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Verfasst von:Aglago, Elom K. [VerfasserIn]   i
 Qu, Conghui [VerfasserIn]   i
 Harlid, Sophia [VerfasserIn]   i
 Phipps, Amanda I [VerfasserIn]   i
 Steinfelder, Robert S [VerfasserIn]   i
 Ogino, Shuji [VerfasserIn]   i
 Thomas, Claire E [VerfasserIn]   i
 Hsu, Li [VerfasserIn]   i
 Toland, Amanda E [VerfasserIn]   i
 Brenner, Hermann [VerfasserIn]   i
 Berndt, Sonja I [VerfasserIn]   i
 Buchanan, Daniel D [VerfasserIn]   i
 Campbell, Peter T [VerfasserIn]   i
 Cao, Yin [VerfasserIn]   i
 Chan, Andrew T [VerfasserIn]   i
 Drew, David A [VerfasserIn]   i
 Figueiredo, Jane C [VerfasserIn]   i
 French, Amy J [VerfasserIn]   i
 Gallinger, Steven [VerfasserIn]   i
 Georgeson, Peter [VerfasserIn]   i
 Giannakis, Marios [VerfasserIn]   i
 Goode, Ellen L [VerfasserIn]   i
 Gruber, Stephen B [VerfasserIn]   i
 Gunter, Marc J [VerfasserIn]   i
 Harrison, Tabitha A [VerfasserIn]   i
 Hoffmeister, Michael [VerfasserIn]   i
 Huang, Wen-Yi [VerfasserIn]   i
 Hullar, Meredith AJ [VerfasserIn]   i
 Huyghe, Jeroen R [VerfasserIn]   i
 Jenkins, Mark A [VerfasserIn]   i
 Lynch, Brigid M [VerfasserIn]   i
 Moreno, Victor [VerfasserIn]   i
 Murphy, Neil [VerfasserIn]   i
 Newton, Christina C [VerfasserIn]   i
 Nowak, Jonathan A [VerfasserIn]   i
 Obón-Santacana, Mireia [VerfasserIn]   i
 Sun, Wei [VerfasserIn]   i
 Ugai, Tomotaka [VerfasserIn]   i
 Um, Caroline Y [VerfasserIn]   i
 Zaidi, Syed H [VerfasserIn]   i
 Tsilidis, Konstantinos K [VerfasserIn]   i
 van Guelpen, Bethany [VerfasserIn]   i
 Peters, Ulrike [VerfasserIn]   i
Titel:Folate intake and colorectal cancer risk according to genetic subtypes defined by targeted tumor sequencing
Verf.angabe:Elom K Aglago, Conghui Qu, Sophia Harlid, Amanda I Phipps, Robert S Steinfelder, Shuji Ogino, Claire E Thomas, Li Hsu, Amanda E Toland, Hermann Brenner, Sonja I Berndt, Daniel D Buchanan, Peter T Campbell, Yin Cao, Andrew T Chan, David A Drew, Jane C Figueiredo, Amy J French, Steven Gallinger, Peter Georgeson, Marios Giannakis, Ellen L Goode, Stephen B Gruber, Marc J Gunter, Tabitha A Harrison, Michael Hoffmeister, Wen-Yi Huang, Meredith AJ Hullar, Jeroen R Huyghe, Mark A Jenkins, Brigid M Lynch, Victor Moreno, Neil Murphy, Christina C Newton, Jonathan A Nowak, Mireia Obón-Santacana, Wei Sun, Tomotaka Ugai, Caroline Y Um, Syed H Zaidi, Konstantinos K Tsilidis, Bethany van Guelpen, Ulrike Peters
E-Jahr:2024
Jahr:September 2024
Umfang:10 S.
Illustrationen:Illustrationen
Fussnoten:Gesehen am 28.04.2025
Titel Quelle:Enthalten in: The American journal of clinical nutrition
Ort Quelle:Amsterdam : Elsevier, 1952
Jahr Quelle:2024
Band/Heft Quelle:120(2024), 3, Seite 664-673
ISSN Quelle:1938-3207
 1938-3215
Abstract:Background - Folate is involved in multiple genetic, epigenetic, and metabolic processes, and inadequate folate intake has been associated with an increased risk of cancer. - Objective - We examined whether folate intake is differentially associated with colorectal cancer (CRC) risk according to somatic mutations in genes linked to CRC using targeted sequencing. - Design - Participants within 2 large CRC consortia with available information on dietary folate, supplemental folic acid, and total folate intake were included. Colorectal tumor samples from cases were sequenced for the presence of nonsilent mutations in 105 genes and 6 signaling pathways (IGF2/PI3K, MMR, RTK/RAS, TGF-β, WNT, and TP53/ATM). Multinomial logistic regression models were analyzed comparing mutated/nonmutated CRC cases to controls to compute multivariable-adjusted odds ratios (ORs) with 95% confidence interval (CI). Heterogeneity of associations of mutated compared with nonmutated CRC cases was tested in case-only analyses using logistic regression. Analyses were performed separately in hypermutated and nonhypermutated tumors, because they exhibit different clinical behaviors. - Results - We included 4339 CRC cases (702 hypermutated tumors, 16.2%) and 11,767 controls. Total folate intake was inversely associated with CRC risk (OR = 0.93; 95% CI: 0.90, 0.96). Among hypermutated tumors, 12 genes (AXIN2, B2M, BCOR, CHD1, DOCK3, FBLN2, MAP3K21, POLD1, RYR1, TET2, UTP20, and ZNF521) showed nominal statistical significance (P < 0.05) for heterogeneity by mutation status, but none remained significant after multiple testing correction. Among these genetic subtypes, the associations between folate variables and CRC were mostly inverse or toward the null, except for tumors mutated for DOCK3 (supplemental folic acid), CHD1 (total folate), and ZNF521 (dietary folate) that showed positive associations. We did not observe differential associations in analyses among nonhypermutated tumors, or according to the signaling pathways. - Conclusions - Folate intake was not differentially associated with CRC risk according to mutations in the genes explored. The nominally significant differential mutation effects observed in a few genes warrants further investigation.
DOI:doi:10.1016/j.ajcnut.2024.07.012
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

kostenfrei: Volltext: https://doi.org/10.1016/j.ajcnut.2024.07.012
 kostenfrei: Volltext: https://www.sciencedirect.com/science/article/pii/S0002916524006099
 DOI: https://doi.org/10.1016/j.ajcnut.2024.07.012
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:colorectal cancer
 folate
 folic acid
 molecular subtypes
 somatic mutations
 tumor
K10plus-PPN:192376294X
Verknüpfungen:→ Zeitschrift

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