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: A large and diverse collection of tumor mutations in cancer patients provides important information on the nature of environmental factors or biological processes that are important causes of human gene mutation, since xenobiotic mutagens as well as endogenous mechanisms of genetic change produce characteristic types of patterns in target DNA.
Abstract: The first p53 gene mutation arising in a human tumor was described a decade ago by Baker et al. [S.J. Baker, E.R. Fearon, J.M. Nigro, S.R. Hamilton, A.C. Preisinger, J.M. Jessup, P. van Tuinen, D.H. Ledbetter, D.F. Barker, Y. Nakamura, R. White, B. Vogelstein, Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas, Science 244 (1989) 217-221]. There are now over 10,000 mutations extracted from the published literature in the IARC database of human p53 tumor mutations [P. Hainaut, T. Hernandez, A. Robinson, P. Rodriguez-Tome, T. Flores, M. Hollstein, C.C. Harris, R. Montesano, IARC database of p53 gene mutations in human tumors and cell lines: updated compilation, revised formats and new visualization tools, Nucleic Acids Res. 26 (1998) 205-213; Version R3, January 1999]. A large and diverse collection of tumor mutations in cancer patients provides important information on the nature of environmental factors or biological processes that are important causes of human gene mutation, since xenobiotic mutagens as well as endogenous mechanisms of genetic change produce characteristic types of patterns in target DNA [J.H. Miller, Mutational specificity in bacteria, Annu. Rev. Genet. 17 (1983) 215-238; T. Lindahl, Instability and decay of the primary structure of DNA, Nature 362 (1993) 709-715; S.P. Hussain, C.C. Harris, Molecular epidemiology of human cancer: contribution of mutation spectra studies of tumor suppressor genes, Cancer Res. 58 (1998) 4023-4037; P. Hainaut, M. Hollstein, p53 and human cancer: the first ten thousand mutations, Adv. Cancer Res. 2000]. P53 gene mutations in cancers can be compared to point mutation spectra at the HPRT locus of human lymphocytes from patients or healthy individuals with known exposure histories, and accumulated data indicate that mutation patterns at the two loci share certain general features. Hypotheses regarding specific cancer risk factors can be tested by comparing p53 tumor mutations typical of a defined patient group against mutations generated experimentally in rodents or in prokaryotic and eukaryotic cells in vitro. Refinements of this approach to hypothesis testing are being explored that employ human p53 sequences introduced artificially into experimental organisms used in laboratory mutagenesis assays. P53-specific laboratory models, combined with DNA microchips designed for high through-put mutation screening promise to unmask information currently hidden in the compilation of human tumor p53 mutations.
193 citations
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TL;DR: A certain amount of overdiagnosis in children under 2 years of age may explain the increased incidence rates and partially the increase in survival and overall 5-year survival in Europe in 1988-1997.
193 citations
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International Agency for Research on Cancer1, University of Toronto2, University of Texas Health Science Center at Houston3, University of Göttingen4, Epigenomics AG5, German Cancer Research Center6, Heidelberg University7, Mayo Clinic8, University of California, San Francisco9, Brown University10, Wayne State University11, National University of Singapore12, University of Bonn13, University of Cologne14, Pennsylvania State University15, National Institute of Occupational Health16, Radboud University Nijmegen17, University of Zaragoza18, deCODE genetics19, University of Iceland20, Seoul National University21, University of California, Los Angeles22, Dartmouth College23, Council on Education for Public Health24, Institut Gustave Roussy25, Cancer Care Ontario26, University of Sheffield27, Ontario Institute for Cancer Research28
TL;DR: Previous associations found in white populations were replicated and new associations were identified in Asian populations, and the associations between the 5p15 variants and lung cancer differed by histology; odds ratios for rs2736100 were highest in adenocarcinoma and for rs402710 were highest for squamous cell carcinomas.
Abstract: BACKGROUND: Genome-wide association studies have identified three chromosomal regions at 15q25, 5p15, and 6p21 as being associated with the risk of lung cancer. To confirm these associations in independent studies and investigate heterogeneity of these associations within specific subgroups, we conducted a coordinated genotyping study within the International Lung Cancer Consortium based on independent studies that were not included in previous genome-wide association studies. METHODS: Genotype data for single-nucleotide polymorphisms at chromosomes 15q25 (rs16969968, rs8034191), 5p15 (rs2736100, rs402710), and 6p21 (rs2256543, rs4324798) from 21 case-control studies for 11 645 lung cancer case patients and 14 954 control subjects, of whom 85% were white and 15% were Asian, were pooled. Associations between the variants and the risk of lung cancer were estimated by logistic regression models. All statistical tests were two-sided. RESULTS: Associations between 15q25 and the risk of lung cancer were replicated in white ever-smokers (rs16969968: odds ratio [OR] = 1.26, 95% confidence interval [CI] = 1.21 to 1.32, P(trend) = 2 x 10(-26)), and this association was stronger for those diagnosed at younger ages. There was no association in never-smokers or in Asians between either of the 15q25 variants and the risk of lung cancer. For the chromosome 5p15 region, we confirmed statistically significant associations in whites for both rs2736100 (OR = 1.15, 95% CI = 1.10 to 1.20, P(trend) = 1 x 10(-10)) and rs402710 (OR = 1.14, 95% CI = 1.09 to 1.19, P(trend) = 5 x 10(-8)) and identified similar associations in Asians (rs2736100: OR = 1.23, 95% CI = 1.12 to 1.35, P(trend) = 2 x 10(-5); rs402710: OR = 1.15, 95% CI = 1.04 to 1.27, P(trend) = .007). The associations between the 5p15 variants and lung cancer differed by histology; odds ratios for rs2736100 were highest in adenocarcinoma and for rs402710 were highest in adenocarcinoma and squamous cell carcinomas. This pattern was observed in both ethnic groups. Neither of the two variants on chromosome 6p21 was associated with the risk of lung cancer. CONCLUSIONS: In this international genetic association study of lung cancer, previous associations found in white populations were replicated and new associations were identified in Asian populations. Future genetic studies of lung cancer should include detailed stratification by histology.
193 citations
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Utrecht University1, International Agency for Research on Cancer2, University of British Columbia3, Aarhus University4, Aalborg University5, Institut Gustave Roussy6, University of Naples Federico II7, Imperial College London8, German Cancer Research Center9, National and Kapodistrian University of Athens10, Umeå University11, University of Cambridge12, University of Oxford13
TL;DR: Findings show that high concentrations of serum HDL are associated with a decreased risk of colon cancer, and the mechanism behind this association needs further elucidation.
Abstract: Objective To examine the association between serum concentrations of total cholesterol, high density lipoprotein cholesterol (HDL), low density lipoprotein cholesterol, triglycerides, apolipoprotein A-I (apoA), apolipoprotein B and the incidence of colorectal cancer (CRC).
Design Nested case–control study.
Setting The study was conducted within the European Prospective Investigation into Cancer and Nutrition (EPIC), a cohort of more than 520 000 participants from 10 western European countries.
Participants 1238 cases of incident CRC, which developed after enrolment into the cohort, were matched with 1238 controls for age, sex, centre, follow-up time, time of blood collection and fasting status.
Main outcome measures Serum concentrations were quantitatively determined by colorimetric and turbidimetric methods. Dietary and lifestyle data were obtained from questionnaires. Conditional logistic regression models were used to estimate incidence rate ratios (RRs) and 95% CIs which were adjusted for height, weight, smoking habits, physical activity, education, consumption of fruit, vegetables, meat, fish, alcohol, fibre and energy.
Results After adjustments, the concentrations of HDL and apoA were inversely associated with the risk of colon cancer (RR for 1 SD increase of 16.6 mg/dl in HDL and 32.0 mg/dl in apoA of 0.78 (95% CI 0.68 to 0.89) and 0.82 (95% CI 0.72 to 0.94), respectively). No association was observed with the risk of rectal cancer. Additional adjustment for biomarkers of systemic inflammation, insulin resistance and oxidative stress or exclusion of the first 2 years of follow-up did not influence the association between HDL and risk of colon cancer.
Conclusions These findings show that high concentrations of serum HDL are associated with a decreased risk of colon cancer. The mechanism behind this association needs further elucidation.
192 citations
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TL;DR: The hypothesis that the associations of circulating oestrogens with breast cancer risk are more likely due to an effect of circulating hormones on the development of cancer than to elevations induced by the tumour is supported.
Abstract: Nine prospective studies have now reported on the association between endogenous sex hormone levels in postmenopausal women and subsequent breast cancer risk (Moore et al, 1986; Wysowski et al, 1987; Barrett-Connor et al, 1990; Gordon et al, 1990; Garland et al, 1992; Helzlsouer et al, 1994; Toniolo et al, 1995; Berrino et al, 1996; Dorgan et al, 1996; Thomas et al, 1997; Zeleniuch-Jacquotte et al, 1997; Hankinson et al, 1998; Cauley et al, 1999; Kabuto et al, 2000). The Endogenous Hormones and Breast Cancer Collaborative Group (TEHBCCG) conducted a pooled analysis of the original data of these studies and concluded that both oestrogen and androgen hormones were strongly associated with risk (TEHBCCG, 2002). Remaining questions include how long prior to diagnosis the associations between hormone levels and breast cancer are observed and whether androgens play a part independent of their role as substrates for oestrogen production. The New York University (NYU) Women's Health Study was one of the first prospective studies to report a positive association between oestrogens and androgens and breast cancer risk (Toniolo et al, 1995). We expand here our initial results that were based on 130 cases for oestrogen analyses and 85 cases for androgen analyses. The present report includes 297 cases diagnosed between 6 months and 12.7 years after enrollment in the study. This study has nearly twice as many cases as any previously published cohort study. Owing to the large sample size and extended follow-up, we were able to assess the association of breast cancer risk with hormone levels in serum samples collected five or more years prior to diagnosis. To explore whether the presence of a growing cancer results in an increase in circulating hormone levels, we also examined the rate of change per year in hormone and sex-hormone binding globulin (SHBG) levels in 95 cases and their matched controls who contributed a second blood donation within 5 years of diagnosis.
192 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 |