Please use this identifier to cite or link to this item: 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 (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))
Articles publicats en revistes (ISGlobal)

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