Evidence map›Paper›PMID 36855205›Full record

ArticleClinical epigenetics2023

Distinct DNA methylation signatures associated with blood lipids as exposures or outcomes among survivors of childhood cancer: a report from the St. Jude lifetime cohort.

Qian Dong, Cheng Chen, Nan Song, Na Qin, Noel-Marie Plonski, Emily R Finch, Kyla Shelton, John Easton, Heather Mulder, Emily Plyer and 10 more

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 4 institutions in 3 countries.

Qian Dong *Department of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, 262 Danny Thomas Place, MS 735, Memphis, TN, 38105, USA.
Cheng Chen *Department of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, 262 Danny Thomas Place, MS 735, Memphis, TN, 38105, USA.
Nan SongCollege of Pharmacy, Chungbuk National University, Cheongju, Korea.
Na QinDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, China.
Noel-Marie PlonskiDepartment of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, 262 Danny Thomas Place, MS 735, Memphis, TN, 38105, USA.
Emily R FinchDepartment of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, 262 Danny Thomas Place, MS 735, Memphis, TN, 38105, USA.
Kyla SheltonDepartment of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, 262 Danny Thomas Place, MS 735, Memphis, TN, 38105, USA.
John EastonDepartment of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Heather MulderDepartment of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Emily PlyerDepartment of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Geoffrey NealeHartwell Center, St. Jude Children's Research Hospital, Memphis, TN, USA.
Emily WalkerHartwell Center, St. Jude Children's Research Hospital, Memphis, TN, USA.
Qian LiDepartment of Biostatistics, St. Jude Children's Research Hospital, Memphis, TN, USA.
I-Chan HuangDepartment of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, 262 Danny Thomas Place, MS 735, Memphis, TN, 38105, USA.
Jinghui ZhangDepartment of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Hui WangSchool of Public Health, Shanghai Jiaotong University, Shanghai, China.
Melissa M HudsonDepartment of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, 262 Danny Thomas Place, MS 735, Memphis, TN, 38105, USA.
Leslie L RobisonDepartment of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, 262 Danny Thomas Place, MS 735, Memphis, TN, 38105, USA.
Kirsten K NessDepartment of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, 262 Danny Thomas Place, MS 735, Memphis, TN, 38105, USA.
Zhaoming WangDepartment of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, 262 Danny Thomas Place, MS 735, Memphis, TN, 38105, USA. Zhaoming.Wang@stjude.org.
St. Jude Children's Research Hospital · USChungbuk National University · KRNanjing Medical University · CNShanghai Jiao Tong University · CN

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Shondra Michelle Miller · 1985 to 2026
$166.9M
The St. Jude Lifetime CohortU01CA195547 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI HUDSON, MELISSA M, NESS, KIRSTEN KIMBERLIE · 2015 to 2024
$14.9M
Training in Pediatric Cancer Survivorship Outcomes and InterventionsT32CA225590 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Kevin R Krull · 2018 to 2026
$2.4M
NCI NIH HHS P30 CA021765NCI NIH HHS T32 CA225590NCI NIH HHS U01 CA195547
6 · The paper itself

Abstract

backgroundDNA methylation (DNAm) plays an important role in lipid metabolism, however, no epigenome-wide association study (EWAS) of lipid levels has been conducted among childhood cancer survivors. Here, we performed EWAS analysis with longitudinally collected blood lipid data from survivors in the St. Jude lifetime cohort study.

methodsAmong 2052 childhood cancer survivors of European ancestry (EA) and 370 survivors of African ancestry (AA), four types of blood lipids, including high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol (TC), and triglycerides (TG), were measured during follow-up beyond 5-years from childhood cancer diagnosis. For the exposure EWAS (i.e., lipids measured before blood draw for DNAm), the DNAm level was an outcome variable and each of the blood lipid level was an exposure variable; vice versa for the outcome EWAS (i.e., lipids measured after blood draw for DNAm).

resultsAmong EA survivors, we identified 43 lipid-associated CpGs in the HDL (n = 7), TC (n = 3), and TG (n = 33) exposure EWAS, and 106 lipid-associated CpGs in the HDL (n = 5), LDL (n = 3), TC (n = 4), and TG (n = 94) outcome EWAS. Among AA survivors, we identified 15 lipid-associated CpGs in TG exposure (n = 6), HDL (n = 1), LDL (n = 1), TG (n = 5) and TC (n = 2) outcome EWAS with epigenome-wide significance (P < 9 × 10

conclusionsWe identified distinct signatures of DNAm for blood lipids as exposures or outcomes and between EA and AA survivors, revealing additional genes involved in lipid metabolism and potential novel targets for controlling blood lipids in childhood cancer survivors.

Indexed as

Cancer SurvivorsNeoplasmsChildCohort StudiesDNA MethylationHumansLipidsLipoproteins, HDLSurvivorsTriglyceridesLipidsLipoproteins, HDLTriglyceridesAfrican ancestryChildhood cancer survivorsDNA methylationEuropean ancestryEWASLipid levels

Identifiers

PMID36855205
PMCPMC9976538
OpenAlexW4322627600

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.