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Amy M. Fulton, PhD

Academic Title:

Professor

Primary Appointment:

Pathology

Additional Title:

Professor Program Leader, UMGCCC

Location:

Bressler Research Building, 10-033

Phone (Primary):

(410) 706-6479

Phone (Secondary):

(410) 706-5938

Education and Training

  • University of Kansas, BA, Microbiology, 1972
  • University of Wisconsin, MS, Medical Microbiology, 1975
  • University of Wisconsin, Ph.D., Medical Microbiology, 1977
  • University of British Columbia, Postdoctoral Study, Cancer Immunobiology, 1980

Biosketch

Dr. Fulton's laboratory is identifying the mechanisms by which breast cancers grow and metastasize. She is working to understand the role of inflammation in promoting tumor progression with the goal of identifying novel strategies to target these mechanisms. Dr. Fulton collaborates with both clinical and basic research investigators to develo innovative approaches to diagnose, treat and prevent breast cancer. Her research has shown that overexpression of Cyclooxygenase-2 is an indicator and mediator of aggressive disease and preclinical studies indicate that cyclooxygenase inhibitors limit tumor growth and spread. Her laboratory was the first to show that the cyclooxygenase-2 product, prostaglandin E2, activates the EP4 G protein-coupled receptor to drive metastasis. Prostaglandin E2-mediated immune suppression is also mediated through activation of EP4 on immune effector cells. In preclinical models, small m.w. antagonists of EP4 inhibit tumor dissemination and protect immune cells from dysregulation. She has recently demonstrated 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 with several clinical collaborators to examine efficacy of an EP4 antagonist in advanced malignancy. Her lab has also discovered that chemokine receptor CXCR3 isoforms differentially promote metastasis and cancer stem cells. They have identified novel allosteric CXCR3 modulators with high efficacy in preclinical models. Working with Dr. Namita Kundu, Dr. Fulton's lab has identified a novel and potent inhibitor of metastasis isolated from the Taro plant, Colocasia esculenta. Current studies in collaboration with Dr. David Weber are designed to identify the active moiety and to discern the mechanism of action.

Research/Clinical Keywords

Tumor biology; biology of metastasis; inflammatory mediators; cyclooxygenase; chemokines; prostaglandins

Highlighted Publications

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

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

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. PMID:21934601. 

 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 July 15, 2011. PMID:21761157.  

 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. 149:403-15, 2015.

 

 

Awards and Affiliations

  • BA with Distinction, U. of Kansas, 1972
  • Departmental Honors, U. of Kansas, 1972
  • Phi Beta Kappa Honors Society, 1972
  • NIH Postdoctoral Fellow, 1978-79
  • Associate Editor, Cancer Research, 2007-2012
  • Editorial Board, AntiCancer Drugs
  • Editorial Board, American J. of Translational Research
  • Editorial Board, Bioactive Lipids in Cancer
  • Advisory Board member, Bentham Science ebook; Bioactive Lipids in Cancer
  • Board of Directors, Women in Cancer Research
  • Scientific Advisory Board, ATCC
  • AACR Breast Cancer Research Scientific Review Committee