Institution
International Agency for Research on Cancer
Government•Lyon, 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.
Topics: Cancer, Population, Breast cancer, Risk factor, European Prospective Investigation into Cancer and Nutrition
Papers published on a yearly basis
Papers
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TL;DR: World Health Organization Collaborating Center for International Histological Classification of Tu-mors, Armed Forces Institute of Pathology, Wash-ington, DC.
Abstract: World Health Organization Collaborating Centerfor International Histological Classification of Tu-mors, Armed Forces Institute of Pathology, Wash-ington, DC.Address for reprints: Leslie H. Sobin, M.D., ArmedForces Institute of Pathology, Alaska Avenue and14th Street, Building 54, Room 3009, Washington,DC 20306-6000.Received March 23, 2000; accepted March 23,2000.
2,578 citations
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TL;DR: The most common cancers in terms of new cases were lung (1.2 million), breast (1,05 million), colorectal (945 000), stomach (876'000), and liver (564'000).
Abstract: Summary Estimation of the burden of cancer in terms of incidence, mortality, and prevalence is a first step to appreciating appropriate control measures in a global context. The latest results of such an exercise, based on the most recent available international data, show that there were 10 million new cases, 6 million deaths, and 22 million people living with cancer in 2000. The most common cancers in terms of new cases were lung (1.2 million), breast (1.05 million), colorectal (945 000), stomach (876 000), and liver (564 000). The profile varies greatly in different populations, and the evidence suggests that this variation is mainly a consequence of different lifestyle and environmental factors, which should be amenable to preventive interventions. World population growth and ageing imply a progressive increase in the cancer burden – 15 million new cases and 10 million new deaths are expected in 2020, even if current rates remain unchanged.
2,365 citations
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TL;DR: The statistical models used used to estimate incidence and mortality data for 25 cancers in 40 European countries in 2008 used to obtain an estimate of the numbers of cancer cases and deaths in Europe in 2008.
2,358 citations
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TL;DR: In this paper, the carcinogenicity of the biological agents classifi ed as "carcinogenic to humans" (Group 1) and to identify additional tumour sites and mechanisms of carcinogenesis (tables 1 and 2).
Abstract: In February, 2009, 36 scientists from 16 countries met at the International Agency for Research on Cancer (IARC) to reassess the carcinogenicity of the biological agents classifi ed as “carcinogenic to humans” (Group 1) and to identify additional tumour sites and mechanisms of carcinogenesis (tables 1 and 2). These assessments will be published as part B of Volume 100 of the IARC Monographs. Hepatitis B virus (HBV) and hepatitis C virus (HCV) infect, res pectively, over 300 million and 170 million people worldwide, mainly in Asia and Africa. Chronic infection with these viruses is known to cause hepatocellular carcinoma. Suffi cient evidence is available to conclude that chronic infection with HCV can also cause non-Hodgkin lymphoma, especially B-cell lymphoma. In an inter vention study, patients with HCV infection and splenic lymphoma who were given the antiviral agent, interferon, showed regression of the lymphoma. Epstein–Barr virus (EBV) infects almost everyone and causes several types of cancer, including nasopharyngeal carcinoma, one of the most common cancers in southeastern Asia, and Burkitt’s lymphoma in children in Africa. New evidence points to a role for EBV in 5–10% of gastric carcinomas worldwide. EBV-positive gastric carcinoma develops early in life and has distinct histopathology, therefore it might belong to a separate clinical entity. In this subset of gastric tumours, presence of the viral genome in a monoclonal form and expression of EBV-transforming proteins are strong evidence for the involvement of EBV. Data from 22 cohort studies and 80 case–control studies show an association between Kaposi’s sarcoma herpes virus (KSHV) and Kaposi’s sarcoma, with relative risks higher than 10. Most studies are of transplant recipients and people infected with HIV-1. In both patients who are and are not infected with HIV-1, risk of Kaposi’s sarcoma increases relative to increasing titre of antibodies directed against KSHV, which are markers of the viral load. Evidence is suffi cient to show that KSHV causes primary eff usion lymphoma, a rare subgroup of B-cell non-Hodgkin lymphoma. Mechanistic data support an oncogenic role for KSHV in Kaposi’s sarcoma and in primary eff usion lymphoma—in individuals who are immunocompromised and in those apparently immunocompetent. KSHV is also associated with multicentric Castleman’s disease. Individuals who are infected with HIV-1 have a high risk of cancer. HIV-1 infection, mainly through immunosuppression, leads to increased replication of oncogenic viruses such as EBV and KSHV. Although antiretroviral therapy lowers the risk of many cancers associated with HIV-1, risks remain high. Cervical cancer is caused by types of human papillomavirus (HPV) that belong to a few phylogenetically related “high-risk” species (alpha-5, 6, 7, 9, 11) of the mucosotropic alpha genus. The types found most frequently in cervical cancer (HPV-16, 18, 31, 33, 35, 45, 52, 58) and four types less constantly found (HPV-39, 51, 56, 59) were classifi ed in
2,349 citations
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University of Cambridge1, National Institutes of Health2, University of Southern California3, International Agency for Research on Cancer4, Academia Sinica5, Princess Anne Hospital6, St Mary's Hospital7, University of London8, The Breast Cancer Research Foundation9, Wellcome Trust Sanger Institute10, QIMR Berghofer Medical Research Institute11, Peter MacCallum Cancer Centre12, University of Copenhagen13, Curie Institute14, Nofer Institute of Occupational Medicine15, University of Helsinki16, Seoul National University17, University of Ulsan18, Harvard University19, Karolinska Institutet20, Agency for Science, Technology and Research21, Hannover Medical School22, Leiden University23, Erasmus University Rotterdam24, University of Minnesota25, University of Sheffield26, Mayo Clinic27, VU University Amsterdam28, Carlos III Health Institute29, University of Melbourne30, Cancer Council New South Wales31, University of Otago32, Cancer Council Victoria33, Bosch34, University of Tübingen35, German Cancer Research Center36, University of Eastern Finland37
TL;DR: To identify further susceptibility alleles, a two-stage genome-wide association study in 4,398 breast cancer cases and 4,316 controls was conducted, followed by a third stage in which 30 single nucleotide polymorphisms were tested for confirmation.
Abstract: Breast cancer exhibits familial aggregation, consistent with variation in genetic susceptibility to the disease. Known susceptibility genes account for less than 25% of the familial risk of breast cancer, and the residual genetic variance is likely to be due to variants conferring more moderate risks. To identify further susceptibility alleles, we conducted a two-stage genome-wide association study in 4,398 breast cancer cases and 4,316 controls, followed by a third stage in which 30 single nucleotide polymorphisms (SNPs) were tested for confirmation in 21,860 cases and 22,578 controls from 22 studies. We used 227,876 SNPs that were estimated to correlate with 77% of known common SNPs in Europeans at r2.0.5. SNPs in five novel independent loci exhibited strong and consistent evidence of association with breast cancer (P,1027). Four of these contain plausible causative genes (FGFR2, TNRC9, MAP3K1 and LSP1). At the second stage, 1,792 SNPs were significant at the P,0.05 level compared with an estimated 1,343 that would be expected by chance, indicating that many additional common susceptibility alleles may be identifiable by this approach.
2,288 citations
Authors
Showing all 3012 results
Name | H-index | Papers | Citations |
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David J. Hunter | 213 | 1836 | 207050 |
Kay-Tee Khaw | 174 | 1389 | 138782 |
Elio Riboli | 158 | 1136 | 110499 |
Silvia Franceschi | 155 | 1340 | 112504 |
Stephen J. Chanock | 154 | 1220 | 119390 |
Paolo Boffetta | 148 | 1455 | 93876 |
Timothy J. Key | 146 | 808 | 90810 |
Hans-Olov Adami | 145 | 908 | 83473 |
Joseph J.Y. Sung | 142 | 1240 | 92035 |
Heiner Boeing | 140 | 1024 | 92580 |
Anne Tjønneland | 139 | 1345 | 91556 |
Kim Overvad | 139 | 1196 | 86018 |
Sheila Bingham | 136 | 519 | 67332 |
Pasi A. Jänne | 136 | 685 | 89488 |
Peter Kraft | 135 | 821 | 82116 |