Association between human blood metabolome and the risk of breast cancer
Breast cancer is the most common cancer among women with limited treatment options. To identify promising drug targets for breast cancer, we conducted a systematical Mendelian randomization (MR) study to screen blood metabolome for potential causal mediators of breast cancer and further predict targ...
Saved in:
Published in | Breast cancer research : BCR Vol. 25; no. 1; pp. 9 - 11 |
---|---|
Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
BioMed Central Ltd
24.01.2023
BioMed Central BMC |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | Breast cancer is the most common cancer among women with limited treatment options. To identify promising drug targets for breast cancer, we conducted a systematical Mendelian randomization (MR) study to screen blood metabolome for potential causal mediators of breast cancer and further predict target-mediated side effects.
We selected 112 unique blood metabolites from 3 large-scale European ancestry-based genome-wide association studies (GWASs) with a total of 147,827 participants. Breast cancer data were obtained from a GWAS in the Breast Cancer Association Consortium (BCAC), involving 122,977 cases and 105,974 controls of European ancestry. We conducted MR analyses to systematically assess the associations of blood metabolites with breast cancer, and a phenome-wide MR analysis was further applied to ascertain the potential on-target side effects of metabolite interventions.
Two blood metabolites were identified as the potential causal mediators for breast cancer, including high-density lipoprotein cholesterol (HDL-C) (odds ratio [OR], 1.09; 95% confidence interval [CI], 1.06-1.12; P = 9.67 × 10
) and acetate (OR, 1.24; 95% CI, 1.13-1.37; P = 1.35 × 10
). In the phenome-wide MR analysis, lowering HDL-C might have deleterious effects on the risk of the circulatory system and foreign body injury, while lowering acetate had deleterious effects on mental disorders disease.
The present systematic MR analysis revealed that HDL-C and acetate may be the causal mediators in the risk of developing breast cancer. Side-effect profiles were characterized to help inform drug target prioritization for breast cancer prevention. HDL-C and acetate might be promising drug targets for preventing breast cancer, but they should be applied under weighting advantages and disadvantages. |
---|---|
AbstractList | Breast cancer is the most common cancer among women with limited treatment options. To identify promising drug targets for breast cancer, we conducted a systematical Mendelian randomization (MR) study to screen blood metabolome for potential causal mediators of breast cancer and further predict target-mediated side effects. We selected 112 unique blood metabolites from 3 large-scale European ancestry-based genome-wide association studies (GWASs) with a total of 147,827 participants. Breast cancer data were obtained from a GWAS in the Breast Cancer Association Consortium (BCAC), involving 122,977 cases and 105,974 controls of European ancestry. We conducted MR analyses to systematically assess the associations of blood metabolites with breast cancer, and a phenome-wide MR analysis was further applied to ascertain the potential on-target side effects of metabolite interventions. Two blood metabolites were identified as the potential causal mediators for breast cancer, including high-density lipoprotein cholesterol (HDL-C) (odds ratio [OR], 1.09; 95% confidence interval [CI], 1.06-1.12; P = 9.67 x 10.sup.-10) and acetate (OR, 1.24; 95% CI, 1.13-1.37; P = 1.35 x 10.sup.-5). In the phenome-wide MR analysis, lowering HDL-C might have deleterious effects on the risk of the circulatory system and foreign body injury, while lowering acetate had deleterious effects on mental disorders disease. The present systematic MR analysis revealed that HDL-C and acetate may be the causal mediators in the risk of developing breast cancer. Side-effect profiles were characterized to help inform drug target prioritization for breast cancer prevention. HDL-C and acetate might be promising drug targets for preventing breast cancer, but they should be applied under weighting advantages and disadvantages. Breast cancer is the most common cancer among women with limited treatment options. To identify promising drug targets for breast cancer, we conducted a systematical Mendelian randomization (MR) study to screen blood metabolome for potential causal mediators of breast cancer and further predict target-mediated side effects. We selected 112 unique blood metabolites from 3 large-scale European ancestry-based genome-wide association studies (GWASs) with a total of 147,827 participants. Breast cancer data were obtained from a GWAS in the Breast Cancer Association Consortium (BCAC), involving 122,977 cases and 105,974 controls of European ancestry. We conducted MR analyses to systematically assess the associations of blood metabolites with breast cancer, and a phenome-wide MR analysis was further applied to ascertain the potential on-target side effects of metabolite interventions. Two blood metabolites were identified as the potential causal mediators for breast cancer, including high-density lipoprotein cholesterol (HDL-C) (odds ratio [OR], 1.09; 95% confidence interval [CI], 1.06-1.12; P = 9.67 × 10 ) and acetate (OR, 1.24; 95% CI, 1.13-1.37; P = 1.35 × 10 ). In the phenome-wide MR analysis, lowering HDL-C might have deleterious effects on the risk of the circulatory system and foreign body injury, while lowering acetate had deleterious effects on mental disorders disease. The present systematic MR analysis revealed that HDL-C and acetate may be the causal mediators in the risk of developing breast cancer. Side-effect profiles were characterized to help inform drug target prioritization for breast cancer prevention. HDL-C and acetate might be promising drug targets for preventing breast cancer, but they should be applied under weighting advantages and disadvantages. Abstract Background Breast cancer is the most common cancer among women with limited treatment options. To identify promising drug targets for breast cancer, we conducted a systematical Mendelian randomization (MR) study to screen blood metabolome for potential causal mediators of breast cancer and further predict target-mediated side effects. Methods We selected 112 unique blood metabolites from 3 large-scale European ancestry-based genome-wide association studies (GWASs) with a total of 147,827 participants. Breast cancer data were obtained from a GWAS in the Breast Cancer Association Consortium (BCAC), involving 122,977 cases and 105,974 controls of European ancestry. We conducted MR analyses to systematically assess the associations of blood metabolites with breast cancer, and a phenome-wide MR analysis was further applied to ascertain the potential on-target side effects of metabolite interventions. Results Two blood metabolites were identified as the potential causal mediators for breast cancer, including high-density lipoprotein cholesterol (HDL-C) (odds ratio [OR], 1.09; 95% confidence interval [CI], 1.06–1.12; P = 9.67 × 10−10) and acetate (OR, 1.24; 95% CI, 1.13–1.37; P = 1.35 × 10−5). In the phenome-wide MR analysis, lowering HDL-C might have deleterious effects on the risk of the circulatory system and foreign body injury, while lowering acetate had deleterious effects on mental disorders disease. Conclusions The present systematic MR analysis revealed that HDL-C and acetate may be the causal mediators in the risk of developing breast cancer. Side-effect profiles were characterized to help inform drug target prioritization for breast cancer prevention. HDL-C and acetate might be promising drug targets for preventing breast cancer, but they should be applied under weighting advantages and disadvantages. BackgroundBreast cancer is the most common cancer among women with limited treatment options. To identify promising drug targets for breast cancer, we conducted a systematical Mendelian randomization (MR) study to screen blood metabolome for potential causal mediators of breast cancer and further predict target-mediated side effects.MethodsWe selected 112 unique blood metabolites from 3 large-scale European ancestry-based genome-wide association studies (GWASs) with a total of 147,827 participants. Breast cancer data were obtained from a GWAS in the Breast Cancer Association Consortium (BCAC), involving 122,977 cases and 105,974 controls of European ancestry. We conducted MR analyses to systematically assess the associations of blood metabolites with breast cancer, and a phenome-wide MR analysis was further applied to ascertain the potential on-target side effects of metabolite interventions.ResultsTwo blood metabolites were identified as the potential causal mediators for breast cancer, including high-density lipoprotein cholesterol (HDL-C) (odds ratio [OR], 1.09; 95% confidence interval [CI], 1.06–1.12; P = 9.67 × 10−10) and acetate (OR, 1.24; 95% CI, 1.13–1.37;P = 1.35 × 10−5). In the phenome-wide MR analysis, lowering HDL-C might have deleterious effects on the risk of the circulatory system and foreign body injury, while lowering acetate had deleterious effects on mental disorders disease.ConclusionsThe present systematic MR analysis revealed that HDL-C and acetate may be the causal mediators in the risk of developing breast cancer. Side-effect profiles were characterized to help inform drug target prioritization for breast cancer prevention. HDL-C and acetate might be promising drug targets for preventing breast cancer, but they should be applied under weighting advantages and disadvantages. Breast cancer is the most common cancer among women with limited treatment options. To identify promising drug targets for breast cancer, we conducted a systematical Mendelian randomization (MR) study to screen blood metabolome for potential causal mediators of breast cancer and further predict target-mediated side effects.BACKGROUNDBreast cancer is the most common cancer among women with limited treatment options. To identify promising drug targets for breast cancer, we conducted a systematical Mendelian randomization (MR) study to screen blood metabolome for potential causal mediators of breast cancer and further predict target-mediated side effects.We selected 112 unique blood metabolites from 3 large-scale European ancestry-based genome-wide association studies (GWASs) with a total of 147,827 participants. Breast cancer data were obtained from a GWAS in the Breast Cancer Association Consortium (BCAC), involving 122,977 cases and 105,974 controls of European ancestry. We conducted MR analyses to systematically assess the associations of blood metabolites with breast cancer, and a phenome-wide MR analysis was further applied to ascertain the potential on-target side effects of metabolite interventions.METHODSWe selected 112 unique blood metabolites from 3 large-scale European ancestry-based genome-wide association studies (GWASs) with a total of 147,827 participants. Breast cancer data were obtained from a GWAS in the Breast Cancer Association Consortium (BCAC), involving 122,977 cases and 105,974 controls of European ancestry. We conducted MR analyses to systematically assess the associations of blood metabolites with breast cancer, and a phenome-wide MR analysis was further applied to ascertain the potential on-target side effects of metabolite interventions.Two blood metabolites were identified as the potential causal mediators for breast cancer, including high-density lipoprotein cholesterol (HDL-C) (odds ratio [OR], 1.09; 95% confidence interval [CI], 1.06-1.12; P = 9.67 × 10-10) and acetate (OR, 1.24; 95% CI, 1.13-1.37; P = 1.35 × 10-5). In the phenome-wide MR analysis, lowering HDL-C might have deleterious effects on the risk of the circulatory system and foreign body injury, while lowering acetate had deleterious effects on mental disorders disease.RESULTSTwo blood metabolites were identified as the potential causal mediators for breast cancer, including high-density lipoprotein cholesterol (HDL-C) (odds ratio [OR], 1.09; 95% confidence interval [CI], 1.06-1.12; P = 9.67 × 10-10) and acetate (OR, 1.24; 95% CI, 1.13-1.37; P = 1.35 × 10-5). In the phenome-wide MR analysis, lowering HDL-C might have deleterious effects on the risk of the circulatory system and foreign body injury, while lowering acetate had deleterious effects on mental disorders disease.The present systematic MR analysis revealed that HDL-C and acetate may be the causal mediators in the risk of developing breast cancer. Side-effect profiles were characterized to help inform drug target prioritization for breast cancer prevention. HDL-C and acetate might be promising drug targets for preventing breast cancer, but they should be applied under weighting advantages and disadvantages.CONCLUSIONSThe present systematic MR analysis revealed that HDL-C and acetate may be the causal mediators in the risk of developing breast cancer. Side-effect profiles were characterized to help inform drug target prioritization for breast cancer prevention. HDL-C and acetate might be promising drug targets for preventing breast cancer, but they should be applied under weighting advantages and disadvantages. Background Breast cancer is the most common cancer among women with limited treatment options. To identify promising drug targets for breast cancer, we conducted a systematical Mendelian randomization (MR) study to screen blood metabolome for potential causal mediators of breast cancer and further predict target-mediated side effects. Methods We selected 112 unique blood metabolites from 3 large-scale European ancestry-based genome-wide association studies (GWASs) with a total of 147,827 participants. Breast cancer data were obtained from a GWAS in the Breast Cancer Association Consortium (BCAC), involving 122,977 cases and 105,974 controls of European ancestry. We conducted MR analyses to systematically assess the associations of blood metabolites with breast cancer, and a phenome-wide MR analysis was further applied to ascertain the potential on-target side effects of metabolite interventions. Results Two blood metabolites were identified as the potential causal mediators for breast cancer, including high-density lipoprotein cholesterol (HDL-C) (odds ratio [OR], 1.09; 95% confidence interval [CI], 1.06-1.12; P = 9.67 x 10.sup.-10) and acetate (OR, 1.24; 95% CI, 1.13-1.37; P = 1.35 x 10.sup.-5). In the phenome-wide MR analysis, lowering HDL-C might have deleterious effects on the risk of the circulatory system and foreign body injury, while lowering acetate had deleterious effects on mental disorders disease. Conclusions The present systematic MR analysis revealed that HDL-C and acetate may be the causal mediators in the risk of developing breast cancer. Side-effect profiles were characterized to help inform drug target prioritization for breast cancer prevention. HDL-C and acetate might be promising drug targets for preventing breast cancer, but they should be applied under weighting advantages and disadvantages. Keywords: Breast cancer, Metabolites, Mendelian randomization |
ArticleNumber | 9 |
Audience | Academic |
Author | Sun, Lulu Wang, Aili Zhu, Zhengbao Wang, Yu Jia, Yiming Yang, Pinni Liu, Fanghua Chen, Guo-Chong Guo, Daoxia Zhang, Yonghong Shi, Mengyao |
Author_xml | – sequence: 1 givenname: Yu surname: Wang fullname: Wang, Yu – sequence: 2 givenname: Fanghua surname: Liu fullname: Liu, Fanghua – sequence: 3 givenname: Lulu surname: Sun fullname: Sun, Lulu – sequence: 4 givenname: Yiming surname: Jia fullname: Jia, Yiming – sequence: 5 givenname: Pinni surname: Yang fullname: Yang, Pinni – sequence: 6 givenname: Daoxia surname: Guo fullname: Guo, Daoxia – sequence: 7 givenname: Mengyao surname: Shi fullname: Shi, Mengyao – sequence: 8 givenname: Aili surname: Wang fullname: Wang, Aili – sequence: 9 givenname: Guo-Chong surname: Chen fullname: Chen, Guo-Chong – sequence: 10 givenname: Yonghong surname: Zhang fullname: Zhang, Yonghong – sequence: 11 givenname: Zhengbao surname: Zhu fullname: Zhu, Zhengbao |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36694207$$D View this record in MEDLINE/PubMed |
BookMark | eNp9kk9vFCEYxompse3qF_BgJvHiZSow_JuLyaZR26SJF028EWBedllnoMKsxm8vu1trtzECCQz83md4Zp5zdBJTBIReEnxBiBJvC-kwVy2mXYuJwH3LnqAzwgRvOaNfTx6sT9F5KRuMiVRcPUOnnRA9o1ieoatlKckFM4cUGwvzT4DYrLeTqU9jSkMzwWxsGtMEjYlDM6-hyaF8a5JvbAZT5saZ6CA_R0-9GQu8uJsX6MuH958vr9qbTx-vL5c3reOim9uB0X4AwYnyAL7rrJLGMyIZ8f0gbU-rJWvr6JVUjBspuMPCK1-tdMrzboGuD7pDMht9m8Nk8i-dTND7jZRX2uQ5uBG0BQLe9kIMxDHqe2OokNRiaZTjxOOq9e6gdbu1EwwO4pzNeCR6fBLDWq_SD10vRxkmVeDNnUBO37dQZj2F4mAcTYS0LZpK0fOeivqLFuj1I3STtjnWT1Wp2lRlu7_UylQDIfpU3-t2onopO8YZ4WpHXfyDqn2AKbgaEh_q_lHBq4dG7x3-yUEF6AFwOZWSwd8jBOtd2PQhbLo60fuwaVaL1KMiF-Z9kup1wvi_0t8ygda- |
CitedBy_id | crossref_primary_10_3389_fgene_2024_1333454 crossref_primary_10_1007_s10528_024_10966_4 crossref_primary_10_1080_2314808X_2024_2355735 crossref_primary_10_3389_fendo_2024_1413777 crossref_primary_10_1038_s41598_024_73337_4 crossref_primary_10_3390_metabo14060322 crossref_primary_10_1371_journal_pone_0304574 crossref_primary_10_2174_0113862073290567240506162553 crossref_primary_10_1016_j_intimp_2024_113593 crossref_primary_10_1186_s12885_024_12908_0 crossref_primary_10_1007_s00240_024_01545_8 crossref_primary_10_2478_ahem_2004_0007 crossref_primary_10_1186_s41065_025_00408_5 crossref_primary_10_1016_j_taap_2024_116855 crossref_primary_10_3390_cells14010005 crossref_primary_10_1002_pmic_202300359 crossref_primary_10_3390_nu16213674 crossref_primary_10_3389_fgene_2024_1385293 crossref_primary_10_1097_MD_0000000000037085 crossref_primary_10_1200_JCO_22_02754 |
Cites_doi | 10.1016/0741-8329(85)90090-4 10.2967/jnumed.115.157834 10.1038/nrm.2016.25 10.1161/CIRCRESAHA.118.311342 10.1007/s11306-021-01823-1 10.1093/ije/dyt179 10.1002/gepi.21758 10.1038/ng.2982 10.1093/ije/dyg070 10.1186/s12916-017-0976-4 10.1007/s00392-017-1106-1 10.1038/nrc.2016.87 10.1007/s10549-019-05165-4 10.3390/metabo11100687 10.1038/ncomms11122 10.1093/hmg/ddy163 10.1161/CIRCRESAHA.117.311002 10.1002/cncr.32802 10.1038/nrclinonc.2017.1 10.1186/s13045-019-0828-0 10.1111/bju.12279 10.1016/j.annonc.2020.01.066 10.1038/s41588-018-0184-y 10.3390/jcm9092846 10.1016/j.ccell.2014.12.002 10.1016/j.jacc.2016.09.972 10.1038/nature24284 10.7554/eLife.34408 10.1161/CIRCULATIONAHA.119.040180 10.1080/19490976.2015.1134082 10.1097/RLU.0b013e3181bed06e 10.1158/1078-0432.CCR-11-0817 10.1038/ng.3314 10.3322/caac.21660 10.1093/ije/dyz242 10.3322/caac.21654 10.1002/gepi.21965 10.1136/bmj.k3225 10.1093/jn/nxz268 |
ContentType | Journal Article |
Copyright | 2023. The Author(s). COPYRIGHT 2023 BioMed Central Ltd. 2023. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. The Author(s) 2023 |
Copyright_xml | – notice: 2023. The Author(s). – notice: COPYRIGHT 2023 BioMed Central Ltd. – notice: 2023. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: The Author(s) 2023 |
DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 3V. 7TO 7X7 7XB 8FI 8FJ 8FK ABUWG AFKRA AZQEC BENPR CCPQU DWQXO FYUFA GHDGH H94 K9. M0S PHGZM PHGZT PIMPY PKEHL PQEST PQQKQ PQUKI PRINS 7X8 5PM DOA |
DOI | 10.1186/s13058-023-01609-4 |
DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Central (Corporate) Oncogenes and Growth Factors Abstracts Health & Medical Collection ProQuest Central (purchase pre-March 2016) Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central ProQuest Central UK/Ireland ProQuest Central Essentials ProQuest Central ProQuest One ProQuest Central Korea Health Research Premium Collection Health Research Premium Collection (Alumni) AIDS and Cancer Research Abstracts ProQuest Health & Medical Complete (Alumni) ProQuest Health & Medical Collection ProQuest Central Premium ProQuest One Academic (New) Publicly Available Content Database ProQuest One Academic Middle East (New) ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Publicly Available Content Database Oncogenes and Growth Factors Abstracts ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest One Academic Eastern Edition ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) ProQuest One Community College ProQuest Hospital Collection Health Research Premium Collection (Alumni) ProQuest Central China ProQuest Hospital Collection (Alumni) ProQuest Central ProQuest Health & Medical Complete Health Research Premium Collection ProQuest One Academic UKI Edition Health and Medicine Complete (Alumni Edition) ProQuest Central Korea AIDS and Cancer Research Abstracts ProQuest Central (New) ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic |
DatabaseTitleList | MEDLINE Publicly Available Content Database MEDLINE - Academic |
Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database – sequence: 4 dbid: BENPR name: ProQuest Central url: https://www.proquest.com/central sourceTypes: Aggregation Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine Anatomy & Physiology |
EISSN | 1465-542X |
EndPage | 11 |
ExternalDocumentID | oai_doaj_org_article_be1efb966d1c42f9aa2672b07a8c51f0 PMC9872401 A734541583 36694207 10_1186_s13058_023_01609_4 |
Genre | Research Support, Non-U.S. Gov't Journal Article |
GeographicLocations | United Kingdom--UK |
GeographicLocations_xml | – name: United Kingdom--UK |
GrantInformation_xml | – fundername: Natural Science Research Project of Jiangsu Provincial Higher Education grantid: 21KJB330006 – fundername: National Natural Science Foundation of China grantid: 82020108028 – fundername: National Natural Science Foundation of China grantid: 82103917 – fundername: ; grantid: 21KJB330006 – fundername: ; grantid: 82020108028; 82103917 |
GroupedDBID | --- 04C 0R~ 23N 2WC 4.4 53G 5GY 5VS 6J9 7X7 8FI 8FJ AAFWJ AAJSJ AASML AAWTL AAYXX ABUWG ACGFO ACGFS ACJQM ACMJI ACPRK ADBBV ADFRT ADUKV AENEX AFKRA AFPKN AHBYD AHMBA AHYZX ALIPV ALMA_UNASSIGNED_HOLDINGS AMKLP AMTXH AOIAM AOIJS BAPOH BAWUL BCNDV BENPR BFQNJ BMC BMSDO BPHCQ BVXVI C6C CCPQU CITATION CS3 DIK DU5 E3Z EBD EBLON EBS EIHBH F5P FYUFA GROUPED_DOAJ GX1 HMCUK HYE IAO ICW IHR INH INR ITC KQ8 O5R O5S OK1 P2P PGMZT PHGZM PHGZT PIMPY PQQKQ PROAC RBZ ROL RPM RSV SBL SOJ TR2 U2A UKHRP WOQ CGR CUY CVF ECM EIF NPM PMFND 3V. 7TO 7XB 8FK AZQEC DWQXO H94 K9. PKEHL PQEST PQUKI PRINS 7X8 5PM PUEGO |
ID | FETCH-LOGICAL-c563t-d429de6518feef33b87af41741f9d7b92305bb5bb987845a765c06f8f46538f53 |
IEDL.DBID | DOA |
ISSN | 1465-542X 1465-5411 |
IngestDate | Wed Aug 27 01:27:02 EDT 2025 Thu Aug 21 18:38:41 EDT 2025 Fri Jul 11 05:21:43 EDT 2025 Mon Jun 30 03:10:20 EDT 2025 Tue Jun 17 20:17:06 EDT 2025 Tue Jun 10 20:20:00 EDT 2025 Tue Mar 18 09:46:16 EDT 2025 Thu Apr 24 22:53:34 EDT 2025 Tue Jul 01 02:43:15 EDT 2025 |
IsDoiOpenAccess | true |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 1 |
Keywords | Metabolites Breast cancer Mendelian randomization |
Language | English |
License | 2023. The Author(s). Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
LinkModel | DirectLink |
MergedId | FETCHMERGED-LOGICAL-c563t-d429de6518feef33b87af41741f9d7b92305bb5bb987845a765c06f8f46538f53 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
OpenAccessLink | https://doaj.org/article/be1efb966d1c42f9aa2672b07a8c51f0 |
PMID | 36694207 |
PQID | 2777782763 |
PQPubID | 2034567 |
PageCount | 11 |
ParticipantIDs | doaj_primary_oai_doaj_org_article_be1efb966d1c42f9aa2672b07a8c51f0 pubmedcentral_primary_oai_pubmedcentral_nih_gov_9872401 proquest_miscellaneous_2769592602 proquest_journals_2777782763 gale_infotracmisc_A734541583 gale_infotracacademiconefile_A734541583 pubmed_primary_36694207 crossref_primary_10_1186_s13058_023_01609_4 crossref_citationtrail_10_1186_s13058_023_01609_4 |
ProviderPackageCode | CITATION AAYXX |
PublicationCentury | 2000 |
PublicationDate | 2023-01-24 |
PublicationDateYYYYMMDD | 2023-01-24 |
PublicationDate_xml | – month: 01 year: 2023 text: 2023-01-24 day: 24 |
PublicationDecade | 2020 |
PublicationPlace | England |
PublicationPlace_xml | – name: England – name: London |
PublicationTitle | Breast cancer research : BCR |
PublicationTitleAlternate | Breast Cancer Res |
PublicationYear | 2023 |
Publisher | BioMed Central Ltd BioMed Central BMC |
Publisher_xml | – name: BioMed Central Ltd – name: BioMed Central – name: BMC |
References | A Beeghly-Fadiel (1609_CR34) 2020; 49 DA Bennett (1609_CR20) 2017; 103 S Burgess (1609_CR25) 2013; 37 N Li (1609_CR2) 2019; 12 CL Silva (1609_CR40) 2021; 17 SY Shin (1609_CR13) 2014; 46 DJ Morrison (1609_CR35) 2016; 7 K Trajanoska (1609_CR29) 2018; 362 J Kettunen (1609_CR14) 2016; 7 N Murphy (1609_CR19) 2020; 31 G Hemani (1609_CR23) 2018; 7 M Chong (1609_CR22) 2019; 140 GD Smith (1609_CR17) 2003; 32 KN Seyed (1609_CR18) 2021; 10 MR Nelson (1609_CR12) 2015; 47 JR Ussher (1609_CR9) 2016; 68 H Sung (1609_CR1) 2021; 71 ZT Schug (1609_CR36) 2016; 16 L Huo (1609_CR42) 2009; 34 SJ Henley (1609_CR3) 2020; 126 RW McGarrah (1609_CR10) 2018; 122 B Pan (1609_CR31) 2012; 18 1609_CR15 ZT Schug (1609_CR41) 2015; 27 J Bowden (1609_CR26) 2016; 40 VA Katzke (1609_CR32) 2017; 15 QWJ Zhao (1609_CR27) 2019; 5 SK Clinton (1609_CR38) 2020; 150 CH Johnson (1609_CR8) 2016; 17 G Hemani (1609_CR28) 2018; 27 H Zhao (1609_CR6) 2019; 176 DK Arnett (1609_CR11) 2018; 122 MJ Brion (1609_CR24) 2013; 42 SM Jung (1609_CR33) 2020; 9 UE Martinez-Outschoorn (1609_CR39) 2017; 14 W März (1609_CR30) 2017; 106 H Nuutinen (1609_CR37) 1985; 2 W Zhou (1609_CR21) 2018; 50 RL Siegel (1609_CR4) 2021; 71 ES McDonald (1609_CR5) 2016; 57 B Mohsen (1609_CR43) 2013; 112 K Michailidou (1609_CR16) 2017; 551 JO Onuh (1609_CR7) 2021; 11 |
References_xml | – volume: 2 start-page: 623 issue: 4 year: 1985 ident: 1609_CR37 publication-title: Alcohol (Fayetteville, NY) doi: 10.1016/0741-8329(85)90090-4 – volume: 57 start-page: 9s issue: Suppl 1 year: 2016 ident: 1609_CR5 publication-title: J Nucl Med doi: 10.2967/jnumed.115.157834 – volume: 17 start-page: 451 issue: 7 year: 2016 ident: 1609_CR8 publication-title: Nat Rev Mol Cell Biol doi: 10.1038/nrm.2016.25 – volume: 103 start-page: 1400 issue: 18 year: 2017 ident: 1609_CR20 publication-title: Heart (British Cardiac Society) – volume: 122 start-page: 1409 issue: 10 year: 2018 ident: 1609_CR11 publication-title: Circ Res doi: 10.1161/CIRCRESAHA.118.311342 – volume: 17 start-page: 72 issue: 8 year: 2021 ident: 1609_CR40 publication-title: Metabolomics doi: 10.1007/s11306-021-01823-1 – volume: 42 start-page: 1497 issue: 5 year: 2013 ident: 1609_CR24 publication-title: Int J Epidemiol doi: 10.1093/ije/dyt179 – volume: 37 start-page: 658 issue: 7 year: 2013 ident: 1609_CR25 publication-title: Genet Epidemiol doi: 10.1002/gepi.21758 – volume: 46 start-page: 543 issue: 6 year: 2014 ident: 1609_CR13 publication-title: Nat Genet doi: 10.1038/ng.2982 – volume: 32 start-page: 1 issue: 1 year: 2003 ident: 1609_CR17 publication-title: Int J Epidemiol doi: 10.1093/ije/dyg070 – volume: 15 start-page: 218 issue: 1 year: 2017 ident: 1609_CR32 publication-title: BMC Med doi: 10.1186/s12916-017-0976-4 – volume: 106 start-page: 663 issue: 9 year: 2017 ident: 1609_CR30 publication-title: Clin Res Cardiol doi: 10.1007/s00392-017-1106-1 – volume: 16 start-page: 708 issue: 11 year: 2016 ident: 1609_CR36 publication-title: Nat Rev Cancer doi: 10.1038/nrc.2016.87 – volume: 176 start-page: 687 issue: 3 year: 2019 ident: 1609_CR6 publication-title: Breast Cancer Res Treat doi: 10.1007/s10549-019-05165-4 – volume: 11 start-page: 63 issue: 10 year: 2021 ident: 1609_CR7 publication-title: Metabolites doi: 10.3390/metabo11100687 – volume: 7 start-page: 11122 year: 2016 ident: 1609_CR14 publication-title: Nat Commun doi: 10.1038/ncomms11122 – volume: 27 start-page: R195 issue: R2 year: 2018 ident: 1609_CR28 publication-title: Hum Mol Genet doi: 10.1093/hmg/ddy163 – volume: 122 start-page: 1238 issue: 9 year: 2018 ident: 1609_CR10 publication-title: Circ Res doi: 10.1161/CIRCRESAHA.117.311002 – volume: 5 start-page: 78 year: 2019 ident: 1609_CR27 publication-title: arXiv – volume: 126 start-page: 2225 issue: 10 year: 2020 ident: 1609_CR3 publication-title: Cancer doi: 10.1002/cncr.32802 – volume: 14 start-page: 113 issue: 2 year: 2017 ident: 1609_CR39 publication-title: Nat Rev Clin Oncol doi: 10.1038/nrclinonc.2017.1 – volume: 12 start-page: 140 issue: 1 year: 2019 ident: 1609_CR2 publication-title: J Hematol Oncol doi: 10.1186/s13045-019-0828-0 – volume: 112 start-page: 1062 issue: 8 year: 2013 ident: 1609_CR43 publication-title: BJU Int doi: 10.1111/bju.12279 – volume: 31 start-page: 641 issue: 5 year: 2020 ident: 1609_CR19 publication-title: Ann Oncol doi: 10.1016/j.annonc.2020.01.066 – volume: 50 start-page: 1335 issue: 9 year: 2018 ident: 1609_CR21 publication-title: Nat Genet doi: 10.1038/s41588-018-0184-y – volume: 9 start-page: 53 issue: 9 year: 2020 ident: 1609_CR33 publication-title: J Clin Med doi: 10.3390/jcm9092846 – volume: 27 start-page: 57 issue: 1 year: 2015 ident: 1609_CR41 publication-title: Cancer Cell doi: 10.1016/j.ccell.2014.12.002 – volume: 68 start-page: 2850 issue: 25 year: 2016 ident: 1609_CR9 publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2016.09.972 – volume: 551 start-page: 92 issue: 7678 year: 2017 ident: 1609_CR16 publication-title: Nature doi: 10.1038/nature24284 – volume: 7 start-page: 80 year: 2018 ident: 1609_CR23 publication-title: eLife doi: 10.7554/eLife.34408 – volume: 140 start-page: 819 issue: 10 year: 2019 ident: 1609_CR22 publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.119.040180 – volume: 7 start-page: 189 issue: 3 year: 2016 ident: 1609_CR35 publication-title: Gut microbes doi: 10.1080/19490976.2015.1134082 – volume: 34 start-page: 874 issue: 12 year: 2009 ident: 1609_CR42 publication-title: Clin Nucl Med doi: 10.1097/RLU.0b013e3181bed06e – volume: 18 start-page: 1246 issue: 5 year: 2012 ident: 1609_CR31 publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-11-0817 – volume: 47 start-page: 856 issue: 8 year: 2015 ident: 1609_CR12 publication-title: Nat Genet doi: 10.1038/ng.3314 – volume: 71 start-page: 209 issue: 3 year: 2021 ident: 1609_CR1 publication-title: CA Cancer J Clin doi: 10.3322/caac.21660 – volume: 49 start-page: 1117 issue: 4 year: 2020 ident: 1609_CR34 publication-title: Int J Epidemiol doi: 10.1093/ije/dyz242 – volume: 10 start-page: 52 issue: 2 year: 2021 ident: 1609_CR18 publication-title: Cells – volume: 71 start-page: 7 issue: 1 year: 2021 ident: 1609_CR4 publication-title: CA Cancer J Clin doi: 10.3322/caac.21654 – volume: 40 start-page: 304 issue: 4 year: 2016 ident: 1609_CR26 publication-title: Genet Epidemiol doi: 10.1002/gepi.21965 – ident: 1609_CR15 – volume: 362 start-page: k3225 year: 2018 ident: 1609_CR29 publication-title: BMJ (Clinical research ed) doi: 10.1136/bmj.k3225 – volume: 150 start-page: 663 issue: 4 year: 2020 ident: 1609_CR38 publication-title: J Nutr doi: 10.1093/jn/nxz268 |
SSID | ssj0017858 |
Score | 2.4982595 |
Snippet | Breast cancer is the most common cancer among women with limited treatment options. To identify promising drug targets for breast cancer, we conducted a... Background Breast cancer is the most common cancer among women with limited treatment options. To identify promising drug targets for breast cancer, we... BackgroundBreast cancer is the most common cancer among women with limited treatment options. To identify promising drug targets for breast cancer, we... Abstract Background Breast cancer is the most common cancer among women with limited treatment options. To identify promising drug targets for breast cancer,... |
SourceID | doaj pubmedcentral proquest gale pubmed crossref |
SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
StartPage | 9 |
SubjectTerms | Acetates Acetic acid Biobanks Biomarkers Blood Breast cancer Breast Neoplasms - etiology Breast Neoplasms - genetics Cancer Cancer therapies Care and treatment Cholesterol Cholesterol, HDL - genetics Circulatory system Clinical trials Collaboration Consortia Development and progression Disease Female Genome-wide association studies Genome-Wide Association Study Genomes Genomics Health aspects High density lipoprotein Humans Mendelian randomization Mental disorders Mental illness Metabolism Metabolites Metabolome NMR Nuclear magnetic resonance Oncology, Experimental Polymorphism, Single Nucleotide Prevention Risk Factors Side effects Statistical power Therapeutic targets Triglycerides |
SummonAdditionalLinks | – databaseName: Health & Medical Collection dbid: 7X7 link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3Ni9QwFA-6gngR3fWjukoE0YOEbdJ89SSjuAzCenJhbqH5UmGnXWe6B_97X9LMOEXY0lOTQtP3_fLyewi9Da3w8O8DobRzhHvrieYuEBlSwqGWbcwJt4tvcnnJv67EqiTctqWscqcTs6L2g0s58jOm4NIMxOHj9W-Sukal3dXSQuMuupegy1JJl1rtA67UeF5Pp4sEEZzS3aEZLc-2oLuFJmCxSMJYawmfGaaM3_-_lj4wU_MSygObdP4IPSzOJF5M1H-M7oT-GJ0segik13_wO5zLO3Pe_Bjdvyi76CdoeUATXAq1cG7Wh3MdO16HEXjjalgH3PUeg4-IUwk6HiK2qYh9xC4xy-YJujz_8v3zkpSOCsQJ2YzEg_XxQQqqYwixaaxWXeQQlNDYemXB2auFtXC3WmkuOiWFq2XUMaGw6Siap-ioH_rwHGFRO-G7mjmgLzgFVifUmBCl44K5wH2F6O53GlfgxlPXiyuTww4tzUQCAyQwmQSGV-jD_p3rCWzj1tmfEpX2MxNQdn4wbH6YInfGBhqihZjOU8dZbLuOScVsrTrtBI11hd4nGpskzvB5riunEmCRCRjLLFTDgXWEbip0OpsJYujmwzsuMUUNbM0_pq3Qm_1wejOVtvVhuElzZCtaCCtZhZ5NTLVfUiNly1mtKqRm7DZb83yk__Uzg4QDBcFZoy9u_6yX6AGbZIAwfoqOxs1NeAVe1mhfZ1H6C-NZIhY priority: 102 providerName: ProQuest |
Title | Association between human blood metabolome and the risk of breast cancer |
URI | https://www.ncbi.nlm.nih.gov/pubmed/36694207 https://www.proquest.com/docview/2777782763 https://www.proquest.com/docview/2769592602 https://pubmed.ncbi.nlm.nih.gov/PMC9872401 https://doaj.org/article/be1efb966d1c42f9aa2672b07a8c51f0 |
Volume | 25 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3Ni9QwFH_oCuJFdNeP6jpEED1I2DbNV48zsssg7CKLC4OX0HyhsNOR3e7B_96XtDNMEfRiKT00CSTvI--95OUXgHehER5pH2hVtY5ybz3V3AUqQ1pwKGUT84Lb-YVcXvHPK7Hau-or5YQN8MAD4U5sqEK06JT7ynEWm7ZlUjFbqlY7UcUcraPN2wZT4_6B0kJvj8hoeXKLM7XQFO0TTYhqDeUTM5TR-v-ck_eM0jRhcs8CnT2Bx6PrSOZDl5_CvdAdwtG8w7B5_Yu8JzmZM6-SH8LD83HP_AiWexwgY1oWyVfzkZy1TtahR0m43qwDaTtP0CMkKeGcbCKxKWW9Jy6Jxs0zuDo7_fppScf7E6gTsu6pR1vjgxSVjiHEurZatZFjCFLFxiuLrl0prMW30Upz0SopXCmjjglzTUdRP4eDbtOFl0BE6YRvS-aQm-gCWJ0wYkKUjgvmAvcFVFtyGjeCi6c7Lq5NDjK0NAMLDLLAZBYYXsDHXZufA7TGX2svEpd2NRMsdv6BwmJGYTH_EpYCPiQem6S82D3XjmcQcJAJBsvMVc0FujS6LuB4UhOVzk2Lt1JiRqW_NUzhoxnO2AW83RWnlimRrQubu1RHNqLBIJIV8GIQqt2QaikbzkpVgJqI22TM05Lux_cMCY4cRNesevU_iPQaHrFBUyjjx3DQ39yFN-h59XYG99VKzeDB4vTiy-Usqxx-LxfffgO_VCz6 |
linkProvider | Directory of Open Access Journals |
linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9QwEB5VWwm4IGh5BAoYiccBWU0c23EOCG2h1ZZ2Vwi1Um8mcWxA6iZldyvUP8VvZOxkl42QemuUU2xLseeblz2eAXhlc1Hh2luaJIWhvCorqrixVFq_4RDL3IUNt_FEjk755zNxtgF_lndhfFjlUiYGQV01xu-R77IMH8WQHT5c_KK-apQ_XV2W0GhhcWSvfqPLNn9_-Anp-5qxg_2TjyPaVRWgRsh0QSuUwJWVIlHOWpempcoKx9EwT1xeZSUaPLEoS3zRG1dcFJkUJpZOOZ-JTDlfJQJF_iZP0ZUZwObe_uTL19W5RaZCRVAUP4IKniTLazpK7s5RWwhFUUdSn9Utp7ynCkPFgP_1wppi7AdtrmnBg3twtzNfybDF233YsPUWbA9rdN2nV-QNCQGlYad-C26Nu3P7bRitoYB0oWEklAckIXKeTO0C0XjeTC0p6oqgVUp80DtpHCl92PyCGA_P2QM4vZHVfgiDuqntYyAiNqIqYmYQUWiGlMrnqbFOGi6YsbyKIFkupzZdgnNfZ-NcB0dHSd2SQCMJdCCB5hG8W425aNN7XNt7z1Np1dOn5g4fmtl33XG6Lm1iXYleZJUYzlxeFExmrIyzQhmRuDiCt57G2gsQ_D1TdPcgcJI-FZceZilH6AiVRrDT64mMb_rNS5ToTvDM9T82ieDlqtmP9MF0tW0ufR-ZixwdWRbBoxZUqymlUuacxVkEWQ9uvTn3W-qfP0JacqQgmofJk-t_6wXcHp2Mj_Xx4eToKdxhLT9QxndgsJhd2mdo4y3K5x1jEfh207z8F6oeX7M |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Association+between+human+blood+metabolome+and+the+risk+of+breast+cancer&rft.jtitle=Breast+cancer+research+%3A+BCR&rft.au=Wang%2C+Yu&rft.au=Liu%2C+Fanghua&rft.au=Sun%2C+Lulu&rft.au=Jia%2C+Yiming&rft.date=2023-01-24&rft.pub=BioMed+Central+Ltd&rft.issn=1465-5411&rft.volume=25&rft.issue=1&rft_id=info:doi/10.1186%2Fs13058-023-01609-4&rft.externalDocID=A734541583 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1465-542X&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1465-542X&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1465-542X&client=summon |