Placental ischemia and breast cancer risk after preeclampsia: Tying the knot

Anne Gingery, Emma L. Bahe, Jeff Gilbert

Research output: Contribution to journalReview articlepeer-review

10 Scopus citations


Although hypertensive disorders of pregnancy, such as preeclampsia, continue to be a significant source of maternal and fetal morbidity and mortality, there is emerging evidence that effects of the preeclamptic syndrome persist into later life. In contrast to recent studies that have reported that formerly preeclamptic women are at increased risk for cardiovascular disease, it appears that preeclampsia may be associated with a decreased risk of breast cancer. Recent investigations have provided exciting new insights into potential mechanisms underlying the pathogenesis of preeclampsia and some of these findings may bear relevance to the anticancer effects reported in the epidemiological literature. Placental ischemia is regarded to be a primary factor in preeclampsia and the ischemic placenta produces a variety of factors that generate profound effects on endothelial cell function and the cardiovascular system during pregnancy. Moreover, several of these factors are reportedly elevated many years after preeclamptic pregnancies. This group of molecules includes factors such as soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin/CD105 (sEng) and various cytokines. Many of these factors have been strongly associated with cancer incidence and, hence, could contribute to the modification of cancer risk observed in these women. Therefore, identifying potential connections between placental dysfunction and future cancer risk is an important endeavor towards realizing novel therapeutic regimens for cancer patients.

Original languageEnglish (US)
Pages (from-to)671-681
Number of pages11
JournalExpert Review of Anticancer Therapy
Issue number5
StatePublished - 2009

Bibliographical note

Funding Information:
This work has been supported in part by grants from the National Institutes of Health GM074628, the Whiteside Institute for Clinical Research and the Graduate School of the University of Minnesota, USA. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.


  • Cytokine
  • Pregnancy
  • sEng
  • sFlt-1


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