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Related Experiment Video

Updated: Jun 25, 2026

Microsatellite DNA Genotyping and Flow Cytometry Ploidy Analyses of Formalin-fixed Paraffin-embedded Hydatidiform Molar Tissues

Microsatellite DNA Genotyping and Flow Cytometry Ploidy Analyses of Formalin-fixed Paraffin-embedded Hydatidiform Molar Tissues

Published on: October 20, 2019

MDM2 309 polymorphism is associated with missed abortion.

Yan Fang¹, Beihua Kong, Qifeng Yang

¹Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, 107 Wenhuaxi Road, Ji'nan 250012, Shandong, People's Republic of China.

Human Reproduction (Oxford, England)

|February 28, 2009

Summary

The murine double minute 2 (MDM2) promoter single nucleotide polymorphism (SNP309) G/G genotype is linked to an increased risk of missed abortion. This genetic factor may contribute to early pregnancy loss.

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Published on: August 20, 2018

Area of Science:

Genetics
Reproductive Medicine
Molecular Biology

Background:

Missed abortion is a pregnancy complication.
The murine double minute 2 (MDM2) gene plays a role in cell cycle regulation and apoptosis.
Single nucleotide polymorphisms (SNPs) in gene promoters can influence gene expression and disease risk.

Purpose of the Study:

To investigate the association between the MDM2 SNP309 polymorphism and the risk of first-trimester missed abortion.

Main Methods:

Genotyping of the MDM2 SNP309 polymorphism was performed using polymerase chain reaction-restriction fragment length polymorphism.
Blood and villous samples were collected from 95 women diagnosed with first-trimester missed abortion.

Main Results:

The MDM2 SNP309 G/G genotype was significantly associated with an increased risk of missed abortion in both blood (P = 0.010; OR: 2.164) and villous samples (P = 0.043; OR: 2.767).
Individuals with the G/G genotype had approximately 2-3 times higher odds of experiencing a missed abortion compared to those with T/T or T/G genotypes.

Conclusions:

The MDM2 SNP309 G/G genotype may serve as a genetic risk factor for missed abortion.
Further research is warranted to elucidate the underlying mechanisms linking this polymorphism to pregnancy loss.