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Platelet count and gastric cancer susceptibility: A Mendelian randomization study
The objective of this study was to ascertain the potential causal linkage between platelet (PLT) counts and the incidence of gastric cancer (GC). This study employed a 2-sample Mendelian randomization (MR) approach, utilizing the inverse variance weighting, weighted median, and MR-Egger regression m...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Lippincott Williams & Wilkins
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10627695/ https://www.ncbi.nlm.nih.gov/pubmed/37933067 http://dx.doi.org/10.1097/MD.0000000000035790 |
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author | Zhu, Yingze Zhou, Miao Kong, Wenyue Li, Congling Su, Xin |
author_facet | Zhu, Yingze Zhou, Miao Kong, Wenyue Li, Congling Su, Xin |
author_sort | Zhu, Yingze |
collection | PubMed |
description | The objective of this study was to ascertain the potential causal linkage between platelet (PLT) counts and the incidence of gastric cancer (GC). This study employed a 2-sample Mendelian randomization (MR) approach, utilizing the inverse variance weighting, weighted median, and MR-Egger regression methodologies. The publicly accessible summary statistics dataset from the genome-wide association study pertaining to individuals of European ancestry (n = 145,648) was employed as the foundational resource for the exposure variable. Concomitantly, the non-cancer disease codes for GC (n = 6563), derived from individuals within the UK Biosample Bank, were utilized as the outcome measure. A set of 132 single-nucleotide polymorphisms exhibiting genome-wide significance were selected as instrumental variables, drawn from the genome-wide association studies focused on PLT counts. The application of the weighted median methodology yielded indications suggesting the possible absence of a causal relationship between PLT counts and GC (beta = 0.139, SE = 0.079, P = .077). Contrarily, the implementation of the inverse variance weighting technique produced results indicative of a potential causal relationship between PLT counts and GC (beta = 0.128, SE = 0.049, P = .009). The assessment of Cochran Q test and the scrutiny of funnel plots unveiled no discernible indications of heterogeneity or asymmetry, thus signifying the absence of directional pleiotropy. The outcomes derived from the MR analysis lend credence to the hypothesis that there exists a plausible causal relationship between erythrocyte pressure and an elevated susceptibility to gastric cancer. |
format | Online Article Text |
id | pubmed-10627695 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Lippincott Williams & Wilkins |
record_format | MEDLINE/PubMed |
spelling | pubmed-106276952023-11-07 Platelet count and gastric cancer susceptibility: A Mendelian randomization study Zhu, Yingze Zhou, Miao Kong, Wenyue Li, Congling Su, Xin Medicine (Baltimore) 3500 The objective of this study was to ascertain the potential causal linkage between platelet (PLT) counts and the incidence of gastric cancer (GC). This study employed a 2-sample Mendelian randomization (MR) approach, utilizing the inverse variance weighting, weighted median, and MR-Egger regression methodologies. The publicly accessible summary statistics dataset from the genome-wide association study pertaining to individuals of European ancestry (n = 145,648) was employed as the foundational resource for the exposure variable. Concomitantly, the non-cancer disease codes for GC (n = 6563), derived from individuals within the UK Biosample Bank, were utilized as the outcome measure. A set of 132 single-nucleotide polymorphisms exhibiting genome-wide significance were selected as instrumental variables, drawn from the genome-wide association studies focused on PLT counts. The application of the weighted median methodology yielded indications suggesting the possible absence of a causal relationship between PLT counts and GC (beta = 0.139, SE = 0.079, P = .077). Contrarily, the implementation of the inverse variance weighting technique produced results indicative of a potential causal relationship between PLT counts and GC (beta = 0.128, SE = 0.049, P = .009). The assessment of Cochran Q test and the scrutiny of funnel plots unveiled no discernible indications of heterogeneity or asymmetry, thus signifying the absence of directional pleiotropy. The outcomes derived from the MR analysis lend credence to the hypothesis that there exists a plausible causal relationship between erythrocyte pressure and an elevated susceptibility to gastric cancer. Lippincott Williams & Wilkins 2023-11-03 /pmc/articles/PMC10627695/ /pubmed/37933067 http://dx.doi.org/10.1097/MD.0000000000035790 Text en Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc. https://creativecommons.org/licenses/by-nc/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial License 4.0 (CCBY-NC) (https://creativecommons.org/licenses/by-nc/4.0/) , where it is permissible to download, share, remix, transform, and buildup the work provided it is properly cited. The work cannot be used commercially without permission from the journal. |
spellingShingle | 3500 Zhu, Yingze Zhou, Miao Kong, Wenyue Li, Congling Su, Xin Platelet count and gastric cancer susceptibility: A Mendelian randomization study |
title | Platelet count and gastric cancer susceptibility: A Mendelian randomization study |
title_full | Platelet count and gastric cancer susceptibility: A Mendelian randomization study |
title_fullStr | Platelet count and gastric cancer susceptibility: A Mendelian randomization study |
title_full_unstemmed | Platelet count and gastric cancer susceptibility: A Mendelian randomization study |
title_short | Platelet count and gastric cancer susceptibility: A Mendelian randomization study |
title_sort | platelet count and gastric cancer susceptibility: a mendelian randomization study |
topic | 3500 |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10627695/ https://www.ncbi.nlm.nih.gov/pubmed/37933067 http://dx.doi.org/10.1097/MD.0000000000035790 |
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