Journal Articles

Permanent URI for this collectionhttps://mro.massey.ac.nz/handle/10179/7915

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    Genotoxic colibactin mutational signature in colorectal cancer is associated with clinicopathological features, specific genomic alterations and better survival.
    (2023-03-12) Georgeson P; Steinfelder RS; Harrison TA; Pope BJ; Zaidi SH; Qu C; Lin Y; Joo JE; Mahmood K; Clendenning M; Walker R; Aglago EK; Berndt SI; Brenner H; Campbell PT; Cao Y; Chan AT; Chang-Claude J; Dimou N; Doheny KF; Drew DA; Figueiredo JC; French AJ; Gallinger S; Giannakis M; Giles GG; Goode EL; Gruber SB; Gsur A; Gunter MJ; Harlid S; Hoffmeister M; Hsu L; Huang W-Y; Huyghe JR; Manson JE; Moreno V; Murphy N; Nassir R; Newton CC; Nowak JA; Obón-Santacana M; Ogino S; Pai RK; Papadimitrou N; Potter JD; Schoen RE; Song M; Sun W; Toland AE; Trinh QM; Tsilidis K; Ugai T; Um CY; Macrae FA; Rosty C; Hudson TJ; Winship IM; Phipps AI; Jenkins MA; Peters U; Buchanan DD
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    Hydrogen cross-feeders of the human gastrointestinal tract.
    (Taylor & Francis Group, 2019-01-01) Smith NW; Shorten PR; Altermann EH; Roy NC; McNabb WC
    Hydrogen plays a key role in many microbial metabolic pathways in the human gastrointestinal tract (GIT) that have an impact on human nutrition, health and wellbeing. Hydrogen is produced by many members of the GIT microbiota, and may be subsequently utilized by cross-feeding microbes for growth and in the production of larger molecules. Hydrogenotrophic microbes fall into three functional groups: sulfate-reducing bacteria, methanogenic archaea and acetogenic bacteria, which can convert hydrogen into hydrogen sulfide, methane and acetate, respectively. Despite different energy yields per molecule of hydrogen used between the functional groups, all three can coexist in the human GIT. The factors affecting the numerical balance of hydrogenotrophs in the GIT remain unconfirmed. There is increasing evidence linking both hydrogen sulfide and methane to GIT diseases such as irritable bowel syndrome, and strategies for the mitigation of such health problems through targeting of hydrogenotrophs constitute an important field for further investigation.
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    Genome-wide interaction analysis of folate for colorectal cancer risk.
    (Elsevier B.V., 2023-11) Bouras E; Kim AE; Lin Y; Morrison J; Du M; Albanes D; Barry EL; Baurley JW; Berndt SI; Bien SA; Bishop TD; Brenner H; Budiarto A; Burnett-Hartman A; Campbell PT; Carreras-Torres R; Casey G; Cenggoro TW; Chan AT; Chang-Claude J; Conti DV; Cotterchio M; Devall M; Diez-Obrero V; Dimou N; Drew DA; Figueiredo JC; Giles GG; Gruber SB; Gunter MJ; Harrison TA; Hidaka A; Hoffmeister M; Huyghe JR; Joshi AD; Kawaguchi ES; Keku TO; Kundaje A; Le Marchand L; Lewinger JP; Li L; Lynch BM; Mahesworo B; Männistö S; Moreno V; Murphy N; Newcomb PA; Obón-Santacana M; Ose J; Palmer JR; Papadimitriou N; Pardamean B; Pellatt AJ; Peoples AR; Platz EA; Potter JD; Qi L; Qu C; Rennert G; Ruiz-Narvaez E; Sakoda LC; Schmit SL; Shcherbina A; Stern MC; Su Y-R; Tangen CM; Thomas DC; Tian Y; Um CY; van Duijnhoven FJ; Van Guelpen B; Visvanathan K; Wang J; White E; Wolk A; Woods MO; Ulrich CM; Hsu L; Gauderman WJ; Peters U; Tsilidis KK
    Background Epidemiological and experimental evidence suggests that higher folate intake is associated with decreased colorectal cancer (CRC) risk; however, the mechanisms underlying this relationship are not fully understood. Genetic variation that may have a direct or indirect impact on folate metabolism can provide insights into folate’s role in CRC. Objectives Our aim was to perform a genome-wide interaction analysis to identify genetic variants that may modify the association of folate on CRC risk. Methods We applied traditional case-control logistic regression, joint 3-degree of freedom, and a 2-step weighted hypothesis approach to test the interactions of common variants (allele frequency >1%) across the genome and dietary folate, folic acid supplement use, and total folate in relation to risk of CRC in 30,550 cases and 42,336 controls from 51 studies from 3 genetic consortia (CCFR, CORECT, GECCO). Results Inverse associations of dietary, total folate, and folic acid supplement with CRC were found (odds ratio [OR]: 0.93; 95% confidence interval [CI]: 0.90, 0.96; and 0.91; 95% CI: 0.89, 0.94 per quartile higher intake, and 0.82 (95% CI: 0.78, 0.88) for users compared with nonusers, respectively). Interactions (P-interaction < 5×10-8) of folic acid supplement and variants in the 3p25.2 locus (in the region of Synapsin II [SYN2]/tissue inhibitor of metalloproteinase 4 [TIMP4]) were found using traditional interaction analysis, with variant rs150924902 (located upstream to SYN2) showing the strongest interaction. In stratified analyses by rs150924902 genotypes, folate supplementation was associated with decreased CRC risk among those carrying the TT genotype (OR: 0.82; 95% CI: 0.79, 0.86) but increased CRC risk among those carrying the TA genotype (OR: 1.63; 95% CI: 1.29, 2.05), suggesting a qualitative interaction (P-interaction = 1.4×10-8). No interactions were observed for dietary and total folate. Conclusions Variation in 3p25.2 locus may modify the association of folate supplement with CRC risk. Experimental studies and studies incorporating other relevant omics data are warranted to validate this finding.