AI Article Synopsis

  • There is a shared relationship between cardiovascular disease (CVD) and cancer, tied to common risk factors and biological pathways, which the study aims to explore across three diverse ethnic cohorts.
  • The researchers employed a two-stage methodology involving epigenome-wide association studies and targeted analysis of differentially methylated positions (DMPs), unveiling significant epigenetic markers for CVD and cancer.
  • The findings indicate interconnected biological pathways for CVD and cancer, suggesting potential for precision prevention strategies, including screening based on epigenetic signatures to identify at-risk patients in early diagnosis stages.

Article Abstract

Background: Emerging evidence reveals a complex relationship between cardiovascular disease (CVD) and cancer, which share common risk factors and biological pathways.

Objectives: The aim of this study was to evaluate common epigenetic signatures for CVD and cancer incidence in 3 ethnically diverse cohorts: Native Americans from the SHS (Strong Heart Study), European Americans from the FHS (Framingham Heart Study), and European Americans and African Americans from the ARIC (Atherosclerosis Risk In Communities) study.

Methods: A 2-stage strategy was used that included first conducting untargeted epigenome-wide association studies for each cohort and then running targeted models in the union set of identified differentially methylated positions (DMPs). We also explored potential molecular pathways by conducting a bioinformatics analysis.

Results: Common DMPs were identified across all populations. In a subsequent meta-analysis, 3 and 1 of those DMPs were statistically significant for CVD only and both cancer and CVD, respectively. No meta-analyzed DMPs were statistically significant for cancer only. The enrichment analysis pointed to interconnected biological pathways involved in cancer and CVD. In the DrugBank database, elements related to 1-carbon metabolism and cancer and CVD medications were identified as potential drugs for target gene products. In an additional analysis restricted to the 950 SHS participants who developed incident CVD, the C index for incident cancer increased from 0.618 (95% CI: 0.570-0.672) to 0.971 (95% CI: 0.963-0.978) when adjusting the models for the combined cancer and CVD DMPs identified in the other cohorts.

Conclusions: These results point to molecular pathways and potential treatments for precision prevention of CVD and cancer. Screening based on common epigenetic signatures of incident CVD and cancer may help identify patients with newly diagnosed CVD at increased cancer risk.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11520201PMC
http://dx.doi.org/10.1016/j.jaccao.2024.07.014DOI Listing

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