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: Population & Cancer. The organization has 2989 authors who have published 9010 publications receiving 929752 citations. The organization is also known as: IARC.
Topics: Population, Cancer, Breast cancer, Risk factor, European Prospective Investigation into Cancer and Nutrition
Papers published on a yearly basis
Papers
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TL;DR: SNPs in the NER genes ERCC1 (Asn118Asn, 15310G>C, 8902G>T), XPA (-4G>A), ERCC2/XPD (Lys751Gln) and ERCC5/X PD (His46His) and MGMT/AGT(Lys178Arg) were found to modulate NSCLC risk.
Abstract: Polymorphisms of DNA repair genes and risk of non-small cell lung cancer Lung cancer is a leading cause of cancer mortality with an inter-individual difference in susceptibility to the disease. The inheritance of low-efficiency genotypes involved in DNA repair and replication may contribute to the difference in susceptibility. We investigated 44 single nucleotide polymorphisms (SNPs) in 20 DNA repair genes including nucleotide excision repair (NER) genes XPA, ERCC1, ERCC2/XPD, ERCC4/XPF and ERCC5/XPG; base excision repair (BER) genes APE1/APEX, OGG1, MPG, XRCC1, PCNA, POLB, POL iota, LIG3 and EXO1; double-strand break repair (DSB-R) genes XRCC2, XRCC3, XRCC9, NBS1 and ATR; and direct damage reversal (DR) gene MGMT/AGT. The study included 343 non-small cell lung cancer (NSCLC) cases and 413 controls from Norwegian general population. Our results indicate that SNPs in the NER genes ERCC1 (Asn118Asn, 15310G > C, 8902G > T), XPA (-4G > A), ERCC2/XPD (Lys751Gln) and ERCC5/XPD (His46His); the BER genes APE1/APEX (Ile64Val), OGG1 (Ser326Cys), PCNA (1876A > G) and XRCC1 (Arg194Trp, Arg280His, Arg399Gln); and the DSB-R genes ATR (Thr211Met), NBS1 (Glu185Gln), XRCC2 (Arg188His) and XRCC9 (Thr297Ile) modulate NSCLC risk. The level of polycyclic aromatic hydrocarbon-DNA (PAH-DNA) adducts in normal lung tissue from 211 patients was analysed. The variant alleles of XRCC1(Arg280His), XRCC1 (Arg399Gln), ERCC1(G8092T), ERCC5(His46His) and MGMT/AGT(Lys178Arg) were more frequent in patients with PAH-DNA adduct levels lower than the mean whereas the XRCC1(Arg194Trp) variant was more frequent in cases with higher adduct levels than the mean.
410 citations
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University of Texas MD Anderson Cancer Center1, Pompeu Fabra University2, University of Southern California3, University of Turin4, American Cancer Society5, Radboud University Nijmegen Medical Centre6, Imperial College London7, Brigham and Women's Hospital8, deCODE genetics9, University of Oxford10, German Cancer Research Center11, National Institutes of Health12, University of Zaragoza13, Science Applications International Corporation14, University of Oviedo15, Hospital Universitario de Canarias16, Dartmouth College17, Washington University in St. Louis18, Memorial Sloan Kettering Cancer Center19, University of Minnesota20, Harvard University21, University of Iceland22, International Agency for Research on Cancer23, Cancer Epidemiology Unit24, Academy of Athens25, Umeå University26, South University27, St James's University Hospital28, Wittenberg University29, Babeș-Bolyai University30, University of Brescia31, French Institute of Health and Medical Research32, Centre national de la recherche scientifique33
TL;DR: Two new regions associated with bladder cancer on chromosomes 22q13.1, 19q12 and 2q37.1 are identified and previous candidate associations for the GSTM1 deletion and a tag SNP for NAT2 acetylation status are validated, and interactions with smoking in both regions are found.
Abstract: We conducted a multi-stage, genome-wide association study of bladder cancer with a primary scan of 591,637 SNPs in 3,532 affected individuals (cases) and 5,120 controls of European descent from five studies followed by a replication strategy, which included 8,382 cases and 48,275 controls from 16 studies In a combined analysis, we identified three new regions associated with bladder cancer on chromosomes 22q131, 19q12 and 2q371: rs1014971, (P = 8 × 10⁻¹²) maps to a non-genic region of chromosome 22q131, rs8102137 (P = 2 × 10⁻¹¹) on 19q12 maps to CCNE1 and rs11892031 (P = 1 × 10⁻⁷) maps to the UGT1A cluster on 2q371 We confirmed four previously identified genome-wide associations on chromosomes 3q28, 4p163, 8q2421 and 8q243, validated previous candidate associations for the GSTM1 deletion (P = 4 × 10⁻¹¹) and a tag SNP for NAT2 acetylation status (P = 4 × 10⁻¹¹), and found interactions with smoking in both regions Our findings on common variants associated with bladder cancer risk should provide new insights into the mechanisms of carcinogenesis
410 citations
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TL;DR: The current patterns of cancer in Africa are reviewed and the opportunities for reducing the burden through the application of resource level interventions, including implementation of vaccinations for liver and cervical cancers, tobacco control policies for smoking‐related cancers, and low‐tech early detection methods for cervical cancer are reviewed.
Abstract: Cancer is an emerging public health problem in Africa. About 715,000 new cancer cases and 542,000 cancer deaths occurred in 2008 on the continent, with these numbers expected to double in the next 20 years simply because of the aging and growth of the population. Furthermore, cancers such as lung, female breast, and prostate cancers are diagnosed at much higher frequencies than in the past because of changes in lifestyle factors and detection practices associated with urbanization and economic development. Breast cancer in women and prostate cancer in men have now become the most commonly diagnosed cancers in many Sub-Saharan African countries, replacing cervical and liver cancers. In most African countries, cancer control programs and the provision of early detection and treatment services are limited despite this increasing burden. This paper reviews the current patterns of cancer in Africa and the opportunities for reducing the burden through the application of resource level interventions, including implementation of vaccinations for liver and cervical cancers, tobacco control policies for smoking-related cancers, and low-tech early detection methods for cervical cancer, as well as pain relief at the palliative stage of cancer.
409 citations
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TL;DR: The current status of genetic alterations and signaling pathways operative in the evolution of astrocytic and oligodendroglial tumors is summarized.
Abstract: Gliomas are the most common primary brain tumors. They account for more than 70% of all neoplasms of the central nervous system and vary considerably in morphology, location, genetic alterations, and response to therapy. Most frequent and malignant are glioblastomas. The vast majority (>90%) develops rapidly after a short clinical history and without evidence of a less malignant precursor lesion (primary or de novo glioblastoma). Secondary glioblastomas develop more slowly through progression from low-grade or anaplastic astrocytoma. These glioblastoma subtypes constitute distinct disease entities that affect patients of different age, develop through distinct genetic pathways, show different RNA and protein expression profiles, and may differ in their response to radio- and chemotherapy. Recently, isocitrate dehydrogenase 1 (IDH1) mutations have been identified as a very early and frequent genetic alteration in the pathway to secondary glioblastomas as well as that in oligodendroglial tumors, providing the first evidence that low-grade astrocytomas and oligodendrogliomas may share common cells of origin. In contrast, primary glioblastomas very rarely contain IDH1 mutations, suggesting that primary and secondary glioblastomas may originate from different progenitor cells, despite the fact that they are histologically largely indistinguishable. In this review, we summarize the current status of genetic alterations and signaling pathways operative in the evolution of astrocytic and oligodendroglial tumors.
409 citations
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Ruhr University Bochum1, Karolinska Institutet2, University of Duisburg-Essen3, University of Bremen4, International Agency for Research on Cancer5, University of Turin6, University of Padua7, Université de Montréal8, Institut national de la recherche scientifique9, University of Milan10, National Institutes of Health11, Russian Academy12, University of Liverpool13, Nofer Institute of Occupational Medicine14, Curie Institute15, French Institute of Health and Medical Research16, Charles University in Prague17, Johns Hopkins University18
TL;DR: The major result that smoking exerted a steeper risk gradient on SqCC and SCLC than on AdCa is in line with previous population data and biological understanding of lung cancer development.
Abstract: Lung cancer is mainly caused by smoking, but the quantitative relations between smoking and histologic subtypes of lung cancer remain inconclusive. By using one of the largest lung cancer datasets ever assembled, we explored the impact of smoking on risks of the major cell types of lung cancer. This pooled analysis included 13,169 cases and 16,010 controls from Europe and Canada. Studies with population controls comprised 66.5% of the subjects. Adenocarcinoma (AdCa) was the most prevalent subtype in never smokers and in women. Squamous cell carcinoma (SqCC) predominated in male smokers. Age-adjusted odds ratios (ORs) were estimated with logistic regression. ORs were elevated for all metrics of exposure to cigarette smoke and were higher for SqCC and small cell lung cancer (SCLC) than for AdCa. Current male smokers with an average daily dose of >30 cigarettes had ORs of 103.5 (95% confidence interval (CI): 74.8-143.2) for SqCC, 111.3 (95% CI: 69.8-177.5) for SCLC and 21.9 (95% CI: 16.6-29.0) for AdCa. In women, the corresponding ORs were 62.7 (95% CI: 31.5-124.6), 108.6 (95% CI: 50.7-232.8) and 16.8 (95% CI: 9.2-30.6), respectively. Although ORs started to decline soon after quitting, they did not fully return to the baseline risk of never smokers even 35 years after cessation. The major result that smoking exerted a steeper risk gradient on SqCC and SCLC than on AdCa is in line with previous population data and biological understanding of lung cancer development.
406 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 |