Helen J. Hathaway, PhD


Research Interests

The focus of our laboratory is to define how cell interactions contribute to tissue morphogenesis in both normal mammary gland development and in neoplastic progression of the breast. It is becoming increasingly apparent that epigenetic factors within the tumor microenvironment contribute to carcinogenesis. This realization has renewed interest in the concept of cancer as a disease of abnormal tissue morphogenesis. This is particularly apparent in the mammary gland, an organ that can undergo multiple cycles of morphologic alterations during puberty, estrous, pregnancy, lactation, and involution. Such extensive tissue remodeling in the adult animal provides numerous opportunities to accumulate errors that can lead to malignancy. Therefore, studies that elucidate the molecular basis for mammary tissue remodeling will impact our knowledge of how these pathways are normally regulated, and what stages are candidates for dysregulation during tumorigenesis.

We use both genetically engineered mouse models as well as three-dimensional culture models that recapitulate the microenvironment of the mammary gland to address several areas of investigation. These include the elucidation of factors that control mammary cell polarity, survival, and apoptosis, extracellular proteinase function in tissue remodeling, and the molecular basis of cell-extracellular matrix interactions in normal morphogenesis and neoplastic progression.

Education, Honors, and Professional Experience

1979, B.S.Ag., Plant Science University of Delaware, Newark, DE.
1986, Ph.D., Biology, Rutgers University, Piscataway, NJ.
1986, Postdoctoral Fellow, University of Texas, M.D. Anderson Cancer Center, Houston, TX.
1991, Research Associate, University of Texas, M.D. Anderson Cancer Center, Houston, TX.
1996, Research Assistant Professor, Emory University School of Medicine, Atlanta, GA.
1983, Steinetz Award, Rutgers University.
1985, Busch Predoctoral Fellowship, Rutgers University.
1986, NIH Training Grant Postdoctoral Fellowship, M.D. Anderson Cancer Center.
1991, M.D. Anderson Basic Science Paper Competition.

Current Lab Personnel

Sarah Vertrees, Research student

Selected Publications

De La Cruz, L., Steffgen, K., McGee, C., Martin, A., and Hathaway, H. J. (2004) Apoptosis and involution in the mammary gland are altered in mice lacking a novel receptor, b1,4-galactosyltransferase I. Dev Biol. 2004 Aug 15;272(2):286-309

Hathaway, H. J. (2003). Cell surface galactosyltransferase function in mammary gland morphogenesis: insights from transgenic and knockout models. J. Mamm. Gland Biol. & Neopl. 8:421-434 .

Hathaway, H. J.*, Evans, S. C.*, Dubois, D., Foote, C., Elder, B., and B. D. Shur. (2003) Mutational analysis of the cytoplasmic domain of b1,4-galactosyltransferase I: influence of phosphorylation on cell surface expression. J. Cell Sci. 116:4319-4330.

Steffgen, K., Dufraux, K., and Hathaway, H. J. (2002). Altered branching morphogenesis in mammary glands of mice lacking the long isoform of b1,4-galactosyltransferase I. Devel. Biol. 244:114-133.

Hathaway, H. J. and B. D. Shur (1996). Mammary gland morphogenesis is inhibited in transgenic mice overexpressing cell surface b1,4-galactosyltransferase. Development, 122:2859-2872.

Youakim, A.*, H. J. Hathaway*, D. J. Miller, X. Gong, and B. D. Shur (1994). Overexpressing sperm surface b1,4-galactosyltransferase in transgenic mice affects multiple aspects of sperm-egg interactions. J. Cell Biol. 126:1573-1584.

Hathaway, H. J. and B. D. Shur (1992). Cell surface b1,4 galactosyltransferase mediates neural crest cell migration and neurulation in vivo. J. Cell Biol. 117:369-382.