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Posted at: Sep 7, 2017, 6:40 PM; last updated: Sep 7, 2017, 6:40 PM (IST)

Six genes linked to pre-term birth identified

Six genes linked to pre-term birth identified
Photo source: Thinkstock

New York

US researchers have found six gene variants that have the potential to influence whether a woman is likely to have a preterm baby, a finding that could lead to new ways to prevent preterm birth and its consequences -- the leading cause of death among children under age 5 worldwide.

The findings showed that mutations in genes called EBF1, EEFSEC, AGTR2, ADCY5, RAP2C and WNT4 could often point to gestational time. Variations of three genes especially - EBF1, EEFSEC and AGTR2 - were associated with preterm birth.

"This is a very exciting discovery that can be expected to lead to the development of new treatments to prevent pregnant women from going into labour too soon and to give more babies a healthy start in life," said Stacey D. Stewart, President at the March of Dimes Prematurity Research Centre in New York.

Preterm birth is defined as any birth occurring before 37 weeks of pregnancy. In addition to the risk of death, babies who survive an early birth often face serious, lifelong health problems, including chronic lung disease, vision and hearing impairment, cerebral palsy, and neurodevelopmental disabilities. 

For the study, published in the New England Journal of Medicine, the team conducted a massive DNA analysis of more than 50,000 pregnant women.

One of the gene areas identified suggests that cells within the lining of the uterus play a larger-than-expected role in the length of pregnancy, which in turn provides a new target for medications to help prevent preterm birth.

Another raises important questions about how a lack of selenium -- a common dietary mineral found in some nuts, certain green vegetables, liver and other meats -- might affect preterm birth risk.

The study could play a key role in reducing newborn deaths and giving every child the chance to grow up smart and strong, the researchers said. — IANS

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