The long-term goal of our research program is to facilitate the development of novel therapies for cancer patients through a better understanding of the role of the tumor microenvironment in lymphoma.
Despite major therapeutic advances in the treatment of cancer, most malignancies remain incurable. There is compelling evidence to suggest that the crosstalk between malignant cells and stromal cells in the tumor microenvironment favors disease progression by promoting malignant cell functions as well as drug resistance. Therefore, disrupting this interaction between the tumor cells and their microenvironment is an attractive strategy for cancer treatment. As the paradigm in the treatment of cancer shifts toward combining therapies that target both malignant cells and the microenvironment, a better understanding of the molecular mechanisms that regulate the crosstalk between malignant cells and the microenvironment are clearly needed. Cytokines within the tumor microenvironment can profoundly affect tumor cells and targeting cytokines has been shown to have therapeutic efficacy in several neoplasms. Therefore, identification of cytokines that are dysregulated in cancer and understanding the mechanisms of their regulation may serve as a therapeutic avenue for targeted cancer therapy.
Our group is studying the following aspects of the tumor microenvironment (TME) using the bone marrow microenvironment as a model for the B cell lymphoma Waldenström macroglobulinemia (WM):
1. Identification and characterization of novel GLI target genes in the tumor microenvironment.
2. Characterizing novel epigenetic regulation of WM and the TME.
3. Identification and characterization of the role of GLI proteins in Waldenström macroglobulinemia and other B cell malignancies.
4. Identification and characterization of novel signaling pathways that regulate GLI proteins.
5. Characterization of the role of GLI in inflammation.
6. Characterization of the role of GLI in B cell biology and immunoglobulin secretion.
If you are interested in any aspect of our research program, please contact us to inquire about joining our group!
Ph.D., Biology, University of North Carolina at Chapel Hill
M.S., Florida Intl University
B.S., Alexandria University
BCHM 999: Doctoral Research
BMS 705: Immunology
BMS 715: Immunology Laboratory\Honors
BMS 730: Ethical Issues in Biomed Sci
MCBS 999: Doctoral Thesis
Targeting IL-6 receptor reduces IgM levels and tumor growth in Waldenström macroglobulinemia (2019). Oncotarget, 10(36). doi:10.18632/oncotarget.26946
Han, W., Cummings, H., Duvuuru, M. K., Fleck, S., Vahabzadeh, S., & Elsawa, S. F. (2019). In Vitro Osteogenic, Angiogenic, and Inflammatory Effects of Copper in β-Tricalcium Phosphate. MRS Advances, 4(21), 1253-1259. doi:10.1557/adv.2018.686
Han, W., Ibarra, G., Gupta, M., Yin, Y., & Elsawa, S. F. (2018). Elevated GLI3 expression in germinal center diffuse large B cell lymphoma. Leukemia & Lymphoma, 59(11), 2743-2745. doi:10.1080/10428194.2018.1439169
Yacout, S., Elsawa, S., & Gaillard, E. (2018). Calf melanin immunomodulates RPE cell attachment to extracellular matrix protein.. Graefes Archive for Clinical and Experimental Ophthalmology, 256(10), 1883-1893.
Jackson, D. A., Misurelli, J. A., & Elsawa, S. F. (2018). GLI Family Zinc Finger 2. In Encyclopedia of Signaling Molecules (pp. 2077-2088). Springer International Publishing. doi:10.1007/978-3-319-67199-4_101917
Lai, J. -P., Oseini, A. M., Moser, C. D., Yu, C., Elsawa, S. F., Hu, C., . . . Roberts, L. R. (2010). The oncogenic effect of sulfatase 2 in human hepatocellular carcinoma is mediated in part by glypican 3-dependent Wnt activation. Hepatology, 52(5), 1680-1689. doi:10.1002/hep.23848
Wilcox, R. A., Wada, D. A., Ziesmer, S. C., Elsawa, S. F., Comfere, N. I., Dietz, A. B., . . . Ansell, S. M. (2009). Monocytes promote tumor cell survival in T-cell lymphoproliferative disorders and are impaired in their ability to differentiate into mature dendritic cells. Blood, 114(14), 2936-2944. doi:10.1182/blood-2009-05-220111
Elsawa, S. F. (2006). B-lymphocyte stimulator (BLyS) stimulates immunoglobulin production and malignant B-cell growth in Waldenstrom macroglobulinemia. Blood, 107(7), 2882-2888. doi:10.1182/blood-2005-09-3552
Zheng, X., Rumie Vittar, N. B., Gai, X., Fernandez-Barrena, M. G., Moser, C. D., Hu, C., . . . Roberts, L. R. (n.d.). The Transcription Factor GLI1 Mediates TGFβ1 Driven EMT in Hepatocellular Carcinoma via a SNAI1-Dependent Mechanism. PLoS ONE, 7(11), e49581. doi:10.1371/journal.pone.0049581