Research Interests
Breast cancer is the most frequent cancer in women and represents the second leading cause
of cancer death among women. It is essential to better understand the mechanistic actions
by which breast cancer occurs in order to develop new treatments. Therefore, my research is
aimed at further elucidating the molecular pathways involved in the pathogenesis of breast cancer.
For example, aberrant activation of the Wnt/β-catenin signaling pathway contributes to the genesis
of breast cancer.
I am interested in the secreted frizzled-related proteins (SFRPs) because they are a family of
proteins that antagonize Wnt signaling and loss of SFRP expression is found in a multitude of cancers,
including breast cancer. Our lab is investigating whether low SFRP levels might lead to breast cancer
development in both humans and mice. I am currently utilizing a SFRP1 knockout mouse model to determine
whether SFRP loss renders the mammary gland more susceptible to breast cancer development.
Additionally, we are manipulating the expression levels of SFRP in both immortal (non-malignant)
mammary epithelial cell lines as well as breast cancer cell lines to determine the mechanisms by
which SFRPs influence the various pathways that lead to tumorigenesis since both Wnt dependent and
independent pathways are involved. For example, the SFRPs exhibit an apoptotic function in several
different tissues and the anti-apoptotic effect of lost SFRP expression has been implicated in
carcinogenesis. Therefore, my research also focuses on has SFRPs regulate the pathways that lead to
cell death how they might be targeted for breast cancer treatment purposes.
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Pre-doctoral Publications
Iannacone, E.A., Yan, A.W., Gauger K.J., Dowling, A.L., Zoeller, R.T. 2002. Thyroid hormone
exerts site specific effects on SRC-1 and N-CoR expression selectively in the neonatal rat brain.
Molecular and Cellular Endocrinology, 15: 186: 49-59.
Zoeller, R.T., Dowling, A.L.S., Herzig, C.T.A., Iannacone, E.A., Gauger, K.J., Bansal, R. 2002.
Thyroid hormone, brain development, and the environment. Environmental Health Perspectives,
110 (Suppl 3): 355-361.
Gauger, K.J., Kato, Y., Haraguchi, K., Lehmler, H.J., Robertson, L.W., Bansal, R., Zoeller, R.T. 2004.
Polychlorinated biphenyls (PCBs) exert thyroid hormone-like effects in the fetal rat brain but do not
bind to thyroid hormone receptors. Environmental Health Perspectives, 112 (Suppl 5): 516-523.
You, S.H., Gauger, K.J., Bansal, R., Zoeller, R.T. 2006. 4-Hydroxy-PCB106 acts a direct thyroid hormone
receptor agonist in rat GH3 cells. Molecular and Cellular Endocrinology, (In Press).
Gauger, K.J., Sharlin, D., Zoeller, R.T. 2006. Polychlorinated biphenyls as disruptors of thyroid
hormone action. In: PCBs:Recent Advances. L.W. Robertson and L.G. Hansen, Eds. Univ Illinois Press,
Champaign IL, (In Press).
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