scispace - formally typeset
Search or ask a question
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.


Papers
More filters
Journal ArticleDOI
TL;DR: HPV testing in primary screening using current mixtures of HPV types and HPV vaccination against main HPV types should reduce the incidence of this cancer worldwide.
Abstract: Background Most cancers of the uterine cervix are squamous cell carcinomas. Although the incidence of such carcinomas of the uterine cervix has declined over time, that of cervical adenocarcinoma has risen in recent years. The extent to which human papillomavirus (HPV) infection and cofactors may explain this differential trend is unclear. Methods We pooled data from eight case-control studies of cervical cancer that were conducted on three continents. A total of 167 case patients with invasive cervical adenocarcinoma (112 with adenocarcinoma and 55 with adenosquamous carcinoma) and 1881 hospital-based control subjects were included. HPV DNA was analyzed in cervical specimens with the GP5+/6+ general primer system followed by type-specific hybridization for 33 HPV genotypes. Blood samples were analyzed for chlamydial and herpes simplex virus 2 (HSV-2) serology. Multivariable unconditional logistic regression modeling was used to calculate odds ratios (ORs) with 95% confidence intervals (CIs). All tests of statistical significance were two-sided. Results The adjusted overall odds ratio for cervical adenocarcinoma in HPV-positive women compared with HPV-negative women was 81.3 (95% CI = 42.0 to 157.1). HPV 16 and HPV 18 were the two most commonly detected HPV types in case patients and control subjects. These two types were present in 82% of the patients. Cofactors that showed clear statistically significant positive associations with cervical adenocarcinoma overall and among HPV-positive women included never schooling, poor hygiene, sexual behavior-related variables, long-term use of hormonal contraception, high parity, and HSV-2 seropositivity. Parity had a weaker association with adenocarcinoma and only among HPV-positive women. Use of an intrauterine device (IUD) had a statistically significant inverse association with risk of adenocarcinoma (for ever use of an IUD compared with never use, OR = .41 [95% CI = 0.18 to 0.93]). Smoking and chlamydial seropositivity were not associated with disease. Conclusions HPV appears to be the key risk factor for cervical adenocarcinoma. HPV testing in primary screening using current mixtures of HPV types and HPV vaccination against main HPV types should reduce the incidence of this cancer worldwide.

647 citations

Journal ArticleDOI
Bonnie R. Joubert1, Janine F. Felix2, Paul Yousefi3, Kelly M. Bakulski4, Allan C. Just5, Carrie V. Breton6, Sarah E. Reese1, Christina A. Markunas1, Christina A. Markunas7, Rebecca C Richmond8, Cheng-Jian Xu9, Leanne K. Küpers9, Sam S. Oh10, Cathrine Hoyo11, Olena Gruzieva12, Cilla Söderhäll12, Lucas A. Salas13, Nour Baïz14, Hongmei Zhang15, Johanna Lepeule16, Carlos Ruiz13, Symen Ligthart2, Tianyuan Wang1, Jack A. Taylor1, Liesbeth Duijts, Gemma C Sharp8, Soesma A Jankipersadsing9, Roy Miodini Nilsen17, Ahmad Vaez9, Ahmad Vaez18, M. Daniele Fallin4, Donglei Hu10, Augusto A. Litonjua19, Bernard F. Fuemmeler7, Karen Huen3, Juha Kere12, Inger Kull12, Monica Cheng Munthe-Kaas20, Ulrike Gehring21, Mariona Bustamante, Marie José Saurel-Coubizolles22, Bilal M. Quraishi15, Jie Ren6, Jörg Tost, Juan R. González13, Marjolein J. Peters2, Siri E. Håberg23, Zongli Xu1, Joyce B. J. van Meurs2, Tom R. Gaunt8, Marjan Kerkhof9, Eva Corpeleijn9, Andrew P. Feinberg24, Celeste Eng10, Andrea A. Baccarelli25, Sara E. Benjamin Neelon4, Asa Bradman3, Simon Kebede Merid12, Anna Bergström12, Zdenko Herceg26, Hector Hernandez-Vargas26, Bert Brunekreef21, Mariona Pinart, Barbara Heude27, Susan Ewart28, Jin Yao6, Nathanaël Lemonnier29, Oscar H. Franco2, Michael C. Wu30, Albert Hofman2, Albert Hofman25, Wendy L. McArdle8, Pieter van der Vlies9, Fahimeh Falahi9, Matthew W. Gillman25, Lisa F. Barcellos3, Ashok Kumar31, Ashok Kumar12, Ashok Kumar32, Magnus Wickman33, Magnus Wickman12, Stefano Guerra, Marie-Aline Charles27, John W. Holloway34, Charles Auffray29, Henning Tiemeier2, George Davey Smith8, Dirkje S. Postma9, Marie-France Hivert25, Brenda Eskenazi3, Martine Vrijheid13, Hasan Arshad34, Josep M. Antó, Abbas Dehghan2, Wilfried Karmaus15, Isabella Annesi-Maesano14, Jordi Sunyer, Akram Ghantous26, Göran Pershagen12, Nina Holland3, Susan K. Murphy7, Dawn L. DeMeo19, Esteban G. Burchard10, Christine Ladd-Acosta4, Harold Snieder9, Wenche Nystad23, Gerard H. Koppelman9, Caroline L Relton8, Vincent W. V. Jaddoe2, Allen J. Wilcox1, Erik Melén33, Erik Melén12, Stephanie J. London1 
TL;DR: This large scale meta-analysis of methylation data identified numerous loci involved in response to maternal smoking in pregnancy with persistence into later childhood and provide insights into mechanisms underlying effects of this important exposure.
Abstract: Epigenetic modifications, including DNA methylation, represent a potential mechanism for environmental impacts on human disease. Maternal smoking in pregnancy remains an important public health problem that impacts child health in a myriad of ways and has potential lifelong consequences. The mechanisms are largely unknown, but epigenetics most likely plays a role. We formed the Pregnancy And Childhood Epigenetics (PACE) consortium and meta-analyzed, across 13 cohorts (n = 6,685), the association between maternal smoking in pregnancy and newborn blood DNA methylation at over 450,000 CpG sites (CpGs) by using the Illumina 450K BeadChip. Over 6,000 CpGs were differentially methylated in relation to maternal smoking at genome-wide statistical significance (false discovery rate, 5%), including 2,965 CpGs corresponding to 2,017 genes not previously related to smoking and methylation in either newborns or adults. Several genes are relevant to diseases that can be caused by maternal smoking (e.g., orofacial clefts and asthma) or adult smoking (e.g., certain cancers). A number of differentially methylated CpGs were associated with gene expression. We observed enrichment in pathways and processes critical to development. In older children (5 cohorts, n = 3,187), 100% of CpGs gave at least nominal levels of significance, far more than expected by chance (p value < 2.2 × 10(-16)). Results were robust to different normalization methods used across studies and cell type adjustment. In this large scale meta-analysis of methylation data, we identified numerous loci involved in response to maternal smoking in pregnancy with persistence into later childhood and provide insights into mechanisms underlying effects of this important exposure.

646 citations

Journal ArticleDOI
TL;DR: Ch Chronically high levels of circulating insulin and IGFs associated with a Western lifestyle may increase colorectal cancer risk, possibly by decreasing IGFBP-1 and increasing the bioactivity of IGF-I.
Abstract: BACKGROUND Leading a Western lifestyle, being overweight, and being sedentary are associated with an increased risk of colorectal cancer. Recent theories propose that the effects of these risk factors may be mediated by increases in circulating insulin levels and in the bioactivity of insulin-like growth factor (IGF)-I. To test this hypothesis, we conducted a case-control study nested within a cohort of 14 275 women in New York. METHODS We used blood samples that had been obtained from these women from March 1985 through June 1991 and stored in a biorepository. C-peptide (a marker for insulin secretion), IGF-I, and IGF-binding proteins (IGFBPs)-1, -2, and -3 were assayed in the serum of 102 women who subsequently developed colorectal cancer and 200 matched control subjects. Logistic regression was used to relate cancer risk to these peptide levels, by adjustment for other risk factors. All statistical tests used are two-sided. RESULTS Colorectal cancer risk increased with increasing levels of C-peptide (P:(trend) =.001), up to an odds ratio (OR) of 2. 92 (95% confidence interval [CI] = 1.26-6.75) for the highest versus the lowest quintiles, after adjustment for smoking. For colon cancer alone (75 case subjects and 146 control subjects), ORs increased up to 3.96 (95% CI = 1.49-10.50; P:(trend) <.001) for the highest versus the lowest quintiles. A statistically significant decrease in colorectal cancer risk was observed for increasing levels of IGFBP-1 (P:(trend) =.02; OR in the upper quintile = 0.48 [95% CI = 0.23-1. 00]), as well as for the highest quintile of IGFBP-2 levels (P:(trend) =.06; OR = 0.38 [95% CI = 0.15-0.94]). Colorectal cancer risk showed a modest but statistically nonsignificant positive association with levels of IGF-I and was statistically significantly increased for the highest quintile of IGFBP-3 (OR = 2.46 [95% CI = 1. 09-5.57]). CONCLUSIONS Chronically high levels of circulating insulin and IGFs associated with a Western lifestyle may increase colorectal cancer risk, possibly by decreasing IGFBP-1 and increasing the bioactivity of IGF-I.

645 citations

Journal ArticleDOI
TL;DR: These assessments will be published as volume 112 of the IARC Monographs in March, 2015.
Abstract: DOI: http://dx.doi.org/10.1016/S1470-2045(15)70134-8 Article Info  Summary  Full Text  Tables and Figures  References In March, 2015, 17 experts from 11 countries met at the International Agency for Research on Cancer (IARC; Lyon, France) to assess the carcinogenicity of the organophosphate pesticides tetrachlorvinphos, parathion, malathion, diazinon, and glyphosate (table). These assessments will be published as volume 112 of the IARC Monographs.

644 citations

Journal ArticleDOI
TL;DR: In this article, the authors quantified maternal mortality throughout the world by underlying cause and age from 1990 to 2015 for ages 10-54 years by systematically compiling and processing all available data sources from 186 of 195 countries and territories.

641 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
Network Information
Related Institutions (5)
German Cancer Research Center
26.3K papers, 1.4M citations

92% related

Fred Hutchinson Cancer Research Center
30.9K papers, 2.2M citations

89% related

University of Texas MD Anderson Cancer Center
92.5K papers, 4.7M citations

89% related

National Institutes of Health
297.8K papers, 21.3M citations

88% related

Memorial Sloan Kettering Cancer Center
65.3K papers, 4.4M citations

88% related

Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20238
202233
2021483
2020495
2019423
2018400