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Amy M. Fulton

Amy M. Fulton Ph.D.

Academic Title: Professor
Primary Appointment: Pathology
Location: Bressler Research Building, 10-033
Phone: (410) 706-6479
Phone: (410) 706-5938

Personal History:

I earned a B.A. (with Distinction; Honors in Microbiology) from the U. of Kansas and the M.S. and Ph.D. in Medical Microbiology from the U. of Wisconsin, Madison. I completed an NIH Postdoctoral Fellowship in the laboratory of Dr. Julia Levy at the U. of British Columbia where I studied aspects of immune dysregulation associated with malignancy. I joined the Department of Immunology at the Michigan Cancer Foundation (now Karmanos Cancer Institute) as a Scientist and Assistant Professor in the Department of Pathology, Wayne State University School of Medicine. I was Chief of the Laboratory of Immunology and Associate Member at MCF until I joined the U. of Maryland as an Associate Professor of Pathology. I am currently Professor of Pathology with Tenure, a member of the Program in Oncology of the Marlene and Stewart Greenebaum Cancer Cancer, Leader of the Hormone Responsive Cancers Program, UMGCC and an Investigator of the Baltimore VA Medical Center. As a member of the Hormone Responsive Cancers Program of the Greenebaum Cancer Center, I collaborate with both clinical and basic research investigators to develop innovative approaches to diagnose, treat and prevent breast and prostate cancer. My research centers on dissecting the role of inflammatory pathways in the promotion of cancer progression.

Research Interests:

Breast cancer; mechanisms of metastasis; inflammation; immune therapy

My laboratory is interested in identifying the mechanisms by which breast cancers grow and metastasize and in developing therapeutic strategies against breast cancer. Our goal is to understand the role of inflammation in promoting tumor progression. We have shown that overexpression of cyclooxygenase-2 is an indicator of aggressive disease and preclinical studies indicate that cyclooxygenase inhibitors limit tumor growth and spread. We have shown that specific targeting of the COX-2 pathway at the level of prostaglandin E receptor EP4 avoids the potential toxicities of COX-2 inhibition while preserving anti-metastatic activity. Recently we have shown that breast cancer stem-like cells with heightened tumorigenic potential and a treatment resistant phenotype have elevated levels of EP4 and are more sensitive to inhibition by EP4 antagonists than the non-stem cell population. These findings have led to the design of a clinical trial to examine efficacy of an EP4 antagonist in advanced malignancy. We have also discovered that the chemokine receptor CXCR3 promotes metastasis. CXCR3 ligands can promote or inhibit tumor growth and metastasis depending on levels of ligand expression. Current studies examine mechanisms by which cyclooxygenase inhibitors enhance anti-tumor immunity. We are also investigating how cytokines and chemokines and their specific receptors modify tumor behavior. We have identified therapeutic activities for several cytokines and are developing strategies to inhibit chemokine receptors that promote tumor metastasis. Working with Dr. Kundu, we have identified a novel and potent inhibitor of metastasis isolated from the Taro plant. Current studies are designed to identify the active moiety and to discern the mechanism of action.


Walser, T.C. and Fulton, A.M. Chemokine Receptors in Cancer in: The Chemokine Receptors (JK Harrison and N Lukacs, eds.), Humana Press, pp. 335-349, 2007.

Ma, X., Kundu, N., Rifat, S., Walser, T and Fulton, A.M. Prostaglandin E receptor EP4 antagonism inhibits breast cancer metastasis. Cancer Research, 66:2923-2927, 2006 (selected for cover and highlights).

Walser, T.C., Rifat, S., Ma, X., Kundu, N., Ward, C., Goloubeva, O., Johnson, M.G., Medina, J.C., Collins, T.L. and Fulton, A.M. Antagonism of CXCR3 inhibits lung metastasis in a murine model of metastatic breast cancer. Cancer Research 66:7701-7707, 2006 (selected for highlights section).

Fulton, A.M.,Ma, X., Kundu, N. Targeting Prostaglandin E EP Receptors to Inhibit Metastasis. Invited Review. Cancer Research 66:9794-9797, 2006.

Walser, T.C., Ma, X., Kundu, N., Dorsey, R., Goloubeva, O. and Fulton, A.M. Immune-mediated modulation of breast cancer growth and metastasis by the chemokine Mig (CXCL9) in a murine model. J. Immunotherapy 30:490-498, 2007.

Kundu, N., Ma, X., Walser, T., Goloubeva, O., Ostrand-Rosenberg, S., and Fulton, A.M. Antagonism of the prostaglandin E receptor EP4 inhibits metastasis and enhances NK function.
Breast Cancer Research and Treatment 117:235-242, 2009.

Ma, X., Norsworthy, K., Kundu, N., Rodgers, W.H., Gimotty, P., Goloubeva, O., Lipsky, M., Li, Y., Holt, D., and Fulton, A.M. CXCR3 expression is associated with poor survival in breast cancer and promotes metastasis in a murine model. Mol. Cancer Ther. 8:490-8, 2009.

Ma, X., Kundu, N., Ioffe, O., Goloubeva, O., Konger, R., Baquet, C., Gimotty, P. and Fulton, A.M. Prostaglandin E receptor EP1 suppresses metastasis, is associated with better survival and may contribute to breast cancer disparities. Mol. Cancer Res. 8:1310-1318, 2010.PMID:20858737.

Kundu, N., Campbell, P., Hampton, B., Lin, C.Y., Ma, X., Ambulos, N., Zhao, X.F., Goloubeva, O., Holt, D. and Fulton, A.M. Antimetastatic activity isolated from Colocasia esculenta (Taro). AntiCancer Drugs, 23:200-11, 2011.

Holt, D., Ma, X., Kundu, N. and Fulton, A.M. Prostaglandin E2 (PGE2) suppresses natural killer cell function through the PGE2 receptor EP4. Cancer Immunol. Immunother. 60:1577-86, 2011.

Ma, X., Kundu, N., Collin P.D., Goloubeva O., and Fulton, A.M. Frondoside A inhibits breast cancer metastasis and antagonizes prostaglandin E receptors EP4 and EP2. Breast Cancer Res. Treatment 132:1001-8, 2012.

Holt, DH, Ma, X., Kundu, N., Collin, PD and Fulton, A.M. Modulation of host natural killer cell functions in breast cancer via prostaglandin E2 receptors EP2 and EP4. J. Immunotherapy 35:179-188, 2012.

Ma, X., Holt D., Kundu, N., Reader, J., Goloubeva O., Nonomura K., Take Y. and Fulton, A.M. Prostaglandin E receptor EP4 antagonist RQ-00015986 inhibits metastasis and protects Natural Killer cells from PGE2-mediated immune suppression. OncoImmunology 2:e22647, 2013.

Kundu S, Ma X, Kochel T, Goloubeva O, Staats P, Thompson K, Martin S, Reader J, Take Y, Collin P and Fulton A. Prostaglandin E receptor EP4 is a therapeutic target in breast cancer cells with stem-like properties. Breast Cancer Res. Treatment 143:19-31, 2014.

Li Y, Reader JC, Ma X, Kundu N, Kochel T, Fulton A. Divergent roles of CXCR3 isoforms in promoting cancer stem-like cell survival and metastasis. Breast Cancer Res. Treatment 149(2):403-15, 2015.