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Faculty Detail Faculty Entry   
Name YANG YANG  
Campus Address WTI 320A Zip 0007
Phone 205-996-6228
E-mail yangyang@uab.edu" id="FacultyDetail1EmailAddress"><a href="mailto:yangyang@uab.edu">yangyang@uab.edu</a>
URL
 
 

Department Affiliations(s)
Appointment Type Department Division Rank
Center  Center for Metabolic Bone Disease  Center for Metabolic Bone Disease Associate Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Associate Professor
Center  General Clinical Research Center  Ctr for Clinical & Translational Sci Associate Professor
Primary  Pathology   Joint Pathology Associate Professor

Biographical Sketch 
Dr. Yang received her M.D. degree from China Medical University and her PhD degree from Third Military Medical University, China. She completed postdoctoral training and was appointed as an Assistant Professor in the Department of Pathology, University of Arkansas for Medical Sciences. In August 2006, Dr. Yang joined the faculty of Department of Pathology at UAB.

Society Memberships
Organization Name Position Held Org Link
American Association for Cancer Research   Member   
American Association for Matrix   Member   
American Society for Bone and Mineral Research  Member   
American Society of Hematology   Member   
International Bone and Mineral Society   Member   
 

Research/Clinical Interest
Title
Cancer-related bone diseases
Description
My lab is focused on the role of syndecan-1 and heparanase in multiple myeloma (MM), cancer-related bone diseases and the translational research of MM. MM is a B-lymphoid malignancy characterized by tumor cell infiltration of the bone marrow, osteolytic lesions, and angiogenesis in the vicinity of the tumor cells. Although new treatments have improved the outlook for patients with MM, it remains an incurable disease.


(1)Syndecan-1 in myeloma. Syndecan-1 is the dominant heparan sulfate (HS) proteoglycan expressed on the surface of myeloma cells. Syndecam-1 is shed from the myeloma cell surface and high levels of syndecan-1 in myeloma patient sera are an indicator of poor prognosis. We demonstrated that the shed syndecan-1 is not simply an indicator of poor prognosis, but it actively promotes the growth and dissemination of myeloma tumors. Moreover, we discovered that syndecan-1 shedding is stimulated by heparanase expressed in myeloma cells. These important discoveries have been published in Blood (2002) and JBC (2007), which have been cited numerous times in peer-reviewed journals.


(2)Heparanase in myeloma and MM-related bone diseases. Heparanase-1 (heparanase) is an endo-beta-glucuronidase that specifically cleaves the saccharide chains of HS proteoglycans, and is upregulated in a variety of human tumors, including MM. In myeloma, We demonstrated that heparanase drives tumor growth, angiogenesis and metastasis and thus plays a major role in promoting the progression of this cancer. Recently, we discovered that heparanase is a major determinant of the osteolytic phenotype in myeloma. Our work on heparanase has been published in high ranking journals (e.g., Blood, JBC, and Cancer Research) and presented orally at several international meetings (e.g., Annual meetings of American Society of Hematology and of American Society for Bone and Mineral Research). In 2011, I received a NIH R01 grant award for studying the mechanism of heparanase-induced bone diseases in MM.


(3)Translational research in myeloma. Based on our work demonstrating that heparanase is a viable target for MM therapy, in 2011 I received a senior award from Multiple Myeloma Research Foundation for the study of the therapeutic potential of heparanase inhibition in MM bone disease.

Postdoc Positions Available
Date Posted Position Title
02/20/2013  Postdoctoral fellow  
We are currently seeking a postdoctoral fellow to study myeloma related bone disease. The candidates must be self-motivated. A strong background in bone and cancer biology is required. Experience with animal experiments is desirable. Please send your CV and a brief statement of your career goals and research interests to Dr. Yang Yang at yangyang@uab.edu.   
 

Selected Publications 
Publication PUBMEDID
1. Yang Y, Macleod V, Bendre M, Huang Y, Theus AM, Miao HQ, Kussie P, Yaccoby S, Epstein J, Suva LJ, Kelly T, and Sanderson RD: Heparanase promotes the spontaneous metastasis of myeloma cells to bone. Blood 2005; 105 (3): 1303-1309.

2. Yang Yang, Veronica MacLeod, Hua-Quan Miao, Allison Theus, Fenghuang Zhan, John D. Shaughnessy, Jr., Jeffrey Sawyer, Jin-Ping Li, Eyal Zcharia, Israel Vlodavsky and Ralph D. Sanderson: Heparanase enhances syndecan-1 shedding: A novel mechanism for stimulation of tumor growth and metastasis. The Journal of Biological Chemistry 2007; 282(18):13326-33.

3. Yang Y, MacLeod V, Dai Y, Khotskaya-Sample Y, Shriver Z, Venkataraman G, Sasisekharan R, Naggi A, Torri G, Casu B, Vlodavsky I, Suva, Epstein J, Yaccoby S, Shaughnessy JD, Barlogie B and Sanderson RD: The syndecan-1 heparan sulfate proteoglycan is a viable target for myeloma therapy. Blood 2007; 110(6): 2041-8.

4. Purushothaman, A., Chen, L., Yang, Y. and Sanderson, R.D. Heparanase stimulation of protease expression implicates it as a master regulator of the aggressive tumor phenotype in myeloma. The Journal of Biological Chemistry 2008; 283 (47): 32628-36

5. Khotskaya, Y.B., Dai, Y., Ritchie, J.P., MacLeod, V., Yang, Y., Zinn, K. and Sanderson, R.D. Syndecan-1 is required for robust growth, vascularization and metastasis of myeloma tumors in vivo. The Journal of Biological Chemistry 2009; 284(38):26085-95

6. Yang, Y., Ren, R., Ramani, V.C., Nan, L., Suva, L.J., and Sanderson, R.D. Heparanase enhances local and systemic osteolysis in multiple myeloma by upregulating the expression and secretion of RANKL. Cancer Res 2010; 70(21): 8329-38.

7. Ramani, V.C., Yang, Y.* (Co-1st author), Ren, Y., Nan, L., Sanderson, R.D. Heparanase plays a dual role in driving hepatocyte growth factor (HGF) signaling by enhancing HGF expression and activity. JBC 2011; in press (*Selected as JBC Paper of the Week).

8. Ritchie, J.P., Ramani, V.C., Naggi, A., Torri, G., Casu, B., Pisano, C., Carminati, P., Tortoreto, M., Zunino, F., Vlodavsky, I., Sanderson, R.D. and Yang, Y. SST0001, a chemically modified heparin, inhibits myeloma growth and angiogenesis via disruption of the heparanase/ syndecan-1 axis. Clinical Cancer Research 2011, 2011 17(6):1382-93 ( This article has been reviewed by the Faculty of 1000 and the Hematologist in 2011).  		  
 

Keywords
cancer-related bone diseases, tumor microenvironment, bone resorption and formation, multiple myeloma

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