Erik Ranheim

About

Erik Ranheim is a Professor and Department Chair in the Department of Pathology and Laboratory Medicine at the University of Wisconsin School of Medicine and Public Health. His research focuses on two broad areas: 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. Dr. Ranheim's laboratory investigates the mechanisms of immune system and tumor interactions, particularly why tumors often prevail despite the presence of anti-tumor lymphocytes, through studies in mouse models and human patients with B cell leukemia/lymphoma and melanoma, in collaboration with the UW Carbone Cancer Center. Additionally, his work on the frizzled/wnt pathway explores its role in regulating beta-catenin levels within cells, which has implications in human tumors such as colon cancer and familial polyposis syndrome. His research has demonstrated that this pathway is critical for the development of lymphoma and leukemia in mouse models and may influence the survival and growth of malignant B cells.

Research topics

• Biology
• Immunology
• Genetics
• Cancer research
• Pathology
• Medicine
• Molecular biology
• Oncology
• Virology
• Cell biology

Selected publications

• B cells infected with Type 2 Epstein-Barr virus (EBV) have increased NFATc1/NFATc2 activity and enhanced lytic gene expression in comparison to Type 1 EBV infection

  PLoS Pathogens · 2020 · 42 citations

  Humans are infected with two distinct strains (Type 1 (T1) and Type 2 (T2)) of Epstein-Barr virus (EBV) that differ substantially in their EBNA2 and EBNA 3A/B/C latency genes and the ability to transform B cells in vitro. While most T1 EBV strains contain the "prototype" form of the BZLF1 immediate-early promoter ("Zp-P"), all T2 strains contain the "Zp-V3" variant, which contains an NFAT binding motif and is activated much more strongly by B-cell receptor signalling. Whether B cells infected wi…

  DOI

• Constructing and deconstructing GATA2-regulated cell fate programs to establish developmental trajectories

  The Journal of Experimental Medicine · 2020 · 40 citations

  Stem and progenitor cell fate transitions constitute key decision points in organismal development that enable access to a developmental path or actively preclude others. Using the hematopoietic system, we analyzed the relative importance of cell fate-promoting mechanisms versus negating fate-suppressing mechanisms to engineer progenitor cells with multilineage differentiation potential. Deletion of the murine Gata2-77 enhancer, with a human equivalent that causes leukemia, downregulates the tra…

  DOI

• A gain-of-function p53 mutant synergizes with oncogenic NRAS to promote acute myeloid leukemia in mice

  Journal of Clinical Investigation · 2023-10-17 · 14 citations

  articleOpen access

  We previously demonstrated that a subset of acute myeloid leukemia (AML) patients with concurrent RAS pathway and TP53 mutations have an extremely poor prognosis and that most of these TP53 mutations are missense mutations. Here, we report that, in contrast to the mixed AML and T cell malignancy that developed in NrasG12D/+ p53-/- (NP-/-) mice, NrasG12D/+ p53R172H/+ (NPmut) mice rapidly developed inflammation-associated AML. Under the inflammatory conditions, NPmut hematopoietic stem and progeni…

  PublisherOA PDFDOI

• Latent Epstein-Barr virus infection collaborates with Myc over-expression in normal human B cells to induce Burkitt-like Lymphomas in mice

  PLoS Pathogens · 2024-04-15 · 8 citations

  articleOpen accessCorresponding

  Epstein-Barr virus (EBV) is an important cause of human lymphomas, including Burkitt lymphoma (BL). EBV+ BLs are driven by Myc translocation and have stringent forms of viral latency that do not express either of the two major EBV oncoproteins, EBNA2 (which mimics Notch signaling) and LMP1 (which activates NF-κB signaling). Suppression of Myc-induced apoptosis, often through mutation of the TP53 (p53) gene or inhibition of pro-apoptotic BCL2L11 (BIM) gene expression, is required for development…

  PublisherOA PDFDOI

• Administration of intratumoral GD2-directed interleukin-2 immunocytokine and local radiation therapy to activate immune rejection of spontaneous canine melanoma

  Melanoma Research · 2024-05-20 · 6 citations

  articleOpen access

  Canine malignant melanoma provides a clinically relevant, large animal parallel patient population to study the GD2-reactive hu14.18-IL-2 immunocytokine as it is similar to human melanoma and expresses GD2. The objectives of this study were to evaluate safety, radiation fractionation, and identify informative biomarkers of an in-situ tumor vaccine involving local radiation therapy plus intratumoral-immunocytokine in melanoma tumor-bearing dogs. Twelve dogs (six dogs/arm) with locally advanced or…

  PublisherOA PDFDOI

Recent grants

• NIH Grant K08CA090450

  NIH · $664k · 2008

Frequent coauthors

• Paul M. Sondel

  University of Wisconsin–Madison

  73 shared

• Mark R. Albertini

  University of Wisconsin Carbone Cancer Center

  62 shared

• Jacquelyn A. Hank

  University of Wisconsin–Madison

  56 shared

• Cindy Zuleger

  University of Wisconsin Carbone Cancer Center

  55 shared

• Richard K. Yang

  47 shared

• KyungMann Kim

  University of Wisconsin–Madison

  46 shared

• Zachary S. Morris

  University of Wisconsin–Madison

  45 shared

• Amy K. Erbe

  University of Wisconsin–Madison

  42 shared

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