Abstract

BOSTON—Studies in mice are bringing researchers a step closer to understanding the molecular miscues that can give rise to neural tube defects in infants of women with diabetes. A new character in this medical scenario is the oncogene p53. Notorious for its role in cancer, p53 takes the stage again, this time cast as a villain that helps undermine embryonic development, according to a new report in Genes and Development (2002;16:676-680). Elucidating the mechanisms that can go awry in embryos of women with diabetes could help investigators devise strategies to reduce the incidence of these defects. The goal is compelling because women with diabetes who become pregnant are two to five times more likely to deliver infants with congenital malformations, such as neural tube defects, said lead author of the new study Mary Loeken, PhD, an investigator at the Joslin Diabetes Center and assistant professor of medicine at Harvard Medical School. To reduce this risk, women with diabetes are advised to strive to achieve optimal glycemic control before conception and throughout pregnancy. But while tight regulation of glucose levels improves chances of delivering a healthy infant, the threat of congenital malformations remains.

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