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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: Population & Cancer. The organization has 2989 authors who have published 9010 publications receiving 929752 citations. The organization is also known as: IARC.


Papers
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Journal ArticleDOI
TL;DR: This paper presents a meta-analyses of the immune system’s response to repeated exposure to carbon monoxide poisoning in rats over a 12-month period and shows clear patterns of decline in the number of immune-related adverse events.
Abstract: Benbrahim-Tallaa, Lamia Baan, Robert A Grosse, Yann Lauby-Secretan, Beatrice El Ghissassi, Fatiha Bouvard, Veronique Guha, Neela Loomis, Dana Straif, Kurt News England Lancet Oncol. 2012 Jul;13(7):663-4.

435 citations

Journal ArticleDOI
TL;DR: Increasing trends in incidence of the most common cancers, except stomach cancer, are bad news to public health but can largely be explained by well-known changes in society in the past decades.

435 citations

Journal ArticleDOI
TL;DR: Evidence is presented that gap junctions could indeed be responsible for a "bystander effect" seen in HSV-tk gene therapy, and that this effect may be due to Cx-mediated GJIC.
Abstract: In gene therapy to treat cancer, typically only a fraction of the tumor cells can be successfully transfected with a gene. However, in the case of brain tumor therapy with the thymidine kinase gene from herpes simplex virus (HSV-tk), not only the cells transfected with the gene but also neighboring others can be killed in the presence of ganciclovir. Such a "bystander" effect is reminiscent of our previous observation that the effect of certain therapeutic agents may be enhanced by their diffusion through gap junctional intercellular communication (GJIC). Herein, we present the evidence, from in vitro studies, that gap junctions could indeed be responsible for such a gene therapy bystander effect. We used HeLa cells for this purpose, since they show very little, if any, ability to communicate through gap junctions. When HeLa cells were transfected with HSV-tk gene and cocultured with nontransfected cells, only HSV-tk-transfected HeLa cells (tk+) were killed by ganciclovir. However, when HeLa cells transfected with a gene encoding for the gap junction protein, connexin 43 (Cx43), were used, not only tk+ cells, but also tk- cells were killed, presumably due to the transfer, via Cx43-mediated GJIC, of toxic ganciclovir molecules phosphorylated by HSV-tk to the tk- cells. Such bystander effect was not observed when tk+ and tk- cells were cocultured without direct cell-cell contact between those two types of cells. Thus, our results give strong evidence that the bystander effect seen in HSV-tk gene therapy may be due to Cx-mediated GJIC.

433 citations

Journal ArticleDOI
TL;DR: The present paper overviews the various DNA modifications induced by exposure to peroxynitrite or NO and superoxide concurrently, with special reference to the formation of 8-nitroguanine and 8-oxoguanine as well as the induction of DNA single strand breakage.

432 citations

Journal ArticleDOI
TL;DR: Overall, the incidence of cancer was increased by 16% in the cohort and the results were essentially unchanged by restriction to the subcohort of 8207 persons in whom obesity was the primary discharge diagnosis, and were also similar in the first year of follow-up after hospital discharge.

432 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