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Faculty Detail    
Campus Address WTI 602B Zip 3300
Phone  205-996-6226
Other websites

Undergraduate  University of Alabama    1975  Bachelor of Science with Honors 
Graduate  University of Alabama at Birmingham    1986  PhD Anatomy and Cell Biology 
Fellowship  Stanford University    1989  Biological Chemistry 

Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Pathology   Molecular & Cellular Pathology Professor
Center  Biomedical Engineering  Biomatrix Eng Regen Med (BERM) Ctr Professor
Center  Center for Biophysical Sciences/Engineering  Center for Biophysical Sciences/Engineering Professor
Center  Comp Arthritis, MSK, Bone & Autoimmunity Ctr  Comp Arthritis, MSK, Bone & Autoimmunity Ctr Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor

Graduate Biomedical Sciences Affiliations
Cancer Biology 
Cell, Molecular, & Developmental Biology 
Medical Scientist Training Program 
Molecular and Cellular Pathology Program 
Pathobiology and Molecular Medicine 

Biographical Sketch 
Dr. Sanderson received his PhD degree in Cell Biology in 1986 from the University of Alabama at Birmingham (Advisor, Richard Mayne) followed by a postdoctoral fellowship in the laboratory of Merton Bernfield at Stanford University. He joined the faculty in Pathology at the University of Arkansas for Medical Sciences in 1989 and rose to the rank of Professor in 2000. There, he held the Drs. Mae and Anderson Nettleship Chair in Oncologic Pathology and also served as Director of Basic Research for the Arkansas Cancer Research Center. He joined the UAB Department of Pathology in 2006, currently is co-leader of the Cancer Cell Biology Program of the UAB Comprehensive Cancer Center and is the UAB Endowed Professor in Cancer Pathobiology.

Society Memberships
Organization Name Position Held Org Link
American Association for Cancer Research 
American Society for Matrix Biology 
International Society for Extracellular Vesicles 
Metastasis Research Society 

Research/Clinical Interest
Molecular Regulation of the Tumor Microenvironment
The tumor microenvironment has emerged as a major regulator of tumor growth and progression. The long-term goal of the Sanderson lab is to determine how tumor-host cell interactions mediated by heparan sulfate and the enzyme heparanase regulate the tumor microenvironment and to use that knowledge to design new cancer therapies. We have shown that heparan sulfate proteoglycans and heparanase promote tumor growth and metastasis of multiple myeloma and breast tumors, two tumors that home to and grow within bone. Our hypothesis is that heparan sulfate drives tumor growth by concentrating heparin-binding growth factors (e.g., FGF-2, VEGF, HGF) within the tumor microenvironment and promoting interactions of these growth factors with their high affinity receptors. Thus, interfering with heparan sulfate function has the potential to attenuate numerous signaling pathways important in tumor growth and metastasis. Our current experimental focus is two-fold. First, we are examining how enzymes that modify heparan sulfate such as heparanase alter tumor behavior and promotes an aggressive tumor phenotype. We have recently discovered that this occurs, at least in part, via heparanase regulation of tumor secreted exosomes. These small vesicles contain proteins and nucleic acids that can be transferred horizontally to other cells within the tumor microenvironment and beyond and thus act as important mediators of intercellular communication. Second, we are developing novel heparanase inhibitors and testing them as potential anti-cancer drugs. One of these recently has entered clinical trials in myeloma patients. This work will lead to a better understanding of the tumor microenvironment and how it can be disrupted to block tumor growth. Our work is currently funded by grants from the National Institutes of Health.

Selected Publications 
Publication PUBMEDID
Stewart, M.D., Ramani, V.C. and Sanderson, R.D. 2015. Shed Syndecan-1 Translocates to the Nucleus of Cells Delivering Growth Factors and Inhibiting Histone Acetylation: A novel mechanism of tumor-host crosstalk. J. Biol. Chem. 290:941-949.  25404732  
Ramani, V.C. and Sanderson, R.D. 2014. Chemotherapy stimulates syndecan-1 shedding: A potentially negative effect of treatment that may promote tumor relapse. Matrix Biol. 35:215-222. Reviewed by Faculty of 1000.  24145151 
Thompson, C. A., Purushothaman, A., Ramani, V. C., Vlodavsky, I., and Sanderson, R. D. (2013) Heparanase regulates secretion, composition and function of tumor cell-derived exosomes. J. Biol. Chem. 288:10093-10099 Selected as a JBC Paper of the Week and JBC "Best of 2013."
Ramani, V. C., Purushothaman, A., Stewart, M. D., Thompson, C. A., Vlodavsky, I., Au, J. L., and Sanderson, R. D. (2013) The heparanase/syndecan-1 axis in cancer: mechanisms and therapies. FEBS J 280:2294-306
Purushothaman, A., Babitz, S. K., and Sanderson, R. D. 2012. Heparanase enhances the insulin receptor signaling pathway to activate extracellular signal-regulated kinase in multiple myeloma. J. Biol. Chem. 287:41288-41296.  23048032 
Ramani, V.C., Pruett, P.S., Thompson, C.A., Delucas, L.D. and Sanderson, R.D. 2012. Heparan sulfate chains of syndecan-1 regulate ectodomain shedding. J. Biol. Chem. 287:9952-61.   22298773 
Purushothaman, A., Hurst, D.R., Pisano, C., Mizumoto, S., Sugahara, K. and Sanderson, R.D. 2011. Heparanase-mediated loss of nuclear syndecan-1 enhances histone acetyltransferase (HAT) activity to promote expression of genes that drive an aggressive tumor phenotype. J. Biol. Chem. 286:30377-83.   21757697 
Ritchie, J.P., Ramani, V.C., Ren, Y., Naggi, A., Torri, G., Casu, B., Penco, S., Carminati, P., Tortoreto, M., Zunino, F., Vlodavsky, I. Sanderson, R.D. and Yang, Y. 2011. SST0001, a chemically modified heparin, inhibits myeloma growth and angiogenesis via disruption of the heparanase/syndecan-1 axis. Clin. Cancer Res. 17:1382-93.  21257720 
Ramani, V.C., Yang, Y., Ren, Y., Nan, L. and Sanderson, R.D.* 2011. Heparanase plays a dual role in driving hepatocyte growth factor (HGF) signaling by enhancing HGF expression and activity. J. Biol. Chem. 286:6490-99. * Selected as a J. Biol. Chem. JBC Paper of the Week and JBC "Best of 2011."  21131364 
Yang, Y., Ren, Y., Ramani, V.C., Nan, L., Suva, L.J., Sanderson, R.D. 2010. Heparanase enhances local and systemic osteolysis in multiple myeloma by upregulating the expression and secretion of RANKL. Cancer Res. 70:8329-8338.  20978204 
Barash, U., Cohen-Kaplan, V., Dowek, I., Sanderson, R.D., Ilan, N., Vlodavsky, I. 2010. Proteoglycans in health and disease: new concepts for heparanase function in tumor progression and metastasis. FEBS J. 277(19):3890-903.  20812981 
Kelly, T., Suva, L.J., Nicks, K.M., MacLeod, V., Sanderson, R.D. 2010. Tumor-derived syndecan-1 mediates distal cross-talk with bone that enhances osteoclastogenesis. J. Bone Miner. Res. 25:1294-304.   20200931 
Purushothaman, A., Uyama, T., Kobayashi, F., Yamada, S., Sugahara, K., Rapraeger, A.C., Sanderson, R.D., 2010. Heparanase enhanced shedding of syndecan-1 by myeloma cells promotes endothelial invasion and angiogenesis. Blood. 115:2449-57.  20097882 
Sanderson, R.D. and Epstein, J. 2009. Myeloma bone disease. J. Bone Miner. Res. 24(11):1783-8.   19839769 
Fux, L., Ilan, N., Sanderson, R.D., and Vlodavsky, I. 2009. Heparanase: busy at the cell surface. Trends Biochem. Sci. 34:511-19.  19733083 
Khotskaya, Y., Dai, Y., Ritchie, J., MacLeod, V., Yang, Y., Zinn, K., and Sanderson, R.D. 2009. Syndecan-1 is required for robust growth, vascularization and metastasis of myeloma tumors in vivo. J. Biol. Chem. 284:26085-95.  19596856 
Chen, L. and Sanderson, R.D. 2009. Heparanase Regulates Levels of Syndecan-1 in the Nucleus. PLoS ONE 4(3): e4947.  19305494 
Purushothaman, A., Chen, L., Yang, Y., and Sanderson, R. D. 2008. Heparanase stimulation of protease expression implicates it as a master regulator of the aggressive tumor phenotype in myeloma. J Biol Chem 283:32628-32636
Sanderson, R.D. and Yang, Y. 2008. Syndecan-1: A dynamic regulator of the myeloma tumor microenvironment. Clin. Exp. Metastasis 25:149-159.   18027090 
Yang, Y., MacLeod, V., Dai, Y., Khotskaya-Sample, Y., Shriver, Z., Venkataraman, G., Sasisekharan, R., Naggi, A., Torri, G., Casu, B., Vlodavsky, I., Suva, L.J., Epstein, J., Yaccoby, S., Shaughnessy, J.r., J.D., Barlogie, B., and Sanderson, R. 2007. The syndecan-1 heparan sulfate proteoglycan is a viable target for myeloma therapy. Blood 110:2041-48.  17536013 
Yang, Y., Macleod, V., Miao, H.Q., Theus, A., Zhan, F., Shaughnessy, J.D., Jr., Sawyer, J., Li, J.P., Zcharia, E., Vlodavsky, I., and Sanderson, R.D. 2007. Heparanase enhances syndecan-1 shedding: A novel mechanism for stimulation of tumor growth and metastasis. J Biol Chem. 282:13326-13333.  17347152 
Sanderson, R.D., Yang, Y., Kelly, T., MacLeod, V., Dai, Y., and Theus, A. 2005. Enzymatic remodeling of heparan sulfate proteoglycans within the tumor microenvironment: growth regulation and the prospect of new cancer therapies. J Cell Biochem 96:897-905.
Kelly, T., Suva, L.J., Huang, Y., Macleod, V., Miao, H.Q., Walker, R.C., and Sanderson, R.D. 2005. Expression of heparanase by primary breast tumors promotes bone resorption in the absence of detectable bone metastases. Cancer Res 65:5778-5784.
Yang, Y., Macleod, V., Bendre, M., Huang, Y., Theus, A.M., Miao, H.Q., Kussie, P., Yaccoby, S., Epstein, J., Suva, L.J., Kelly, T., and Sanderson, R.D. 2005. Heparanase promotes the spontaneous metastasis of myeloma cells to bone. Blood 105:1303-1309.

tumor, microenvironment, cancer, heparan sulfate, proteoglycan, heparanase, exosomes, metastasis, bone, myeloma, breast cancer, drug resistance