The research in the Van Ness lab is directed at defining genetic deregulation that contributes to lymphoid malignancies, particularly multiple myeloma. Multiple myeloma results from plasma cell expansion in the bone marrow, and unfortunately is very hard to treat. This difficulty comes in part from the variability in genetic and signaling pathways that are deregulated in the plasma cells as well as the cells in the bone marrow microenvironment. The lab is developing both cell lines and mouse models to explore how different genes can influence disease progression and therapeutic response. The lab is identifying some of the complexity of gene expression through expression profiling; and we have undertaken a collaborative project to target gene deregulation that will contribute to models of plasma cell malignancy in the mouse. The Van Ness lab is also working with both national and international clinical groups to correlate genetic defects with disease outcome and response to different therapies. The ultimate goal is to contribute to genetic characterization of patients that will direct individualized therapy.
Van Ness, B. (2016) Applications and limitations in translating genomics to clinical practice. Translational Res. 168:1-5.
Mitra, A, Mukherjee, U, Jang, J, Harding,T, Stessman, H, Li, Y, Abyzov, A, Jen, J, Kumar, S, Rajkumar, V, Van Ness, B. (2016) Single-cell analysis of targeted transcriptome (SCATTome) predicts drug sensitivity of single cells within human myeloma tumors. Leukemia. 30(5):1094-10102.
Rabellino,A, Melegari, M, Tompkins, VS, Chen, W, Van Ness, BG, TGeruya-Feldstein J. Conacci-Sorrell, M, Janz, S, Scaglioni, PP. (2016) PIAS1 promotes lymphomagenesis through MYC upregulation. Cell Rep. 15:2266-2278.
Baughn, LB, Mitra, A, Van Ness, BG, Noble-Orcutt, K, Sachs, Z, Linden, M. (2016) Phenotypic and functional characterization of a bortezomib resistant multiple myeloma cell line by flow and mass cytometry. Leuk Lymphoma 16:1-10.
Mitra, A, Dodge, J, Van Ness, J, Sokeye, I, and Van Ness, B. (2016) A de novo splice site mutation in EHMT1 resulting in Kleefstra Syndrome with pharmacogenomics screening and behavior therapy for regressive behaviors. Mol Gen & Genomic Med. 5:130-140.
Mitra, AK, Harding, T, Muherjee UK, Jang, JS, Li, Y, HongZen, R, Jen, J, Sonneveld, P, Kumar, S, Kuehl WM, Rajkumar, V, Van Ness, B. (2017) A gene expression signature distinguishes innate response and resistance to proteasome inhibitors in multiple myeloma. Blood Cancer J 7:e581
Thompson, RM, Dytfeld, D, Reyes, L, Robinson, RM, Smith, B, Maencih, Y, Jakubowiak, A, Przybylowicz-Chalecka, A, Szczepaniak, T, Mitra, A, Van Ness, B, Luczak, M, Dollof, N. (2017) Glutaminase inhibitor CB-839 synergizes with carfilzomib in resistant myeloma cells. Oncotarget. 8:35863-35876.
Petersen, GM and Van Ness, B. (2015) Returning a research participant’s genomic results to relatives: Perspectives from mangers of two distinct research biobanks. J Law, Medicine & Ethics, In press.
Van Ness, B. (2015) Applications and limitations in translating genomics to clinical practice. Translational Res. In press.
Fall , D, Stessman, H, Patel, S S, Sachs, Z, Van Ness BG, Baughn LB, Linden, MA. (2014) Utilization of translational bioinformatics to identify novel biomarkers of bortezomib resistance in multiple myeloma. J of Cancer. 5:720-727.
Stessman, H, Lulla, A, Xia, T, Mitra, A, Harding, T, Mansoor, A, Myers, C, Van Ness, B*, Dolloff, N* (*Co-senior corresponding authors) (2014) High throughput drug screening identifies compounds and molecular strategies for targeting proteasome inhibitor resistant multiple myeloma. Leukemia. 28:2263-2267
Mitra, A, Stessman, H, Shaughnessy, J, and Van Ness, B (2014) Profiling bortezomib resistance in multiple myeloma: implications in personalized pharmacotherapy. In Resistance to Proteasome Inhibitors in Cancer: Molecular Mechanisms and Reversal Strategies. (Ping Dou, ed., Springer publisher.)
Stessman, H, Mansoor, BS, Zhan, F, Janz, S, Lindens, MA, *Baughn LB, *Van Ness, B. (2013) Reduced CXCR4 expression is associated with extramedullary disease in a mouse model of myeloma and predicts poor survival in multiple myeloma patients treated with bortezomib. (*co-corresponding authors) Leukemia. 27:2075-2077. PMID: 23728080
Stessman, H, Mansoor, Zhan, F, A, Linden, M, *Van Ness, B, *Baughn, L (2013). Bortezomib resistance can be reversed by induced expression of plasma cell maturation markers in a mouse in vitro model of multiple myeloma. ß. PLOS One. 8(10):e77608. (*co-corresponding authors) PMID: 24204892
Stessman, H, Baughn, L, Sarver, A, Xia, T, Deshpande, R, Mansoor, A, Linden, M, Wu, T, Zhan, F, Janz, S, Meyers, C, Van Ness, B. (2013). Profiling bortezomib resistance and identification of secondary therapies in a mouse myeloma model. Molecular Cancer Therap. 12:1140-1150. PMID: 23536725
Fang, G., Haznadar, M., Wang, W., Haoyu, H., Steinbach, M., Church TR, Oetting, W, Van Ness, B, and Kumar, V. (2012) High-order SNP Combinations Associated with Complex Diseases: Efficient Discovery, Statistical Power and Functional Interactions. PLOS One. 7(4):e33531. PMID: 22536319
Linden, MA, Kirchoff, N, Carlson, CS, Van Ness, B. (2012) Targeted overexpression of an activated N-ras gene results in B- and plasma cell lymphoproliferation and cooperates with c-myc to induce fatal B-cell neoplasia. Exp Hematology. 40(3):216-227. PMID: 22120021