Michael E. Fant, MD, PhD

Dr. Fant joined USF in 2009 as Professor of Pediatrics with a joint appointment in the Department of Pathology and Cell Biology. He received his MD and PhD degrees from Vanderbilt University Medical School and completed a pediatric residency at Children’s Hospital in Boston, Massachusetts. This training was followed by a fellowship in newborn medicine at Harvard Medical School (Joint Program in Neonatology) and a post-doctoral research fellowship at the Massachusetts Institute of Technology, where he pursued his special interests in fetal growth restriction, placental growth regulation, and perinatal metabolism. Since completing his training, Dr. Fant has devoted his investigative career to studying the cellular mechanisms that regulate normal placental growth, as a prerequisite to understanding abnormal fetal growth, and has served on a variety of NIH and FDA advisory panels related to these areas. Throughout his career he has mentored a number of students and post-doctoral fellows and currently serves as Co-Director of the Neonatal-Perinatal Fellowship Program at USF.

Education & Training

Board Certifications

• American Board of Pediatrics
• Neonatal-Perinatal Medicine

Scholarly Activity

The Fant lab, located at the USF/All Children's Hospital Children's Research Institute in St. Petersburg, studies placental development using both human and mouse models. Specifically, trophoblast-specific genes and mesenchymal-trophoblast signaling interactions important in placental development are examined. His laboratory was the first to demonstrate that insulin-like growth factors (IGFs) are produced by the placenta that act locally to regulate placental development. His lab also demonstrated that placental mesenchymal cells exhibit proliferation rates and growth factor responsiveness that are developmentally regulated as part of their intrinsic developmental program. His laboratory is currently studying Plac1, a novel placenta-specific gene, and its role in supporting normal pregnancy. While Plac1 expression in normal tissue is restricted primarily to the placenta, it is expressed by a variety of human cancers, suggesting its relevance to cancer biology as well. Defining its role in placental development, pregnancy maintenance, and cancer biology constitutes the focus of the investigative effort.

Selected Publications

Fant ME. The in vitro growth rate of placental fibroblasts is developmentally regulated. J Clin Invest 1991; 88:1697-1702.

Fang J, Furesz T, Laurent R, Smith CH, Fant ME. Spatial polarization of IGF receptors on the syncytiotrophoblast cell membrane. Pediatric Research, 1997, 41: 258-265.

Fant M, Weisoly DL, Cocchia M, Huber R, Khan S, Lunt T, Schlessinger D. Plac1, a trophoblast-specific gene, is expressed throughout pregnancy in the human placenta and modulated by keratinocyte growth factor (KGF). Molecular Reproduction and Development, 2002, 4:430-436.

Md. Badiul Bhuiyan, Ferid Murad, Michael E. Fant The Placental Cholinergic System: Localization to the Cytotrophoblast and Modulation of Nitric Oxide. Cell Communication and Signaling, 2006. 4:4.

Fant ME, Barrera-Saldana H, Poindexter B, Bick R, and Dubinsky W. PLAC1 protein localizes to the apical region of the differentiated trophoblast and is associated with its apical, microvillous membrane surface, Mol. Reprod. Dev., 2007, 74:922-2

Dong XY, Peng JR, Ye YJ, Chen HS, Zhang LJ, Pang XW, Li Y, Zhang Y, Wang S, Fant ME, Yin YH, Chen WF 2008 Plac1 is a tumor-specific antigen capable of eliciting spontaneous antibody responses in human cancer patients, Int J Cancer, 2008, 122:2038-2043.

Liu F-F, Dong XY, Pang XW, Xing Q, Wang HC, Zhang HG, Li Y, Yin YH, Fant M, Ye YJ, Shen DH, Zhang Y, Wang S, Chen WF 2008 The specific immune response to tumor antigen CP1(PLAC1) and its correlation with improved survival in colon cancer patients. Gastroenterology, 2008, 134:473-477.