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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 ArticleDOI
TL;DR: A population‐based case‐control study was conducted between July 1984 and February 1988 in the Spanish island of Majorca and a 4‐fold increase in the risk of colorectal cancer and a highly significant statistical trend was found for high consumption of fresh meat, dairy products and cereals combined with low consumption of cruciferae.
Abstract: A population-based case-control study was conducted between July 1984 and February 1988 in the Spanish island of Majorca; 286 incident colorectal cancer cases, 295 population controls and 203 hospital controls were interviewed using a food frequency questionnaire. In a multivariate analysis, an increased risk of colon cancer was found for high consumption of fresh meats (RR = 2.87) while a high consumption of cruciferous vegetables afforded protection (RR = 0.48). For rectal cancer an increased risk was associated with dairy products (RR = 3.08) while a protection was afforded by consumption of cruciferae (RR = 0.50). For colorectal cancer, the cereal food group also showed an increase in risk (RR = 1.92). When cases were compared to hospital controls, the effects of cruciferae in colon and rectum and those of dairy products in rectal cancer remained. The magnitude of the RR estimates was decreased for most comparisons, although in general terms the direction of the associations was the same. In addition, univariate analyses of food groups also suggested significant increases in risk of colorectal cancer for increasing consumption of cereals, potatoes, pastry, eggs and number of meals per day. An indication was found of a reduction in risk for consumers of coffee. An analysis based on risk scores was also conducted and a 4-fold increase in the risk of colorectal cancer and a highly significant statistical trend was found for high consumption of fresh meat, dairy products and cereals combined with low consumption of cruciferae.

266 citations

Journal Article
TL;DR: The results suggest that all of the connexin genes examined could induce recovery of GJIC of HeLa cells, but only the cx 26 gene exerts strong negative growth control on He La cells; thus, thisConnexin gene may have different functions from other connexIn genes.
Abstract: In order to examine whether different connexin gene species exert different degrees of tumor-suppressing activity, we characterized growth characteristics of a gap junction-deficient human cancer cell line, HeLa cells, before and after transfection with cDNA for three different connexins, connexin (cx) 26, cx 40, and cx 43. All transfected cell lines (3 clones transfected with the cx 26 gene, 2 clones with cx 40, and 1 with cx 43) showed establishment of gap junctional intercellular communication (GJIC). Two of the cx 26-transfected clones showed significantly slower growth compared with the parental HeLa cells. When transfectants were grown in soft agar, the three cx 26-transfected clones grew much less than the other transfectants and parent HeLa cells. When injected into nude mice, the two cx 26 clones which exhibited the highest amount of cx 26 transcript induced almost no tumors, whereas other transfectants, including the cx 26 clone which exhibited the lowest amount of cx 26 transcript, were tumorigenic. Among transfectants of various connexin genes, there was no good inverse correlation between their GJIC and tumorigenicity. GJIC levels were significantly higher in tumors induced in nude mice by clone cx 26 A and E transfectants. These results suggest that all of the connexin genes examined could induce recovery of GJIC of HeLa cells, but only the cx 26 gene exerts strong negative growth control on HeLa cells; thus, this connexin gene may have different functions from other connexin genes.

266 citations

Journal ArticleDOI
01 May 2002-Gut
TL;DR: The results support earlier findings of increased risk of colon cancer in subjects with elevated plasma IGF-1, and do not support the hypothesis that the risk of rectal cancer could also be directly related to IGF- 1 levels.
Abstract: Background: Insulin-like growth factor 1 (IGF-1) has antiapoptotic and mitogenic effects on various cell types, and raised IGF-1 levels are increasingly being implicated as potential risk factors for cancer. Aims: To examine the relationship between IGF-1 and its major plasma binding protein, IGF binding protein 3 (IGFBP-3), and the risk of colorectal cancer. Methods: We conducted a case-control study nested within the Northern Sweden Health and Disease Cohort. IGF-1 and IGFBP-3 were measured in prediagnostic plasma samples from 168 men and women who developed cancers of the colon (n=110) or rectum (n=58), and from 336 matched controls. Results: Conditional logistic regression analyses showed an increase in colon cancer risk with increasing levels of IGF-1 (odds ratios (ORs) 1.00, 1.89, 2.30, 2.66; p trend =0.03) and IGFBP-3 (ORs 1.00, 0.91, 1.80, 1.93; p trend =0.02). Rectal cancer risk was inversely related to levels of IGF-1 (ORs 1.00, 0.45, 0.33, 0.33; p trend =0.09) and IGFBP-3 (ORs 1.00, 0.75, 0.66, 0.49; p trend =0.21). Mutual adjustments between IGF-1 and IGFBP-3 did not materially alter these relationships. Conclusions: These results support earlier findings of increased risk of colon cancer in subjects with elevated plasma IGF-1. Our results however do not support the hypothesis that the risk of rectal cancer could also be directly related to IGF-1 levels.

265 citations

Journal ArticleDOI
TL;DR: HPV16 is by far the most carcinogenic HPV type in the anus, with enrichment of HPV16 even from high-grade lesions to anal cancer, both in individuals who are HIV negative and those who is HIV positive, and the fraction of anal cancer attributable to HPV16 is smaller in the HIV-positive population.
Abstract: Summary Background Data on carcinogenicity of human papillomavirus (HPV) types in the anus are needed to inform anal cancer prevention through vaccination and screening. This is particularly the case for people infected with HIV, who are at an increased risk of anal cancer. Methods We did a systematic review of studies published from January, 1986, to July, 2017, in MEDLINE, Embase, and the Cochrane Library on anal HPV infection, without any language restrictions. Eligible studies reported type-specific HPV prevalence by strata of cytopathological or histopathological anal diagnosis, sex, and HIV status. Data requests were made to authors when necessary. We did a meta-analysis of type-specific HPV prevalence across the full spectrum of anal diagnoses, from normal cytology to anal cancer. We assessed the main outcome of type-specific HPV prevalence ratios [PR], calculated across strata of anal diagnoses, gender, or HIV status, by use of generalised linear models. Findings 95 studies were identified from the search, published between 1992–2017, from which 18 646 individuals fulfilled the criteria for inclusion in the analyses: 8534 people with normal cytology, 5730 with low-grade lesions, 2024 with high-grade lesions, and 2358 with anal cancer. HPV prevalence varied in normal cytology from 42% in HIV-negative women to 76% in HIV-positive men and, for each diagnosis, was higher in individuals who were HIV positive than those who were HIV negative. HPV16 positivity increased with diagnosis severity, being the only HPV type accounting for more HPV infection in anal cancer than normal cytology, both in individuals who were HIV negative (PR 5·0, 95% CI 3·8–6·6, p Interpretation HPV16 is by far the most carcinogenic HPV type in the anus, with enrichment of HPV16 even from high-grade lesions to anal cancer, both in individuals who are HIV negative and those who are HIV positive. Nevertheless, the fraction of anal cancer attributable to HPV16 is smaller in the HIV-positive population. Funding International Agency for Research on Cancer.

265 citations

Journal ArticleDOI
TL;DR: The results indicate no association between childhood exposure to ETS and lung cancer risk and weak evidence of a dose-response relationship between risk of lung cancer and exposure to spousal and workplace ETS is found.
Abstract: Background: An association between exposure to environmental tobacco smoke (ETS) and lung cancer risk has been suggested. To evaluate this possible association better, researchers need more precise estimates of risk, the relative contribution of different sources of ETS, and the effect of ETS exposure on different histologic types of lung cancer. To address these issues, we have conducted a case-control study of lung cancer and exposure to ETS in 12 centers from seven European countries. Methods: A total of 650 patients with lung cancer and 1542 control subjects up to 74 years of age were interviewed about exposure to ETS. Neither case subjects nor control subjects had smoked more than 400 cigarettes in their lifetime. Results: ETS exposure during childhood was not associated with an increased risk of lung cancer (odds ratio [OR] for ever exposure = 0.78; 95% confidence interval [CI] = 0.64-0.96). The OR for ever exposure to spousal ETS was 1.16 (95% CI = 0.93-1.44). No clear dose-response relationship could be demonstrated for cumulative spousal ETS exposure. The OR for ever exposure to workplace ETS was 1.17 (95% CI = 0.94-1.45), with possible evidence of increasing risk for increasing duration of exposure. No increase in risk was detected in subjects whose exposure to spousal or workplace ETS ended more than 15 years earlier. Ever exposure to ETS from other sources was not associated with lung cancer risk. Risks from combined exposure to spousal and workplace ETS were higher for squamous cell carcinoma and small-cell carcinoma than for adenocarcinoma, but the differences were not statistically significant. Conclusions: Our results indicate no association between childhood exposure to ETS and lung cancer risk. We did find weak evidence of a dose-response relationship between risk of lung cancer and exposure to spousal and workplace ETS. There was no detectable risk after cessation of exposure.

265 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