Blood metabolites reflect the effect of gut microbiota on differentiated thyroid cancer: a Mendelian randomization analysis
Background Studies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have not been well defined. Our study investigated the causal relationships between the gut microbiome, papillary thyroid cancer (PTC) and follic...
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| Vydáno v: | BMC cancer Ročník 25; číslo 1; s. 368 - 10 |
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| Médium: | Journal Article |
| Jazyk: | angličtina |
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BioMed Central
28.02.2025
BioMed Central Ltd Springer Nature B.V BMC |
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| Abstract | Background
Studies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have not been well defined. Our study investigated the causal relationships between the gut microbiome, papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC), as well as the mediating effect of potential blood metabolites, using genetic approaches.
Methods
Leveraging the summary statistics of gut microbial taxa, blood metabolites, PTC and FTC from the largest genome-wide association studies (GWAS) to date, we applied the bidirectional and mediation Mendelian randomization (MR) design. The multivariable MR approach based on Bayesian model averaging (MR-BMA) was used to prioritize the most likely causal taxa. Furthermore, metabolic pathway analysis was performed via the web-based Metaconflict 4.0.
Results
After sensitivity analyses, we identified 4 taxa, 19 blood metabolites, and 5 gut bacterial pathways were causally associated with PTC. Similarly, 3 taxa, 31 blood metabolites, and 3 gut bacterial pathways were found to be causally associated with FTC, with 2 blood metabolites exhibiting bidirectional causal relationships. Metabolic pathway analysis revealed 8 significant pathways in PTC and FTC. MR-BMA analysis pinpointed species
Bifidobacterium longum
as the primary causal taxon for PTC and genus
Bacteroides
for FTC. The mediation MR analysis showed that sphingomyelin (d18:2/23:0, d18:1/23:1, d17:1/24:1) and 2-hydroxysebacate mediated the causal effects of specific gut microbiota on PTC and FTC, respectively.
Conclusion
The study suggested a causal relationship between several gut microbial taxa and DTC, and that specific blood metabolites might mediate this relationship. |
|---|---|
| AbstractList | Studies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have not been well defined. Our study investigated the causal relationships between the gut microbiome, papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC), as well as the mediating effect of potential blood metabolites, using genetic approaches.
Leveraging the summary statistics of gut microbial taxa, blood metabolites, PTC and FTC from the largest genome-wide association studies (GWAS) to date, we applied the bidirectional and mediation Mendelian randomization (MR) design. The multivariable MR approach based on Bayesian model averaging (MR-BMA) was used to prioritize the most likely causal taxa. Furthermore, metabolic pathway analysis was performed via the web-based Metaconflict 4.0.
After sensitivity analyses, we identified 4 taxa, 19 blood metabolites, and 5 gut bacterial pathways were causally associated with PTC. Similarly, 3 taxa, 31 blood metabolites, and 3 gut bacterial pathways were found to be causally associated with FTC, with 2 blood metabolites exhibiting bidirectional causal relationships. Metabolic pathway analysis revealed 8 significant pathways in PTC and FTC. MR-BMA analysis pinpointed species Bifidobacterium longum as the primary causal taxon for PTC and genus Bacteroides for FTC. The mediation MR analysis showed that sphingomyelin (d18:2/23:0, d18:1/23:1, d17:1/24:1) and 2-hydroxysebacate mediated the causal effects of specific gut microbiota on PTC and FTC, respectively.
The study suggested a causal relationship between several gut microbial taxa and DTC, and that specific blood metabolites might mediate this relationship. Background Studies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have not been well defined. Our study investigated the causal relationships between the gut microbiome, papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC), as well as the mediating effect of potential blood metabolites, using genetic approaches. Methods Leveraging the summary statistics of gut microbial taxa, blood metabolites, PTC and FTC from the largest genome-wide association studies (GWAS) to date, we applied the bidirectional and mediation Mendelian randomization (MR) design. The multivariable MR approach based on Bayesian model averaging (MR-BMA) was used to prioritize the most likely causal taxa. Furthermore, metabolic pathway analysis was performed via the web-based Metaconflict 4.0. Results After sensitivity analyses, we identified 4 taxa, 19 blood metabolites, and 5 gut bacterial pathways were causally associated with PTC. Similarly, 3 taxa, 31 blood metabolites, and 3 gut bacterial pathways were found to be causally associated with FTC, with 2 blood metabolites exhibiting bidirectional causal relationships. Metabolic pathway analysis revealed 8 significant pathways in PTC and FTC. MR-BMA analysis pinpointed species Bifidobacterium longum as the primary causal taxon for PTC and genus Bacteroides for FTC. The mediation MR analysis showed that sphingomyelin (d18:2/23:0, d18:1/23:1, d17:1/24:1) and 2-hydroxysebacate mediated the causal effects of specific gut microbiota on PTC and FTC, respectively. Conclusion The study suggested a causal relationship between several gut microbial taxa and DTC, and that specific blood metabolites might mediate this relationship. Keywords: Papillary thyroid cancer, Follicular thyroid cancer, Blood metabolites, Gut Microbiota, Mendelian randomization Studies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have not been well defined. Our study investigated the causal relationships between the gut microbiome, papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC), as well as the mediating effect of potential blood metabolites, using genetic approaches. Leveraging the summary statistics of gut microbial taxa, blood metabolites, PTC and FTC from the largest genome-wide association studies (GWAS) to date, we applied the bidirectional and mediation Mendelian randomization (MR) design. The multivariable MR approach based on Bayesian model averaging (MR-BMA) was used to prioritize the most likely causal taxa. Furthermore, metabolic pathway analysis was performed via the web-based Metaconflict 4.0. After sensitivity analyses, we identified 4 taxa, 19 blood metabolites, and 5 gut bacterial pathways were causally associated with PTC. Similarly, 3 taxa, 31 blood metabolites, and 3 gut bacterial pathways were found to be causally associated with FTC, with 2 blood metabolites exhibiting bidirectional causal relationships. Metabolic pathway analysis revealed 8 significant pathways in PTC and FTC. MR-BMA analysis pinpointed species Bifidobacterium longum as the primary causal taxon for PTC and genus Bacteroides for FTC. The mediation MR analysis showed that sphingomyelin (d18:2/23:0, d18:1/23:1, d17:1/24:1) and 2-hydroxysebacate mediated the causal effects of specific gut microbiota on PTC and FTC, respectively. The study suggested a causal relationship between several gut microbial taxa and DTC, and that specific blood metabolites might mediate this relationship. Abstract Background Studies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have not been well defined. Our study investigated the causal relationships between the gut microbiome, papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC), as well as the mediating effect of potential blood metabolites, using genetic approaches. Methods Leveraging the summary statistics of gut microbial taxa, blood metabolites, PTC and FTC from the largest genome-wide association studies (GWAS) to date, we applied the bidirectional and mediation Mendelian randomization (MR) design. The multivariable MR approach based on Bayesian model averaging (MR-BMA) was used to prioritize the most likely causal taxa. Furthermore, metabolic pathway analysis was performed via the web-based Metaconflict 4.0. Results After sensitivity analyses, we identified 4 taxa, 19 blood metabolites, and 5 gut bacterial pathways were causally associated with PTC. Similarly, 3 taxa, 31 blood metabolites, and 3 gut bacterial pathways were found to be causally associated with FTC, with 2 blood metabolites exhibiting bidirectional causal relationships. Metabolic pathway analysis revealed 8 significant pathways in PTC and FTC. MR-BMA analysis pinpointed species Bifidobacterium longum as the primary causal taxon for PTC and genus Bacteroides for FTC. The mediation MR analysis showed that sphingomyelin (d18:2/23:0, d18:1/23:1, d17:1/24:1) and 2-hydroxysebacate mediated the causal effects of specific gut microbiota on PTC and FTC, respectively. Conclusion The study suggested a causal relationship between several gut microbial taxa and DTC, and that specific blood metabolites might mediate this relationship. Background Studies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have not been well defined. Our study investigated the causal relationships between the gut microbiome, papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC), as well as the mediating effect of potential blood metabolites, using genetic approaches. Methods Leveraging the summary statistics of gut microbial taxa, blood metabolites, PTC and FTC from the largest genome-wide association studies (GWAS) to date, we applied the bidirectional and mediation Mendelian randomization (MR) design. The multivariable MR approach based on Bayesian model averaging (MR-BMA) was used to prioritize the most likely causal taxa. Furthermore, metabolic pathway analysis was performed via the web-based Metaconflict 4.0. Results After sensitivity analyses, we identified 4 taxa, 19 blood metabolites, and 5 gut bacterial pathways were causally associated with PTC. Similarly, 3 taxa, 31 blood metabolites, and 3 gut bacterial pathways were found to be causally associated with FTC, with 2 blood metabolites exhibiting bidirectional causal relationships. Metabolic pathway analysis revealed 8 significant pathways in PTC and FTC. MR-BMA analysis pinpointed species Bifidobacterium longum as the primary causal taxon for PTC and genus Bacteroides for FTC. The mediation MR analysis showed that sphingomyelin (d18:2/23:0, d18:1/23:1, d17:1/24:1) and 2-hydroxysebacate mediated the causal effects of specific gut microbiota on PTC and FTC, respectively. Conclusion The study suggested a causal relationship between several gut microbial taxa and DTC, and that specific blood metabolites might mediate this relationship. Studies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have not been well defined. Our study investigated the causal relationships between the gut microbiome, papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC), as well as the mediating effect of potential blood metabolites, using genetic approaches.BACKGROUNDStudies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have not been well defined. Our study investigated the causal relationships between the gut microbiome, papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC), as well as the mediating effect of potential blood metabolites, using genetic approaches.Leveraging the summary statistics of gut microbial taxa, blood metabolites, PTC and FTC from the largest genome-wide association studies (GWAS) to date, we applied the bidirectional and mediation Mendelian randomization (MR) design. The multivariable MR approach based on Bayesian model averaging (MR-BMA) was used to prioritize the most likely causal taxa. Furthermore, metabolic pathway analysis was performed via the web-based Metaconflict 4.0.METHODSLeveraging the summary statistics of gut microbial taxa, blood metabolites, PTC and FTC from the largest genome-wide association studies (GWAS) to date, we applied the bidirectional and mediation Mendelian randomization (MR) design. The multivariable MR approach based on Bayesian model averaging (MR-BMA) was used to prioritize the most likely causal taxa. Furthermore, metabolic pathway analysis was performed via the web-based Metaconflict 4.0.After sensitivity analyses, we identified 4 taxa, 19 blood metabolites, and 5 gut bacterial pathways were causally associated with PTC. Similarly, 3 taxa, 31 blood metabolites, and 3 gut bacterial pathways were found to be causally associated with FTC, with 2 blood metabolites exhibiting bidirectional causal relationships. Metabolic pathway analysis revealed 8 significant pathways in PTC and FTC. MR-BMA analysis pinpointed species Bifidobacterium longum as the primary causal taxon for PTC and genus Bacteroides for FTC. The mediation MR analysis showed that sphingomyelin (d18:2/23:0, d18:1/23:1, d17:1/24:1) and 2-hydroxysebacate mediated the causal effects of specific gut microbiota on PTC and FTC, respectively.RESULTSAfter sensitivity analyses, we identified 4 taxa, 19 blood metabolites, and 5 gut bacterial pathways were causally associated with PTC. Similarly, 3 taxa, 31 blood metabolites, and 3 gut bacterial pathways were found to be causally associated with FTC, with 2 blood metabolites exhibiting bidirectional causal relationships. Metabolic pathway analysis revealed 8 significant pathways in PTC and FTC. MR-BMA analysis pinpointed species Bifidobacterium longum as the primary causal taxon for PTC and genus Bacteroides for FTC. The mediation MR analysis showed that sphingomyelin (d18:2/23:0, d18:1/23:1, d17:1/24:1) and 2-hydroxysebacate mediated the causal effects of specific gut microbiota on PTC and FTC, respectively.The study suggested a causal relationship between several gut microbial taxa and DTC, and that specific blood metabolites might mediate this relationship.CONCLUSIONThe study suggested a causal relationship between several gut microbial taxa and DTC, and that specific blood metabolites might mediate this relationship. BackgroundStudies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have not been well defined. Our study investigated the causal relationships between the gut microbiome, papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC), as well as the mediating effect of potential blood metabolites, using genetic approaches.MethodsLeveraging the summary statistics of gut microbial taxa, blood metabolites, PTC and FTC from the largest genome-wide association studies (GWAS) to date, we applied the bidirectional and mediation Mendelian randomization (MR) design. The multivariable MR approach based on Bayesian model averaging (MR-BMA) was used to prioritize the most likely causal taxa. Furthermore, metabolic pathway analysis was performed via the web-based Metaconflict 4.0.ResultsAfter sensitivity analyses, we identified 4 taxa, 19 blood metabolites, and 5 gut bacterial pathways were causally associated with PTC. Similarly, 3 taxa, 31 blood metabolites, and 3 gut bacterial pathways were found to be causally associated with FTC, with 2 blood metabolites exhibiting bidirectional causal relationships. Metabolic pathway analysis revealed 8 significant pathways in PTC and FTC. MR-BMA analysis pinpointed species Bifidobacterium longum as the primary causal taxon for PTC and genus Bacteroides for FTC. The mediation MR analysis showed that sphingomyelin (d18:2/23:0, d18:1/23:1, d17:1/24:1) and 2-hydroxysebacate mediated the causal effects of specific gut microbiota on PTC and FTC, respectively.ConclusionThe study suggested a causal relationship between several gut microbial taxa and DTC, and that specific blood metabolites might mediate this relationship. |
| ArticleNumber | 368 |
| Audience | Academic |
| Author | Zhang, Hanfei Li, Lin Li, Yuhao |
| Author_xml | – sequence: 1 givenname: Hanfei surname: Zhang fullname: Zhang, Hanfei organization: Department of Nuclear Medicine, West China Hospital, Sichuan University – sequence: 2 givenname: Yuhao surname: Li fullname: Li, Yuhao organization: Department of Nuclear Medicine, West China Hospital, Sichuan University – sequence: 3 givenname: Lin orcidid: 0000-0001-8349-9588 surname: Li fullname: Li, Lin email: lilinhuaxi@sina.com organization: Department of Nuclear Medicine, West China Hospital, Sichuan University |
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| Cites_doi | 10.1210/jc.2007-0606 10.1080/17474124.2022.2064273 10.1007/978-1-0716-0239-3_17 10.1038/nature15394 10.1038/s41588-018-0099-7 10.1016/j.canlet.2021.10.002 10.1111/cen.13437 10.18632/oncotarget.11603 10.3389/fendo.2022.893164 10.1210/endocr/bqad184 10.1080/19490976.2023.2282795 10.1007/s00284-014-0640-6 10.1021/acs.chemrev.2c00431 10.1093/femsre/fuu010 10.3389/fgene.2023.1299930 10.1093/eurjpc/zwad171 10.1007/s11523-021-00861-y 10.1080/01635589109514163 10.1038/nrc.2017.96 10.1038/s41569-022-00771-0 10.1038/srep14869 10.1007/s00432-023-05535-y 10.1093/carcin/18.4.833 10.18632/oncotarget.9124 10.1002/ijc.32007 10.1016/j.jchromb.2017.10.004 10.4158/EP15844.OR 10.1016/j.tem.2019.05.008 10.1016/j.semcancer.2021.09.007 10.1038/s41467-019-13870-3 10.1016/j.chom.2013.07.007 10.1039/c1mb05029j 10.1016/j.jare.2021.04.001 10.1055/s-0035-1559631 10.3390/nu15122680 10.1007/s13311-017-0600-5 10.1038/nrm2329 10.1038/s42003-021-02587-z 10.7150/jca.66816 10.1097/MOL.0000000000000308 10.3389/fmolb.2022.1039121 10.1093/ije/dyr036 10.3390/metabo11090614 10.1016/j.yexcr.2017.07.009 |
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| References | J Zhou (13598_CR16) 2024; 150 A Rizzo (13598_CR4) 2022; 16 V Zuber (13598_CR23) 2020; 11 A Fernandes (13598_CR1) 2023; 15 V Mollica (13598_CR3) 2022; 17 CT Shen (13598_CR10) 2017; 87 Z Yao (13598_CR11) 2011; 7 PH Sudmant (13598_CR20) 2015; 526 RM Chakaroun (13598_CR45) 2023; 20 Y Rong (13598_CR32) 2017; 358 E Fröhlich (13598_CR8) 2019; 30 X Chen (13598_CR40) 2016; 7 M Koo (13598_CR30) 1991; 16 B Ogretmen (13598_CR36) 2018; 18 T Hou (13598_CR17) 2023; 165 H Dai (13598_CR19) 2023; 30 J Li (13598_CR41) 2017; 8 YA Hannun (13598_CR35) 2008; 9 J Singh (13598_CR31) 1997; 18 HM Ishaq (13598_CR33) 2022; 13 EC Lauritano (13598_CR6) 2007; 92 G Lu (13598_CR43) 2022; 13 L Zhou (13598_CR9) 2014; 69 G Cui (13598_CR46) 2023; 15 LH Duntas (13598_CR26) 2015; 47 H Neuman (13598_CR29) 2015; 39 D Huo (13598_CR25) 2021; 4 A Rizzo (13598_CR2) 2022; 86 AD Kostic (13598_CR7) 2013; 14 DQY Quek (13598_CR38) 2021; 11 DC Guven (13598_CR5) 2022; 9 S Burgess (13598_CR21) 2011; 40 Z Wang (13598_CR39) 2016; 27 X Yu (13598_CR14) 2022; 35 X Shao (13598_CR34) 2021; 523 J Chong (13598_CR24) 2020; 2104 R Farrokhi Yekta (13598_CR13) 2017; 22 N Aggarwal (13598_CR44) 2023; 123 SI Do (13598_CR37) 2017; 37 Y Tian (13598_CR12) 2015; 5 S Shen (13598_CR42) 2017; 1068–1069 A Farzi (13598_CR28) 2018; 15 J Feng (13598_CR15) 2019; 144 M Verbanck (13598_CR22) 2018; 50 Y Song (13598_CR27) 2016; 22 Z Quan (13598_CR18) 2023; 14 |
| References_xml | – volume: 92 start-page: 4180 issue: 11 year: 2007 ident: 13598_CR6 publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2007-0606 – volume: 16 start-page: 333 issue: 4 year: 2022 ident: 13598_CR4 publication-title: Expert Rev Gastroenterol Hepatol doi: 10.1080/17474124.2022.2064273 – volume: 2104 start-page: 337 year: 2020 ident: 13598_CR24 publication-title: Methods Mol Biol. doi: 10.1007/978-1-0716-0239-3_17 – volume: 526 start-page: 75 issue: 7571 year: 2015 ident: 13598_CR20 publication-title: Nature doi: 10.1038/nature15394 – volume: 50 start-page: 693 issue: 5 year: 2018 ident: 13598_CR22 publication-title: Nat Genet doi: 10.1038/s41588-018-0099-7 – volume: 523 start-page: 170 year: 2021 ident: 13598_CR34 publication-title: Cancer Lett doi: 10.1016/j.canlet.2021.10.002 – volume: 87 start-page: 844 issue: 6 year: 2017 ident: 13598_CR10 publication-title: Clin Endocrinol (Oxf) doi: 10.1111/cen.13437 – volume: 8 start-page: 46834 issue: 29 year: 2017 ident: 13598_CR41 publication-title: Oncotarget doi: 10.18632/oncotarget.11603 – volume: 13 start-page: 893164 year: 2022 ident: 13598_CR43 publication-title: Front Endocrinol (Lausanne) doi: 10.3389/fendo.2022.893164 – volume: 165 start-page: bqad184 issue: 1 year: 2023 ident: 13598_CR17 publication-title: Endocrinology. doi: 10.1210/endocr/bqad184 – volume: 15 start-page: 2282795 issue: 2 year: 2023 ident: 13598_CR46 publication-title: Gut Microbes doi: 10.1080/19490976.2023.2282795 – volume: 69 start-page: 675 issue: 5 year: 2014 ident: 13598_CR9 publication-title: Curr Microbiol doi: 10.1007/s00284-014-0640-6 – volume: 123 start-page: 31 issue: 1 year: 2023 ident: 13598_CR44 publication-title: Chem Rev doi: 10.1021/acs.chemrev.2c00431 – volume: 39 start-page: 509 issue: 4 year: 2015 ident: 13598_CR29 publication-title: FEMS Microbiol Rev doi: 10.1093/femsre/fuu010 – volume: 22 start-page: 595 issue: 7 year: 2017 ident: 13598_CR13 publication-title: Biomarkers – volume: 14 start-page: 1299930 year: 2023 ident: 13598_CR18 publication-title: Front Genet doi: 10.3389/fgene.2023.1299930 – volume: 30 start-page: 1274 issue: 12 year: 2023 ident: 13598_CR19 publication-title: Eur J Prev Cardiol doi: 10.1093/eurjpc/zwad171 – volume: 17 start-page: 61 issue: 1 year: 2022 ident: 13598_CR3 publication-title: Target Oncol doi: 10.1007/s11523-021-00861-y – volume: 16 start-page: 249 issue: 3–4 year: 1991 ident: 13598_CR30 publication-title: Nutr Cancer doi: 10.1080/01635589109514163 – volume: 18 start-page: 33 issue: 1 year: 2018 ident: 13598_CR36 publication-title: Nat Rev Cancer doi: 10.1038/nrc.2017.96 – volume: 20 start-page: 217 issue: 4 year: 2023 ident: 13598_CR45 publication-title: Nat Rev Cardiol doi: 10.1038/s41569-022-00771-0 – volume: 5 start-page: 14869 year: 2015 ident: 13598_CR12 publication-title: Sci Rep doi: 10.1038/srep14869 – volume: 150 start-page: 75 issue: 2 year: 2024 ident: 13598_CR16 publication-title: J Cancer Res Clin Oncol doi: 10.1007/s00432-023-05535-y – volume: 18 start-page: 833 issue: 4 year: 1997 ident: 13598_CR31 publication-title: Carcinogenesis doi: 10.1093/carcin/18.4.833 – volume: 7 start-page: 36622 issue: 24 year: 2016 ident: 13598_CR40 publication-title: Oncotarget doi: 10.18632/oncotarget.9124 – volume: 144 start-page: 2728 issue: 11 year: 2019 ident: 13598_CR15 publication-title: Int J Cancer doi: 10.1002/ijc.32007 – volume: 1068–1069 start-page: 41 year: 2017 ident: 13598_CR42 publication-title: J Chromatogr B Analyt Technol Biomed Life Sci doi: 10.1016/j.jchromb.2017.10.004 – volume: 22 start-page: 420 issue: 4 year: 2016 ident: 13598_CR27 publication-title: Endocr Pract doi: 10.4158/EP15844.OR – volume: 30 start-page: 479 issue: 8 year: 2019 ident: 13598_CR8 publication-title: Trends Endocrinol Metab doi: 10.1016/j.tem.2019.05.008 – volume: 86 start-page: 1058 issue: Pt 3 year: 2022 ident: 13598_CR2 publication-title: Semin Cancer Biol doi: 10.1016/j.semcancer.2021.09.007 – volume: 11 start-page: 29 issue: 1 year: 2020 ident: 13598_CR23 publication-title: Nat Commun doi: 10.1038/s41467-019-13870-3 – volume: 37 start-page: 5399 issue: 10 year: 2017 ident: 13598_CR37 publication-title: Anticancer Res – volume: 14 start-page: 207 issue: 2 year: 2013 ident: 13598_CR7 publication-title: Cell Host Microbe doi: 10.1016/j.chom.2013.07.007 – volume: 7 start-page: 2608 issue: 9 year: 2011 ident: 13598_CR11 publication-title: Mol Biosyst doi: 10.1039/c1mb05029j – volume: 35 start-page: 61 year: 2022 ident: 13598_CR14 publication-title: J Adv Res doi: 10.1016/j.jare.2021.04.001 – volume: 47 start-page: 721 issue: 10 year: 2015 ident: 13598_CR26 publication-title: Horm Metab Res doi: 10.1055/s-0035-1559631 – volume: 15 start-page: 2680 issue: 12 year: 2023 ident: 13598_CR1 publication-title: Nutrients. doi: 10.3390/nu15122680 – volume: 15 start-page: 5 issue: 1 year: 2018 ident: 13598_CR28 publication-title: Neurotherapeutics doi: 10.1007/s13311-017-0600-5 – volume: 9 start-page: 139 issue: 2 year: 2008 ident: 13598_CR35 publication-title: Nat Rev Mol Cell Biol doi: 10.1038/nrm2329 – volume: 4 start-page: 1046 issue: 1 year: 2021 ident: 13598_CR25 publication-title: Commun Biol doi: 10.1038/s42003-021-02587-z – volume: 13 start-page: 2014 issue: 6 year: 2022 ident: 13598_CR33 publication-title: J Cancer doi: 10.7150/jca.66816 – volume: 27 start-page: 216 issue: 3 year: 2016 ident: 13598_CR39 publication-title: Curr Opin Lipidol doi: 10.1097/MOL.0000000000000308 – volume: 9 start-page: 1039121 year: 2022 ident: 13598_CR5 publication-title: Front Mol Biosci doi: 10.3389/fmolb.2022.1039121 – volume: 40 start-page: 755 issue: 3 year: 2011 ident: 13598_CR21 publication-title: Int J Epidemiol doi: 10.1093/ije/dyr036 – volume: 11 start-page: 614 issue: 9 year: 2021 ident: 13598_CR38 publication-title: Metabolites. doi: 10.3390/metabo11090614 – volume: 358 start-page: 352 issue: 2 year: 2017 ident: 13598_CR32 publication-title: Exp Cell Res doi: 10.1016/j.yexcr.2017.07.009 |
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Studies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have... Studies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have not been... Background Studies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have... BackgroundStudies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating factors have... Abstract Background Studies have linked gut microbiome and differentiated thyroid cancer (DTC). However, their causal relationships and potential mediating... |
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| SubjectTerms | Adenocarcinoma, Follicular - blood Adenocarcinoma, Follicular - genetics Adenocarcinoma, Follicular - microbiology Adenocarcinoma, Follicular - pathology Bayes Theorem Bayesian analysis Biomedical and Life Sciences Biomedicine Blood Blood metabolites Cancer Research Causes of Development and progression Follicular thyroid cancer Gastrointestinal Microbiome Gastrointestinal system Genome-wide association studies Genome-Wide Association Study Genomes Gut Microbiota Health aspects Health Promotion and Disease Prevention Humans Intestinal microflora Medicine/Public Health Mendelian randomization Mendelian Randomization Analysis Metabolic Networks and Pathways Metabolic pathways Metabolism Metabolites Microbiomes Microbiota Microbiota (Symbiotic organisms) Oncology Papillary thyroid cancer Physiological aspects Sensitivity analysis Sphingomyelin Statistical analysis Statistics Surgical Oncology Thyroid cancer Thyroid Cancer, Papillary - blood Thyroid Cancer, Papillary - genetics Thyroid Cancer, Papillary - microbiology Thyroid Cancer, Papillary - pathology Thyroid Neoplasms - blood Thyroid Neoplasms - genetics Thyroid Neoplasms - microbiology Thyroid Neoplasms - pathology |
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| Title | Blood metabolites reflect the effect of gut microbiota on differentiated thyroid cancer: a Mendelian randomization analysis |
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