Causal effects of COVID‐19 on cancer risk: A Mendelian randomization study

Li, Jia; Bai, Haocheng; Hao, Qiao; Du, Chong; Yao, Peizhuo; Cai, Yifan; Jia, Yiwei; Wei, Xinyu; Li, Chaofan; Liu, Xuanyu; Wang, Weiwei; Sun, Shiyu; Feng, Cong; Hu, Yutian; Zhou, Zhangjian; Zhang, Shuqun; Zhang, Yinbin

doi:10.1002/jmv.28722

Cited by 21 publications

(16 citation statements)

References 51 publications

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“…A strong correlation between COVID-19 and GC has been reported[24,26], and in addition, the receptor ACE2 of SARS-CoV-2 infected hosts is expressed in the gastric mucosa[25]. Gastric cancer patients are relatively more susceptible to viral infection than ordinary people after surgery, chemotherapy or radiotherapy.…”

Section: Discussionmentioning

confidence: 99%

Exploration of the link between COVID-19 and gastric cancer from the perspective of bioinformatics and systems biology

Ma,

Huang,

et al. 2024

Preprint

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Background: Coronavirus disease 2019 (COVID-19), an infectious disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has caused a global pandemic. Gastric cancer (GC) poses a great threat to people's health, which is a high-risk factor for COVID-19. Previous studies have found some associations between GC and COVID-19, whereas the underlying molecular mechanisms are not well understood. Methods: We used a bioinformatics and systems biology approach to investigate the relationship between GC and COVID-19. The gene expression profiles of COVID-19 (GSE196822) and GC (GSE179252) were downloaded from the Gene Expression Omnibus (GEO) database. After identifying the shared differentially expressed genes (DEGs) for GC and COVID-19, functional annotation, protein-protein interaction (PPI) network, hub genes, transcriptional regulatory networks and candidate drugs were analyzed. Results: A total of 209 shared DEGs were identified to explore the linkages between COVID-19 and GC. Functional analyses showed that Immune-related pathway collectively participated in the development and progression of COVID-19 and GC. In addition, there are selected 10 hub genes including CDK1, KIF20A, TPX2, UBE2C, HJURP, CENPA, PLK1, MKI67, IFI6, and IFIT2. The transcription factor/gene and miRNA/gene interaction networks identified 38 transcription factors (TFs) and 234 miRNAs. More importantly, we identified ten potential therapeutic agents, including ciclopirox, resveratrol, etoposide, methotrexate, trifluridine, enterolactone, troglitazone, calcitriol, dasatinib and deferoxamine, some of which have been reported to improve and treat GC and COVID-19. This study also provides insight into the diseases most associated with mutual DEGs, which may provide new ideas for research on the treatment of COVID-19. Conclusions: This research has the possibility to be contributed to effective therapeutic in COVID-19 and GC.

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Section: Discussionmentioning

confidence: 99%

Exploration of the link between COVID-19 and gastric cancer from the perspective of bioinformatics and systems biology

Ma,

Huang,

et al. 2024

Preprint

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“…Finally, several other sensitivity analyses, such as leave-one-out analysis and funnel plots, were applied to identify the presence of heterogeneity and pleiotropy and to assess the robustness of the results. After Bonferroni correction, a P value below 0.008(0.05/6) was considered statistically signi cant and p-value between 0.008 and 0.05 was regarded as suggestive evidence for a potential causal association [33]. All analyses were conducted by using the R package "TwoSampleMR" in R (version 4.2.1).…”

Section: Discussionmentioning

confidence: 99%

Comparison of two different frailty metrics and associations with COVID-19: A bidirectional Mendelian randomization study

Han

Chen

Liu

et al. 2023

Preprint

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Background Several traditional observational studies suggested a strong association between frailty with coronavirus disease 2019 (COVID-19). However, whether the observed association reflects causality remained unclear. We employed a bidirectional Mendelian randomization (MR) study to investigate the causal relationship of frailty, measured by the Frailty Index and Fried Frailty Score, with COVID-19. Methods We extracted summary genome-wide association statistics for the Frailty Index (N = 164,610), Fried Frailty Score (N = 386,565), COVID-19 (Ncase = 159,840, Ncontrol = 2,782,977), hospitalized COVID-19 (Ncase = 44,986, Ncontrol = 2,356,386) and severe COVID-19 (Ncase = 18,152, Ncontrol = 1,145,546). Independent single nucleotide polymorphisms at genome-wide significance for each phenotype were taken as instruments. The random-effects inverse‐variance weighted method was applied as the primary method, followed by various sensitivity and validation analyses. Results No causal effect of Frailty Index between COVID-19 was observed. Genetically predicted Fried Frailty Score was significantly associated with increased risk of COVID-19 hospitalization (odds ratio [OR] 2.06, 95% confidence interval [CI] 1.45–2.91, P < 0.0001), and suggestively associated with higher risk of COVID-19 susceptibility (OR = 1.19, 95% CI 1.01–1.39; P = 0.035) and COVID-19 severity (OR = 2.10, 95% CI 1.10–4.01; P = 0.025). Sensitivity and validation analyses also received broadly concordant results. There is no insignificant association for reverse causation. Conclusion Our study demonstrated that Fried Frailty Score could increase the risk of COVID-19. Future development should focus on long-term mutual influence between frailty and COVID-19 to alleviate the complications of diseases.

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“…In contrast, MR-Egger enables causal analysis through the examination of the slope coefficient, thereby providing an alternative avenue for assessing causality. Conversely, the weighted median method showcases its capacity to compute unbiased estimates, even in the presence of a significant fraction of invalid instrumental variables (IVs) ( 23–25 ). Therefore, given the prevalent use of the IVW in two-sample Mendelian randomization studies, we have utilized IVW as the primary analytical approach, with the remaining four methods serving as supplementary tools to enhance the findings derived from IVW.…”

Section: Methodsmentioning

confidence: 99%

The causal relationship between COVID-19 and ten esophageal diseases: a study utilizing Mendelian randomization

He,

Li,

Liu

et al. 2024

Front. Med.

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BackgroundClinical signs of dysphagia, pancreatic achalasia, and esophagitis have been reported in patients with COVID-19. However, the causal relationship between COVID-19 and esophageal diseases is not clear. Therefore, we utilized Mendelian randomization to explore the potential association between COVID-19 and esophageal diseases.MethodsThe summary statistics for a Genome-wide association study (GWAS) were obtained from The COVID-19 Host Genetics Initiative, encompassing four types of COVID-19 as exposure: severe COVID-19, hospitalized COVID-19 versus ambulatory COVID-19, hospitalized COVID-19 versus uninfected, and confirmed COVID-19. Additionally, summary statistics for ten esophageal diseases as outcomes were sourced from the GWAS Catalog and FinnGen databases. Univariate Mendelian randomization (MR) analysis was utilized to thoroughly investigate and validate the potential causal association between COVID-19 and various esophageal conditions, including esophageal varices, Barrett’s esophagus, esophagitis, esophageal obstruction, esophageal ulcer, esophageal perforation, gastroesophageal reflux, congenital esophageal malformations, benign esophageal tumors, and esophageal adenocarcinoma.ResultsAn inverse variance-weighted (IVW) model was utilized for univariate Mendelian randomization (MR) analysis, which revealed that genetic liability in patients with confirmed COVID-19 was associated with esophageal obstruction (OR [95% CI]: 0.5275458 [0.2822400–0.9860563]; p-value = 0.0450699). Furthermore, a suggestive causal association was found between genetic liability and a reduced risk of benign esophageal tumors (OR [95% CI]: 0.2715453 [0.09368493–0.7870724]; p-value = 0.0163510), but with a suggestively increased risk of congenital esophageal malformations (OR [95% CI]: 6.959561 [1.1955828–40.51204]; p-value = 0.03086835). Additionally, genetic liability in hospitalized COVID-19 patients, compared to non-hospitalized COVID-19 patients, was suggestively associated with an increased risk of esophagitis (OR [95% CI]: 1.443859 [1.0890568–1.914252]; p-value = 0.01068201). The reliability of these causal findings is supported by Cochran’s Q statistic and the MR-Egger intercept test.ConclusionThe results of this study suggest the existence of a causal relationship between COVID-19 and esophageal diseases, highlighting differing risk effects of COVID-19 on distinct esophageal conditions.

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Causal effects of COVID‐19 on cancer risk: A Mendelian randomization study

Abstract: In contemporary literature, little attention has been paid to the association between coronavirus disease-2019 (COVID-19) and cancer risk. We performed the Mendelian randomization (MR) to investigate the causal associations between the three types of COVID-19 exposures (critically ill

Cited by 21 publications

References 51 publications

Exploration of the link between COVID-19 and gastric cancer from the perspective of bioinformatics and systems biology

Exploration of the link between COVID-19 and gastric cancer from the perspective of bioinformatics and systems biology

Comparison of two different frailty metrics and associations with COVID-19: A bidirectional Mendelian randomization study

The causal relationship between COVID-19 and ten esophageal diseases: a study utilizing Mendelian randomization

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