help set priorities for liver cancer prevention. High-coverage HBV vaccination will be transformational in HBV-endemic countries but the prevention of HCV transmission and the treatment of chronic carriers of both viruses requires new scalable solutions.
Institute of Cancer Research1, University of North Carolina at Chapel Hill2, National Institutes of Health3, Karolinska Institutet4, Harvard University5, University of Pisa6, City of Hope National Medical Center7, Boston University8, Institut Gustave Roussy9, New York University10, Johns Hopkins University11, International Agency for Research on Cancer12, University of Melbourne13, Cancer Council Victoria14, University of Massachusetts Amherst15, German Cancer Research Center16, University of Oxford17, University of Toronto18, National University of Singapore19, Imperial College London20, Aarhus University21, Radiation Effects Research Foundation22, Utrecht University23, Yeshiva University24, Umeå University25, University of Southern California26, University of Oslo27, Norwegian University of Science and Technology28, University of Pittsburgh29
TL;DR: It is suggested that increased adiposity is associated with a reduced risk of premenopausal breast cancer at a greater magnitude than previously shown and across the entire distribution of BMI.
Abstract: IMPORTANCE The association between increasing body mass index (BMI; calculated as wei ght in kilograms divided by height in meters squared) and risk of breast cancer is unique in cancer epidemiolog ...
TL;DR: A substantial number of cancer cases are attributable to diabetes and high BMI, and clinical and public health efforts should focus on identifying optimal preventive and screening measures for whole populations and individual patients.
Imperial College London1, University College London2, University of Ioannina3, Utrecht University4, University of Cambridge5, University of Bristol6, Carlos III Health Institute7, International Agency for Research on Cancer8, Umeå University9, Basque Government10, National and Kapodistrian University of Athens11, French Institute of Health and Medical Research12, University of Rennes13, University of Antioquia14, Lund University15, German Cancer Research Center16, Cancer Epidemiology Unit17, University of Turin18, University of Granada19, Aalborg University20, Aarhus University21, University of Naples Federico II22, Prevention Institute23, University of Tromsø24, National Institute for Health Research25, Wellcome Trust Sanger Institute26
TL;DR: Irrespective of BMI, metabolically unhealthy individuals had higher CHD risk than their healthy counterparts and population-wide strategies to tackle obesity are challenged, challenging the concept of 'metabolically healthy obesity.
Abstract: EPIC-CVD has been supported by the European Union Framework 7 (HEALTH-F2-2012-279233), the European Research Council (268834), the UK Medical Research Council (G0800270 and MR/L003120/1), the British Heart Foundation (SP/09/002 and RG/08/014 and RG13/13/30194), and the UK National Institute of Health Research. EPIC Asturias was also supported by the Regional Government of Asturias. EPIC-Greece is also supported by the Hellenic Health Foundation. EPIC- Heidelberg was also supported by the German Cancer Aid, German Cancer Research Centre, German Federal Ministry of Education and Research. EPIC-Oxford was also supported by the UK Medical Research Council (MR/M012190/1) and Cancer Research UK (570/A16491). EPIC-Ragusa was also supported by the Sicilian Government, AIRE ONLUS Ragusa, and AVIS Ragusa. EPIC-Turin was supported also by the Compagnia di San Paolo and the Human Genetics Foundation-Torino (HuGeF).
TL;DR: It is concluded that screening for colorectal cancer with stool-based tests and with lower endoscopy (either colonoscopy or sigmoidoscopy) saves lives.
Abstract: IARC View on Colorectal Screening The International Agency for Research on Cancer concluded that screening for colorectal cancer with stool-based tests and with lower endoscopy (either colonoscopy or sigmoidoscopy) saves lives. Comparative effectiveness data were inconclusive.
TL;DR: In this article, the authors predicted the future burden of primary liver cancer (PLC) in 30 countries around 2030 using age-period-cohort models (NORDPRED software).
Johns Hopkins University1, Harvard University2, Yale University3, National Institutes of Health4, German Cancer Research Center5, New York University6, Mayo Clinic7, University of Toronto8, University of California, San Francisco9, International Agency for Research on Cancer10, University of Pisa11, Sapienza University of Rome12, Vita-Salute San Raffaele University13, Leidos14, University of Amsterdam15, Yale Cancer Center16, Veterans Health Administration17, National and Kapodistrian University of Athens18, Monash University19, University of Melbourne20, Cancer Council Victoria21, Fred Hutchinson Cancer Research Center22, Heidelberg University23, University of Southern California24, University of Texas MD Anderson Cancer Center25, University of Szeged26, Charles University in Prague27, American Cancer Society28, University of Ostrava29, University of Cambridge30, Cleveland Clinic31, Lithuanian University of Health Sciences32, Memorial Sloan Kettering Cancer Center33, University of Hawaii34, Carlos III Health Institute35, National Institute for Health and Welfare36, QIMR Berghofer Medical Research Institute37, University of Padua38, University of Bologna39, Autonomous University of Barcelona40, Pompeu Fabra University41, Université Paris-Saclay42, Vanderbilt University43, Georgetown University44, Umeå University45, Casa Sollievo della Sofferenza46, Kaiser Permanente47, University of Hamburg48, Academy of Sciences of the Czech Republic49, University at Buffalo50, University of Washington51
TL;DR: The largest pancreatic cancer GWAS to date, including 9040 patients and 12,496 controls of European ancestry from the PANScan and the Pancreatic Cancer Case Control Consortium (PanC4), was performed in this paper.
Abstract: In 2020, 146,063 deaths due to pancreatic cancer are estimated to occur in Europe and the United States combined. To identify common susceptibility alleles, we performed the largest pancreatic cancer GWAS to date, including 9040 patients and 12,496 controls of European ancestry from the Pancreatic Cancer Cohort Consortium (PanScan) and the Pancreatic Cancer Case-Control Consortium (PanC4). Here, we find significant evidence of a novel association at rs78417682 (7p12/TNS3, P = 4.35 × 10−8). Replication of 10 promising signals in up to 2737 patients and 4752 controls from the PANcreatic Disease ReseArch (PANDoRA) consortium yields new genome-wide significant loci: rs13303010 at 1p36.33 (NOC2L, P = 8.36 × 10−14), rs2941471 at 8q21.11 (HNF4G, P = 6.60 × 10−10), rs4795218 at 17q12 (HNF1B, P = 1.32 × 10−8), and rs1517037 at 18q21.32 (GRP, P = 3.28 × 10−8). rs78417682 is not statistically significantly associated with pancreatic cancer in PANDoRA. Expression quantitative trait locus analysis in three independent pancreatic data sets provides molecular support of NOC2L as a pancreatic cancer susceptibility gene.
TL;DR: There remain clear disparities in the cancer burden according to national Human Development Index scores, and international efforts are needed to aid countries in social and economic transition to reduce the widening gap in cancer occurrence and survival worldwide.
Abstract: Aims: This review examines the links between human development and cancer overall and for specific types of cancer, as well as cancer-related risk-factors and outcomes, such as disability and life ...
TL;DR: Much work remains to be done to achieve optimal effectiveness of cancer screening in the EU, and continued monitoring, regular feedbacks and periodic reporting are needed to ensure the desired impacts of the programmes.
Abstract: The second report on the implementation status of cancer screening in European Union (EU) was published in 2017. The report described the implementation status, protocols and organization (updated till 2016) and invitation coverage (for index year 2013) of breast, cervical and colorectal cancer screening in the EU. Experts in screening programme monitoring (N=80) from the EU Member States having access to requisite information in their respective countries provided data on breast, cervical and colorectal cancer screening through online questionnaires. Data was collected for screening performed in the framework of publicly mandated programmes only. Filled in questionnaires were received from 26 Member States for all three sites and from one Member State for breast cancer only.
Substantial improvement in screening implementation using population-based approach was documented. Among the age-eligible women, 94.7% were residents of Member States implementing or planning population-based breast cancer screening in 2016, compared to 91.6% in 2007. The corresponding figures for cervical cancer screening were 72.3% and 51.3% in 2016 and 2007 respectively. Most significant improvement was documented for colorectal cancer screening with roll-out ongoing or completed in 17 Member States in 2016, compared to only five in 2007. So the access to population-based screening increased to 72.4% of the age-eligible populations in 2016 as opposed to only 42.6% in 2007. The invitation coverage was highly variable, ranging from 0.2%-111% for breast cancer, 7.6%-105% for cervical cancer and 1.8%-127% for colorectal cancer in the target populations.
In spite of the considerable progress, much work remains to be done to achieve optimal effectiveness. Continued monitoring, regular feedbacks and periodic reporting are needed to ensure the desired impacts of the programmes. This article is protected by copyright. All rights reserved.
TL;DR: This study updates previously published lists of known occupational carcinogens while providing additional information on cancer type, exposure scenarios and routes, and discussing trends in the identification of carcinogens over time.
Abstract: The recognition of occupational carcinogens is important for primary prevention, compensation and surveillance of exposed workers, as well as identifying causes of cancer in the general population. This study updates previously published lists of known occupational carcinogens while providing additional information on cancer type, exposure scenarios and routes, and discussing trends in the identification of carcinogens over time. Data were extracted from International Agency for Research on Cancer (IARC) Monographs covering the years 1971–2017, using specific criteria to ensure occupational relevance and provide high confidence in the causality of observed exposure-disease associations. Selected agents were substances, mixtures or types of radiation classified in IARC Group 1 with ‘sufficient evidence of carcinogenicity’ in humans from studies of exposed workers and evidence of occupational exposure documented in the pertinent monograph. The number of known occupational carcinogens has increased over time: 47 agents were identified as known occupational carcinogens in 2017 compared with 28 in 2004. These estimates are conservative and likely underestimate the number of carcinogenic agents present in workplaces. Exposure to these agents causes a wide range of cancers; cancers of the lung and other respiratory sites, followed by skin, account for the largest proportion. The dominant routes of exposure are inhalation and dermal contact. Important progress has been made in identifying occupational carcinogens; nevertheless, there is an ongoing need for research on the causes of work-related cancer. Most workplace exposures have not been evaluated for their carcinogenic potential due to inadequate epidemiologic evidence and a paucity of quantitative exposure data.
TL;DR: Patients with LCNEC tumors that carry a wild-type RB1 gene or express the RB1 protein do better with NSCLC-GEM/TAX treatment than with SCLc-PE chemotherapy, but no difference was observed for RB1 mutated or with lost protein expression.
Abstract: Purpose: Previous genomic studies have identified two mutually exclusive molecular subtypes of large-cell neuroendocrine carcinoma (LCNEC): the RB1 mutated (mostly comutated with TP53) and the RB1 wild-type groups. We assessed whether these subtypes have a predictive value on chemotherapy outcome.Experimental Design: Clinical data and tumor specimens were retrospectively obtained from the Netherlands Cancer Registry and Pathology Registry. Panel-consensus pathology revision confirmed the diagnosis of LCNEC in 148 of 232 cases. Next-generation sequencing (NGS) for TP53, RB1, STK11, and KEAP1 genes, as well as IHC for RB1 and P16 was performed on 79 and 109 cases, respectively, and correlated with overall survival (OS) and progression-free survival (PFS), stratifying for non-small cell lung cancer type chemotherapy including platinum + gemcitabine or taxanes (NSCLC-GEM/TAX) and platinum-etoposide (SCLC-PE).Results:RB1 mutation and protein loss were detected in 47% (n = 37) and 72% (n = 78) of the cases, respectively. Patients with RB1 wild-type LCNEC treated with NSCLC-GEM/TAX had a significantly longer OS [9.6; 95% confidence interval (CI), 7.7-11.6 months] than those treated with SCLC-PE [5.8 (5.5-6.1); P = 0.026]. Similar results were obtained for patients expressing RB1 in their tumors (P = 0.001). RB1 staining or P16 loss showed similar results. The same outcome for chemotherapy treatment was observed in LCNEC tumors harboring an RB1 mutation or lost RB1 protein.Conclusions: Patients with LCNEC tumors that carry a wild-type RB1 gene or express the RB1 protein do better with NSCLC-GEM/TAX treatment than with SCLC-PE chemotherapy. However, no difference was observed for RB1 mutated or with lost protein expression. Clin Cancer Res; 24(1); 33-42. ©2017 AACR.
University of Copenhagen1, International Agency for Research on Cancer2, University of Eastern Finland3, University of Auvergne4, University College Dublin5, Wageningen University and Research Centre6, University of Alberta7, University of Barcelona8, Carlos III Health Institute9, Ulster University10, European Food Safety Authority11
TL;DR: This position paper on biomarker of food intake validation outlines the second step of the BFIRev procedure but may also be used as such for validation of new candidate biomarkers identified, e.g., in food metabolomic studies.
Abstract: Biomarkers of food intake (BFIs) are a promising tool for limiting misclassification in nutrition research where more subjective dietary assessment instruments are used. They may also be used to assess compliance to dietary guidelines or to a dietary intervention. Biomarkers therefore hold promise for direct and objective measurement of food intake. However, the number of comprehensively validated biomarkers of food intake is limited to just a few. Many new candidate biomarkers emerge from metabolic profiling studies and from advances in food chemistry. Furthermore, candidate food intake biomarkers may also be identified based on extensive literature reviews such as described in the guidelines for Biomarker of Food Intake Reviews (BFIRev). To systematically and critically assess the validity of candidate biomarkers of food intake, it is necessary to outline and streamline an optimal and reproducible validation process. A consensus-based procedure was used to provide and evaluate a set of the most important criteria for systematic validation of BFIs. As a result, a validation procedure was developed including eight criteria, plausibility, dose-response, time-response, robustness, reliability, stability, analytical performance, and inter-laboratory reproducibility. The validation has a dual purpose: (1) to estimate the current level of validation of candidate biomarkers of food intake based on an objective and systematic approach and (2) to pinpoint which additional studies are needed to provide full validation of each candidate biomarker of food intake. This position paper on biomarker of food intake validation outlines the second step of the BFIRev procedure but may also be used as such for validation of new candidate biomarkers identified, e.g., in food metabolomic studies.
Research Triangle Park1, deCODE genetics2, Anschutz Medical Campus3, Boston University4, University of Helsinki5, VU University Amsterdam6, Dartmouth College7, University of Iceland8, National Institutes of Health9, West Virginia University10, Washington University in St. Louis11, Radboud University Nijmegen12, Virginia Commonwealth University13, University of Pennsylvania14, Veterans Health Administration15, International Agency for Research on Cancer16, Lunenfeld-Tanenbaum Research Institute17, University of Pittsburgh18, University of Wisconsin-Madison19
TL;DR: The well-known CHRNA5-CHRNA3-CHRNB4 genes were reconfirmed and a novel association in the DNA methyltransferase gene DNMT3B yielded, which highlights the importance of genetically influenced regulation in brain on the risks of nicotine dependence, heavy smoking and consequent lung cancer.
Abstract: Cigarette smoking is a leading cause of preventable mortality worldwide. Nicotine dependence, which reduces the likelihood of quitting smoking, is a heritable trait with firmly established associations with sequence variants in nicotine acetylcholine receptor genes and at other loci. To search for additional loci, we conducted a genome-wide association study (GWAS) meta-analysis of nicotine dependence, totaling 38,602 smokers (28,677 Europeans/European Americans and 9925 African Americans) across 15 studies. In this largest-ever GWAS meta-analysis for nicotine dependence and the largest-ever cross-ancestry GWAS meta-analysis for any smoking phenotype, we reconfirmed the well-known CHRNA5-CHRNA3-CHRNB4 genes and further yielded a novel association in the DNA methyltransferase gene DNMT3B. The intronic DNMT3B rs910083-C allele (frequency=44–77%) was associated with increased risk of nicotine dependence at P=3.7 × 10−8 (odds ratio (OR)=1.06 and 95% confidence interval (CI)=1.04–1.07 for severe vs mild dependence). The association was independently confirmed in the UK Biobank (N=48,931) using heavy vs never smoking as a proxy phenotype (P=3.6 × 10−4, OR=1.05, and 95% CI=1.02–1.08). Rs910083-C is also associated with increased risk of squamous cell lung carcinoma in the International Lung Cancer Consortium (N=60,586, meta-analysis P=0.0095, OR=1.05, and 95% CI=1.01–1.09). Moreover, rs910083-C was implicated as a cis-methylation quantitative trait locus (QTL) variant associated with higher DNMT3B methylation in fetal brain (N=166, P=2.3 × 10−26) and a cis-expression QTL variant associated with higher DNMT3B expression in adult cerebellum from the Genotype-Tissue Expression project (N=103, P=3.0 × 10−6) and the independent Brain eQTL Almanac (N=134, P=0.028). This novel DNMT3B cis-acting QTL variant highlights the importance of genetically influenced regulation in brain on the risks of nicotine dependence, heavy smoking and consequent lung cancer.
Necker-Enfants Malades Hospital1, Paris Descartes University2, Stockholm County Council3, International Agency for Research on Cancer4, Technische Universität München5, Icahn School of Medicine at Mount Sinai6, Dartmouth College7, University of Cincinnati8, Research Triangle Park9, University of Nevada, Reno School of Medicine10, University of Paris11, University of Grenoble12, Harvard University13, National Institute for Environmental Studies14
TL;DR: A number of criteria are proposed that are critical to support the primary contribution of epigenetics in DOHaD and intergenerational transmission of environmental stressors effects as well as providing insight for future research.
TL;DR: The leukaemia burden worldwide is examined and the distinct incidence patterns are highlighted in order to elucidate explanatory factors that may support preventive measures and health resource planning.