Research Program: Genetic Mechanisms of Cancer
Professor and Department Head, Department of Genetics, Cell Biology and Development

vanne001@umn.edu
612-624-9944 — office
612-624-9663 — lab
Preferred method of contact: e-mail

Research Interests

The research in the Van Ness lab is directed at defining genetic deregulation that contributes to lymphoid malignancies, particularly multiple myeloma. Multiple myeloma resultsfrom 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 microarray 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

Selected Publications

Kyle, RA, Leong, T, Li, S, Oken MM, Kay, NE, Van Ness, B, and Greipp, PR. (2006) Complete Response in Multiple Myeloma: An Eastern Cooperative Oncology Group Study. Cancer. 2006 May 1;106(9):1958-66.

Cheung, WC, Kim, JS, Linden, M, Peng, L, Van Ness, B, Polakiewicz, RD, and Janz, S. (2005) The perils of abrogating myc-dependent apoptosis. CCR Frontiers in Science. 4:4-5.

Linden, M, Kirchoff, N, Kvitrud, M, and Van Ness, B. (2004) Abl-myc retroviral infection elicits bone marrow plasma cell tumors in Bcl-xL transgenic mice. Leuk Res. 4:435-444.

Croonquist, P and Van Ness, B. (2005) The polycomb group protein Enhancer of Zeste Homologue2 (EZH2) is an oncogene required for myeloma cell growth and the ras proliferative phenotype. Oncogene. 24:6269-6280.

Linden, M, Kirchhof, N, Carlson, C, and Van Ness, B. (2004) Targeted overexpression of BCL-xL in B lymphoid cells results in lymphoproliferative disease and plasma cell malignancies. Blood. 103:2779-2790.