Krahasoni metodat

	Multi-omics epigenome-wide association study	Studimi i asociacionit në nivel të epigenomit (EWAS)
Fusha	Bioinformatikë	Bioinformatikë
Familja	Process / pipeline	Process / pipeline
Viti i origjinës	2011 (EWAS foundation); multi-omics integration ~2015–2020	2008–2011 (term and framework established c. 2011)
Krijuesi	Rakyan, Down, Balding & Beck (EWAS framework); multi-omics integration extended by multiple groups (~2015–2020)	Rakyan, Down, Balding & Beck (conceptual framework); Illumina arrays enabled large-scale application
Lloji	Integrative association study	Population-scale epigenomic association study
Burimi themelues	Rakyan, V. K., Down, T. A., Balding, D. J., & Beck, S. (2011). Epigenome-wide association studies for common human diseases. Nature Reviews Genetics, 12(8), 529–541.	Rakyan, V. K., Down, T. A., Balding, D. J., & Beck, S. (2011). Epigenome-wide association studies for common human diseases. Nature Reviews Genetics, 12(8), 529–541.
Emërtime të tjera	multi-omics EWAS, integrative EWAS, multi-layer epigenome-wide association, multi-omics epigenomic integration	EWAS, methylome-wide association study, epigenetic association study, DNA methylation association study
Të lidhura	4	5
Përmbledhja	A multi-omics epigenome-wide association study (multi-omics EWAS) systematically scans the entire epigenome — typically DNA methylation at CpG sites — for associations with a phenotype of interest, then integrates findings across additional omics layers such as transcriptomics, genomics, proteomics, or metabolomics. By linking epigenetic variation to molecular changes at multiple biological levels simultaneously, this approach identifies regulatory mechanisms and biomarkers that single-omics EWAS cannot resolve.	An epigenome-wide association study (EWAS) is a hypothesis-free, genome-scale method that systematically tests whether epigenetic marks — predominantly CpG-site DNA methylation — differ between individuals with and without a trait, disease, or exposure. By scanning hundreds of thousands of genomic positions simultaneously, EWAS identifies loci where the epigenome is reproducibly associated with a phenotype, offering a layer of biological regulation that classical GWAS does not capture.