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http://hdl.handle.net/2445/171331
Title: | Mendelian randomization analysis rules out disylipidaemia as colorectal cancer cause |
Author: | Ibáñez Sanz, Gemma Díez Villanueva, Anna Riera Ponsati, Marina Fernández Villa, Tania Fernández Navarro, Pablo Bustamante, Mariona Llorca, Javier Amiano, Pilar Ascunce, Nieves Fernández Tardón, Guillermo Salcedo Bellido, Inmaculada Salas, Dolores Capelo Álvarez, Rocío Crous Bou, Marta Ortega Valín, Luis Pérez Gómez, Beatriz Castaño-Vinyals, Gemma Palazuelos-Calderón, Camilo Altzibar, Jone M. Ardanaz, Eva Tardón, Adonina Jiménez Moleón, José Juan Olmos Juste, Valle Aragonès Sanz, Núria Pollán, Marina Kogevinas, Manolis Moreno Aguado, Víctor |
Keywords: | Càncer colorectal Malalties de les glàndules endocrines Trastorns del metabolisme Colorectal cancer Endocrine diseases Disorders of metabolism |
Issue Date: | 16-Sep-2019 |
Publisher: | Nature Publishing Group |
Abstract: | Dyslipidemia and statin use have been associated with colorectal cancer (CRC), but prospective studies have shown mixed results. We aimed to determine whether dyslipidemia is causally linked to CRC risk using a Mendelian randomization approach and to explore the association of statins with CRC. A case-control study was performed including 1336 CRC cases and 2744 controls (MCC-Spain). Subjects were administered an epidemiological questionnaire and were genotyped with an array which included polymorphisms associated with blood lipids levels, selected to avoid pleiotropy. Four genetic lipid scores specific for triglycerides (TG), high density lipoprotein cholesterol (HDL), low density lipoprotein cholesterol (LDL), or total cholesterol (TC) were created as the count of risk alleles. The genetic lipid scores were not associated with CRC. The ORs per 10 risk alleles, were for TG 0.91 (95%CI: 0.72-1.16, p = 0.44), for HDL 1.14 (95%CI: 0.95-1.37, p = 0.16), for LDL 0.97 (95%CI: 0.81-1.16, p = 0.73), and for TC 0.98 (95%CI: 0.84-1.17, p = 0.88). The LDL and TC genetic risk scores were associated with statin use, but not the HDL or TG. Statin use, overall, was a non-significant protective factor for CRC (OR 0.84; 95%CI: 0.70-1.01, p = 0.060), but lipophilic statins were associated with a CRC risk reduction (OR 0.78; 95%CI 0.66-0.96, p = 0.018). Using the Mendelian randomization approach, our study does not support the hypothesis that lipid levels are associated with the risk of CRC. This study does not rule out, however, a possible protective effect of statins in CRC by a mechanism unrelated to lipid levels. |
Note: | Reproducció del document publicat a: https://doi.org/10.1038/s41598-019-49880-w |
It is part of: | Scientific Reports, 2019, vol. 9, p. 13407 |
URI: | http://hdl.handle.net/2445/171331 |
Related resource: | https://doi.org/10.1038/s41598-019-49880-w |
ISSN: | 2045-2322 |
Appears in Collections: | Articles publicats en revistes (Ciències Clíniques) Articles publicats en revistes (ISGlobal) Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
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