Jennifer Sims-Mourtada, Ph.D.
Senior Clinical Scientist
Jennifer Sims-Mourtada, Ph.D., is a senior research scientist and the Director of Translational Breast Cancer Research in the Center for Translational Cancer Research. Dr. Sims-Mourtada earned her doctorate in Immunology in 2004 from University of Texas Graduate School of Biomedical Sciences in Houston and completed her post-doctoral training in the Department of Experimental Radiation Oncology at the University of Texas M.D. Anderson Cancer Center in Houston. Prior to joining ChristianaCare in 2011, she was the director of molecular research and development for RadioMedix Inc., a biotechnology company in Houston TX focused on the development of targeted radiotherapeutics for the detection and treatment of cancers. In addition to her research work, she is an Affiliated Associate Professor in the Departments of Medical Laboratory Sciences and Biological Sciences at the University of Delaware. She also sits on the Board of Directors for RadioMedix , Inc. and the Radioisotope Therapy of America (RITA) Foundation. She has published numerous papers on her research and has served as the principle investigator or co- investigator on numerous grants from the Department of Defense and National Institutes of Health. She serves as a reviewer for numerous journals and serves as the associate editor for Cancer Studies and Molecular Medicine. She has been a regular member of the Radiation Therapeutics and Biology (ONC-R) study section at the National Institutes of Health since 2008 and has also served as an ad-hoc reviewer for numerous other NIH panels. Additionally, she serves as a reviewer for the Congressionally Directed Medical Research Breast Cancer Program. Dr. Sims-Mourtada is a member of the American Association of Cancer Researchers, and the Society of Nuclear Medicine and Molecular Imaging.
Radiation and chemotherapy resistance
Cancer stem cells
Women with triple negative breast cancer (TNBC) have worse outcomes than women with hormone receptor positive breast cancer. TNBC disproportionately affects younger women who are pre-menopausal, especially African American women. Treatment for TNBC is an unmet clinical need. Survival rates for women diagnosed with TNBC, who relapse within 5 years of treatment, are significantly lower than women with hormone receptor (ER/PR+) breast cancer. Understanding the mechanisms that drive growth of TNBC may lead to better treatment, and predictive biomarkers that may identify women at risk for early relapse.
Inflammation as a driver of triple negative breast cancer
Dr. Sims-Mourtada’s research seeks to provide insight as to what drives TNBC growth and resistance to current therapy. She proposes that the aggressive nature of TNBC is due to cells that are present in the microenvironment surrounding the tumor. Her team has found that TNBCs have high levels of inflammatory cells in and around the tumor. Inflammatory cells are present in TN breast lesions even before they become invasive, suggesting a role for these cells in tumor formation and progression. Data generated in the Sims-Mourtada lab indicate that inflammation is an early event in TNBC as opposed to other types of breast cancers. Her team is currently investigating the hypothesis that inflammatory cells found associated to pre-malignant breast lesions release factors that initiate a cascade of events that not only result in malignant transformation and growth of breast cancer, but may determine the type of breast cancer that develops. If that is the case, understanding how inflammation affects breast tissue can also aid prevention efforts and help to identify high risk populations. The lab is also investigating whether genetic variances in regions that increase chronic inflammation, or other chronic inflammatory conditions are associated to an increased risk of TNBC and if treatment with anti-inflammatory drugs, many of which are already FDA approved for the treatment of certain autoimmune conditions, may improve treatment outcomes for women with TNBC.
Chronic Inflammation as a regulator of stem cell plasticity
Dr. Sims-Mourtada’s team is also investigating how mechanisms which are normally involved in wound healing may promote resistance in breast cancer. Her lab has shown that a growth factor associated with inflammation and wound healing, known as hedgehog, can promote growth of a population of highly resistant cells after treatment with radiation and chemotherapy. These cells, known as breast cancer stem cells, resemble normal mammary stem cells, and have an unlimited life-span. They are not killed by standard treatments and can remain either locally within the breast tissue, or travel to distant sites and eventually lead to local or systemic recurrence. Her team is currently investigating how hedgehog interacts with other pathways involved in chronic inflammation and wound healing to promote de-differentiation of tumor cells into stem-like cancer cells with increased resistance and metastatic potential.
Complete List of Published Work in MyBibliography http://www.ncbi.nlm.nih.gov/sites/myncbi/1v9JyrWJc8T5h/bibliography/41240546/public/?sort=date&direction=ascending
Mourtada, F and Sims-Mourtada, J. Boosting Response: The Impact of Immune Checkpoint Inhibitors on Radiation Treatment Schedules Cancer Studies and Molecular Medicine, 2015. In press.
Sims-Mourtada, J., Opdenaker, L.M., Davis, J. and Wu, C. Long Term, Low Dose Genistein decreases Stem Cell Populations and Sensitizes Inflammatory Breast Cancer Cell Lines to Radiation, Cancer Studies and Molecular Medicine, 2015, In press
Arnold, K.M., Opdenaker, L., Flynn, D.C. and Sims-Mourtada, J. Wound healing and breast cancer stem cells: inflammation as a driver of resistance in breast cancer, Cancer Metastasis, 2015, 2015 Jan 29;8:1-13. doi: 10.4137/CGM.S11286.
Opdenaker, L, Arnold, K.M., Flynn, D.C. and Sims-Mourtada, J. Immunohistochemical Analysis of Aldehyde Dehydrogenase isoforms in breast cancer, Breast Cancer Targets and Therapy, 2014 Dec 12;6:205-9. doi: 10.2147/BCTT.S73674. eCollection 2014. PMID: 25540596 [PubMed]
Sims-Mourtada, J. , Opdenaker, L., Davis, J., Arnold, K., Flynn, D. Taxane induced hedgehog signaling is linked to expansion of breast cancer stem-like populations after chemotherapy. Molecular Carcinogenesis, 2014 Sep 27. doi: 10.1002/mc.22225. [Epub ahead of print]. PMID: 25263583.
Smith, D.L., Kong, F., Yang, D, Larson, R., Sims-Mourtada, J., Woodward, W. Hedgehog targeting peptides for imaging and therapy of breast cancer., Biomed Research International, Volume 2014 (2014), Article ID 525680. (corresponding author)
Sims-Mourtada, J, Niamat RA, Samuel S, Eskridge C, Kmiec EB. Enrichment of breast cancer stem-like cells by growth on electrospun polycaprolactone-chitosan nanofiber scaffolds., International Journal of Nanotechnology, February 2014 Volume 2014:9(1) Pages 995 – 1003.
Smith, D.L., Breeman, WAP, Sims-Mourtada, J. The untapped potential of 68-Gallium-PET: the next wave of 68-gallium agents. Journal of Applied Radiation and Isotopes, 2012, 2012 Oct 29 (12)00537-4.
Sims-Mourtada,J. Yang,D., Tworowka, I, Larson, R, Smith, D, Tsao, N, Opdenaker, L., Mourtada, F. Woodward, W. Detection of canonical hedgehog signaling in breast cancer by 131-Iodine-labeled derivatives of the sonic hedgehog protein. Journal of Biomedicine and Biotechnology, 2012, Article ID 639562.
Delpassand,E., Samarghandi,,A., Sims Mourtada,J, Zamanian,S ., Espanan,G., Sharif,R., MacKenzie,S., Kosari,K., Barakat, B., Naqvi,S.,Seng,JE., Lowell Anthony,L. Long-term survival and toxicity profile of patients with progressive neuroendocrine tumors following Peptide Receptor Radionuclide Therapy with high activity 111In pentetreotide Theranostics,2012, 2(5):472-80. doi: 10.7150/thno.3739. Epub 2012 May 11.