Erik Ranheim, MD, PhD
- Professor (CHS)
- Vice Chair of Education
Department of Pathology and Laboratory Medicine
Beta-catenin in normal and neoplastic lymphoid development; tumor immunology; hematopoietic and leukemic stem cell biology
Dr. Ranheim's 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.