Allele-specific DNA methylation is increased in cancers and its dense mapping in normal plus neoplastic cells increases the yield of disease-associated regulatory SNPs.
Catherine DoEmmanuel L P DumontMartha SalasAngelica CastanoHuthayfa MujahedLeonel MaldonadoArunjot SinghSonia C DaSilva-ArnoldGovind BhagatSoren LehmanAngela M ChristianoSubha MadhavanPeter L NagyPeter H R GreenRena FeinmanCornelia TrimbleNicholas P IllsleyKaren MarderLawrence HonigCatherine MonkAndre GoyKar ChowSamuel GoldlustGeorge KaptainDavid SiegelBenjamin TyckoPublished in: Genome biology (2020)
ASM is increased in cancers but occurs by a shared mechanism involving disruptive SNPs in CTCF and transcription factor binding sites in both normal and neoplastic cells. Dense ASM mapping in normal plus cancer samples reveals candidate rSNPs that are difficult to find by other approaches. Together with GWAS data, these rSNPs can nominate specific transcriptional pathways in susceptibility to autoimmune, cardiometabolic, neuropsychiatric, and neoplastic diseases.
Keyphrases
- transcription factor
- induced apoptosis
- dna methylation
- genome wide
- cell cycle arrest
- high resolution
- gene expression
- endoplasmic reticulum stress
- oxidative stress
- squamous cell carcinoma
- signaling pathway
- childhood cancer
- machine learning
- mass spectrometry
- dna binding
- heat shock
- pi k akt
- deep learning
- heat shock protein
- drug induced
- heat stress