To serve patients, health care providers, research scientists, scholars, and society by providing excellence and innovation in diagnostic services and educational resources in a respectful, professional and culturally diverse atmosphere.
Our Vision
To become a preeminent leader in academic anatomic and clinical pathology while translating basic science discovery to improved clinical care.
Stephen P. Ethier, PhD.
Professor
Department of Pathology & Laboratory Medicine
Professor
Department of Medicine
Interim Director, Center for Genomic Medicine
Program Leader, Cancer Genes and Molecular Regulation Program
Office: Bioengineering Building 4th floor
Phone: (843) 876-2537
EDUCATION:
Advanced Education: 1982, PhD, University of Tennessee, Oak Ridge, TN
Postdoctoral Training: 1982 - 1984: Fellowship, Chemical Carcinogenesis The Michigan Cancer Foundation, Lathrup Village, MI
Primary Specialty: Breast Cancer
RESEARCH INTERESTS:
Cancer Genetics/Genomics and Molecular Regulation
The goals of the Ethier lab are to understand the genetic basis for the development and progression of human breast cancer and to understand how
specific genetic alterations contribute to specific aspects of the transformed phenotype. For many years, the Ethier lab has worked to understand the
nature of the altered signaling pathways activated by the HER-2 oncoprotein and by the epidermal growth factor receptor when it is over expressed
in breast cancer cells. More recently, the lab has developed a focus on discovering novel oncogenes in human breast cancer by investigating specific
genomic regions that are commonly increased in copy number in breast cancer. Current studies are centered on the 8p11 region of the genome, which is
amplified in approximately 25% of all breast cancers. To date, three novel breast cancer oncogenes have been mapped to this region. The Ethier lab
is using state-of-the-science bioinformatics methodologies to better understand the mechanistic basis for the transforming properties of newly
discovered breast cancer oncogenes. More recently, the Ethier lab has expanded its focus to genome wide studies of breast and other cancers.
Genome wide sequencing and screening platforms are being used to distinguish novel oncogenes from passenger genes, and to identify novel oncogenomic
targets. These screening strategies are also being used to identify synthetic lethal interactions between genef1clgenomic factors •m cancer cells to
lay the ground work for therapeutic strategies using multiple targeted drugs.
SELECTED PUBLICATIONS:
Yang, Z.Q., Streicher, K.L., Ray, M.E., Abrams, J. and Ethier, S.P. “Multiple
interacting oncogenes on the 8p11-p12 amplicon in human breast cancer.” Cancer
Research, 66(24): 11632-43, 2006.
Streicher, K.L., Willmarth, N.E., Garcia, J., Boerner, J.L., Dewey, T.G., Ethier
S.P. “Activation of a nuclear factor kappaB/interleukin-1 positive feedback loop
by amphiregulin in human breast cancer cells.” Mol Cancer Res., 5(8):847-61,
2007.
Willmarth, N.E., Baillo, A., Dziubinski, M.L., Wilson, K., Riese II, D.J.,
Ethier, S.P. “Altered EGFR Localization and Degradation in Human Breast Cancer
Cells with an Amphiregulin/EGFR Autocrine Loop.” Cell Signal., 21(2):212-9,
2008.
Yang, Z.Q., Liu, G., Bollig-Fischer, A., Haddad, R., Tarca, A.L., Ethier, S.P.
“Methylation-associated silencing of SFRP1 with an 8p11-12 amplification
inhibits canonical and non-canonical WNT pathways in breast cancers.”
International Journal of Cancer, 125(7):1613-1621, 2009.
Bollig-Fischer, A., Dziubinski, M., Boyer, A, Haddad, R., Giroux, C., and
Ethier, S.P. HER-2 signaling in the progressive acquisition of growth factor
independence and regulation of biological networks associated with cell
transformation. Cancer Research, 70: 7862-7873, 2010.
Baillo, A., Giroux, C., and Ethier, S.P. Knock-down of Amphiregulin Inhibits
Cellular invasion in Inflammatory Breast Cancer. J. Cell. Physiol.
226:2691-2701, 2011. PubMed PMID: 21302279
Bollig-Fischer, A., Ethier, S.P. Oncogene activation induces metabolic
transformation resulting in insulin-independence in human breast cancer cells.
PLoS One 6(3) e17959, 2011. PubMed PMID: 21437235