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Correction

Correction

This article refers to:
Associations between placental CpG methylation of metastable epialleles and childhood body mass index across ages one, two and ten in the Extremely Low Gestational Age Newborns (ELGAN) cohort

Article title: Associations between placental CpG methylation of metastable epialleles and childhood body mass index across ages one, two and ten in the Extremely Low Gestational Age Newborns (ELGAN) cohort

Table 1. Demographic characteristics of the subset of the ELGAN cohort comprising the present study (n = 411)

Table 2. Placental CpG sites (n = 39) corresponding to metastable epialleles that are associated with BMI z-score across ages one, two, and ten globally

Table 3. Placental CpG sites (n = 57) corresponding to metastable epialleles that are associated with BMI z-score across ages one, two, and ten among females

Table 4. Placental CpG sites (n = 35) corresponding to metastable epialleles that are associated with BMI z-score across ages one, two, and ten among males

Authors: Jeliyah Clark, Elizabeth Martin, Catherine M. Bulka, Lisa Smeester, Hudson P. Santos, Jr., T. Michael O’Shea, Rebecca C. Fry

Journal: Epigenetics

Bibliometrics: Volume 14, Number 11, pages 1102- 1111

DOI: http://dx.doi.org/10.1080/15592294.2019.1633865

It has come to the attention of the authors that an error occurred during sample processing which influenced results from the article originally published online. Placental DNA samples on a 96-well plate were misoriented to their matching barcodes. This resulted in a mismatch between methylation and clinical data. Once correctly aligned, a small number of samples were identified for which reported infant sex and methylation-predicted sex (using the minfi R package) differed. Correction for these errors resulted in changes in demographic distributions, beta-estimates, p-values, and the CpG probes identified as significant.

The data were re-analyzed, accordingly. The correction of the sample processing error influenced study subject inclusion, decreasing the sample size from n=426 to n=411. Five observations were excluded with a sex mismatch, and 10 additional observations were excluded due to missingness of data required to link samples to phenotype data. In the prior analysis, one CpG site was identified to be differentially methylated among girls (q < 0.05) at PLAGL1. Upon re-analysis, this association was not conserved among females but was identified among males. Specifically, an additional 28 FDR-significant associations were identified in sex-stratified analyses: two among males and 26 among females. Here, we provide corrected tables corresponding to these results. The authors apologize for this error.

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