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October 17-21 2015 Baltimore Maryland

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potential of monosomy embryos is negligible compared to their trisomy<br />

counterparts, yet the cause for this is unknown. Our previous investigation<br />

of epigenetic modifiers uncovered a decreased expression of DNA methyltransferase<br />

enzymes in monosomy blastocysts, as well as a hypomethylated<br />

state limited to the monosomic chromosome. This study was thus extended to<br />

determine the DNA methylation profiles of imprinting control regions (ICRs)<br />

present on the affected chromosomes.<br />

DESIGN: Research study.<br />

MATERIALS AND METHODS: Surplus cryopreserved human blastocysts<br />

were donated with IRB approval. Trophectoderm biopsies followed<br />

by comprehensive chromosomal screening using qPCR (RMA-NJ) determined<br />

chromosome constitution. Individual monosomy 11 (n¼10) or 15<br />

(n¼10), trisomy 11 (n¼10) or 15 (n¼10), and euploid oocyte donor blastocysts<br />

(controls; n¼20) underwent bisulfite conversion and PCR amplification<br />

to determine the DNA methylation profiles of two maternally<br />

methylated ICRs, KCNQ1OT1 (11p15.5) and SNRPN (15q11.2). Statistical<br />

analysis was calculated using the Student’s t-Test, with significance at<br />

p

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