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Erik A. Ranheim, MD, PhD

earanheim@wisc.edu

Erik A. Ranheim, MD, PhD

Assistant Professor of Pathology and Laboratory Medicine

Member of the University of Wisconsin Paul P. Carbone Comprehensive Cancer Center

Dr. Ranheim grew up in Minneapolis, MN. He attended the University of Pennsylvania where he played college hockey. He completed his M.D. and Ph.D. in immunology at the University of Minnesota and University of California, San Diego. As a graduate student, he studied how different receptors on the surface of normal and cancerous white blood cells interact during immune responses, and how these pathways might be used to generate immune responses against malignant cells. Dr. Ranheim did his clinical training in hematopathology (pathology of the blood, bone marrow, and lymph nodes) at Stanford University and was a post-doctoral fellow in the lab of Irving Weissman where he studied B cell development, stem cell biology, and anti-tumor immunity. He joined the faculty at the University of Wisconsin, Madison in 2003.

His laboratory has two broad areas of interest, the interaction of the immune system with tumor cells, and the role of the frizzled/wnt/beta-catenin pathway in normal and neoplastic lymphoid development and function. The field of tumor immunology is replete with studies showing that immunization of mice prior to tumor introduction can prevent cancer. While this demonstrates the potential of the immune system in treating cancer, it says almost nothing about the true clinical situation of a patient with a long standing tumor presenting for treatment. He hopes to step back and examine the mechanisms of how the immune system and tumor interact and why, even with evidence that anti-tumor lymphocytes are present, the tumor usually wins. Dr. Ranheim is involved in anti-tumor immunity research in both mouse models and human patients in B cell leukemia/lymphoma and melanoma, in collaboration with other members of the UW Carbone Cancer Center.

The second area of interest involves the frizzled/wnt pathway, a family of receptors and ligands that regulate the level of beta-catenin within cells that has been implicated in a number of human tumors, most notably colon cancer and the familial polyposis syndrome. His interest stems from the fact that work in Irv Weissman's laboratory showed that beta-catenin signaling may be a critical signal directing hematopoietic stem cells to self-renew rather than differentiate. His examination of frizzled 9 knockout mice suggests that this pathway may offer a similar signal to developing cells in the B lymphoid lineage as well as affecting plasma cell function. Malignant cells also seem to be signaled to “self-renew” rather than differentiate, and the beta-catenin pathway is likely to be involved in this decision. Dr. Ranheim's laboratory has found that particular members of this signaling pathway are critical for development of lymphoma/leukemia in a mouse model of human chronic lymphocytic leukemia and is exploring whether other B cell malignancies may also use this pathway to enhance survival and growth of the malignant cells.

If you have questions about these projects, or about the role of the hematopathologist in diagnosis of lymphoma, please email Dr. Ranheim at earanheim@wisc.edu.

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