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Institution

International Agency for Research on Cancer

GovernmentLyon, France
About: International Agency for Research on Cancer is a government organization based out in Lyon, France. It is known for research contribution in the topics: Cancer & Population. The organization has 2989 authors who have published 9010 publications receiving 929752 citations. The organization is also known as: IARC.


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Journal Article
TL;DR: Excesses in high female socioeconomic strata were seen in most populations for cancers of the colon, breast and ovary and for skin melanoma, while in the two Latin American populations for which data were available, lung cancer was more frequent in higher social strata.
Abstract: This chapter summarizes accumulated data on the presence, magnitude and consistency of socioeconomic differentials in mortality and incidence of all malignant neoplasms and 24 individual types of neoplasms in 37 populations in 21 countries. More or less consistent excess risks in men in lower social strata were observed for all respiratory cancers (nose, larynx and lung) and cancers of the oral cavity and pharynx, oesophagus, stomach, and, with a number of exceptions, liver, as well as for all malignancies taken together. For women, low-class excesses were consistently encountered for cancers of the oesophagus, stomach, cervix uteri and, less consistently, liver. Men in higher social strata displayed excesses of colon and brain cancers and skin melanoma. In the two Latin American populations for which data were available, lung cancer was more frequent in higher social strata. Excesses in high female socioeconomic strata were seen in most populations for cancers of the colon, breast and ovary and for skin melanoma. Longitudinal data from England and Wales suggested widening over time of social class differences in men for all cancers combined and for cancers of the lung, larynx and stomach, and in women for all cancers combined and for cervical cancer.

391 citations

Journal ArticleDOI
TL;DR: This work shows that mice with a disrupted gene coding for poly (ADP-ribose) polymerase (PARP–/– mice) are completely resistant to the development of diabetes induced by the beta-cell toxin streptozocin, identifying NAD+ depletion caused by PARP activation as the dominant metabolic event in islet-cell destruction.
Abstract: Human type 1 diabetes results from the selective destruction of insulin-producing pancreatic beta cells during islet inflammation. Cytokines and reactive radicals released during this process contribute to beta-cell death. Here we show that mice with a disrupted gene coding for poly (ADP-ribose) polymerase (PARP–/– mice) are completely resistant to the development of diabetes induced by the beta-cell toxin streptozocin. The mice remained normoglycemic and maintained normal levels of total pancreatic insulin content and normal islet ultrastructure. Cultivated PARP–/– islet cells resisted streptozocin-induced lysis and maintained intracellular NAD+ levels. Our results identify NAD+ depletion caused by PARP activation as the dominant metabolic event in islet-cell destruction, and provide information for the development of strategies to prevent the progression or manifestation of the disease in individuals at risk of developing type 1 diabetes.

390 citations

Journal ArticleDOI
TL;DR: This Expert Consensus Statement reflects on how these ten KCs can be used to identify, organize and utilize mechanistic data when evaluating chemicals as EDCs, and uses diethylstilbestrol, bisphenol A and perchlorate as examples to illustrate this approach.
Abstract: Endocrine-disrupting chemicals (EDCs) are exogenous chemicals that interfere with hormone action, thereby increasing the risk of adverse health outcomes, including cancer, reproductive impairment, cognitive deficits and obesity. A complex literature of mechanistic studies provides evidence on the hazards of EDC exposure, yet there is no widely accepted systematic method to integrate these data to help identify EDC hazards. Inspired by work to improve hazard identification of carcinogens using key characteristics (KCs), we have developed ten KCs of EDCs based on our knowledge of hormone actions and EDC effects. In this Expert Consensus Statement, we describe the logic by which these KCs are identified and the assays that could be used to assess several of these KCs. We reflect on how these ten KCs can be used to identify, organize and utilize mechanistic data when evaluating chemicals as EDCs, and we use diethylstilbestrol, bisphenol A and perchlorate as examples to illustrate this approach.

390 citations

Journal ArticleDOI
TL;DR: This review emphasizes the need to identify new dietary biomarkers and highlights the emerging field of nutritional metabonomics as an analytical method to assess metabolic profiles as measures of dietary exposures and indicators of dietary patterns, dietary changes or effectiveness of dietary interventions.
Abstract: Modern epidemiology suggests a potential interactive association between diet, lifestyle, genetics and the risk of many chronic diseases. As such, many epidemiologic studies attempt to consider assessment of dietary intake alongside genetic measures and other variables of interest. However, given the multi-factorial complexities of dietary exposures, all dietary intake assessment methods are associated with measurement errors which affect dietary estimates and may obscure disease risk associations. For this reason, dietary biomarkers measured in biological specimens are being increasingly used as additional or substitute estimates of dietary intake and nutrient status. Genetic variation may influence dietary intake and nutrient metabolism and may affect the utility of a dietary biomarker to properly reflect dietary exposures. Although there are many functional dietary biomarkers that, if utilized appropriately, can be very informative, a better understanding of the interactions between diet and genes as potentially determining factors in the validity, application and interpretation of dietary biomarkers is necessary. It is the aim of this review to highlight how some important biomarkers are being applied in nutrition epidemiology and to address some associated questions and limitations. This review also emphasizes the need to identify new dietary biomarkers and highlights the emerging field of nutritional metabonomics as an analytical method to assess metabolic profiles as measures of dietary exposures and indicators of dietary patterns, dietary changes or effectiveness of dietary interventions. The review will also touch upon new statistical methodologies for the combination of dietary questionnaire and biomarker data for disease risk assessment. It is clear that dietary biomarkers require much further research in order to be better applied and interpreted. Future priorities should be to integrate high quality dietary intake information, measurements of dietary biomarkers, metabolic profiles of specific dietary patterns, genetics and novel statistical methodology in order to provide important new insights into gene-diet-lifestyle-disease risk associations.

388 citations

Journal ArticleDOI
01 Dec 2019-Gut
TL;DR: CRC incidence increased exclusively in young adults in nine high-income countries spanning three continents, potentially signalling changes in early-life exposures that influence large bowel carcinogenesis.
Abstract: Objective Early-onset colorectal cancer (CRC) is increasing in the USA despite rapid declines in older ages. Similar patterns are reported in Australia and Canada, but a comprehensive global analysis of contemporary data is lacking. Design We extracted long-term data from Cancer Incidence in Five Continents and supplemental sources to report on worldwide CRC incidence rates and trends by age (20–49 years and ≥50 years) through diagnosis year 2012 or beyond (Australia, Finland, New Zealand, Norway, Sweden, USA). Results During 2008–2012, age-standardised CRC incidence rates in adults Conclusion CRC incidence increased exclusively in young adults in nine high-income countries spanning three continents, potentially signalling changes in early-life exposures that influence large bowel carcinogenesis.

388 citations


Authors

Showing all 3012 results

NameH-indexPapersCitations
David J. Hunter2131836207050
Kay-Tee Khaw1741389138782
Elio Riboli1581136110499
Silvia Franceschi1551340112504
Stephen J. Chanock1541220119390
Paolo Boffetta148145593876
Timothy J. Key14680890810
Hans-Olov Adami14590883473
Joseph J.Y. Sung142124092035
Heiner Boeing140102492580
Anne Tjønneland139134591556
Kim Overvad139119686018
Sheila Bingham13651967332
Pasi A. Jänne13668589488
Peter Kraft13582182116
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20238
202233
2021483
2020495
2019423
2018400