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Professor of Pathology Voice: 319-335-9986 Email: siegfried-janz@uiowa.edu After obtaining his medical degree from the University of Leipzig, Germany, where he also took post-graduate training in Pathology and received his board-certification in Clinical Immunology, Siegfried Janz joined the laboratory of Dr. Michael Potter at the National Cancer Institute, Bethesda, Maryland, to study a type of immunoglobulin-producing extraosseous plasma cell tumor, plasmacytoma, that can be readily induced in genetically susceptible BALB/c mice. In these formative years, his research interest in mouse models of human B cell and plasma cell neoplasms was shaped. Siegfried Janz’ chief scientific goal is to elucidate the pathogenesis of B cell and plasma cell malignancies that are induced by the deregulated expression of Myc, one of the most important oncogenes in humans and mice. Since the primary mechanism of Myc deregulation in human non-Hodgkin lymphomas and mouse plasmacytomas is chromosomal translocation, he is particularly interested in furthering our understanding of Myc-activating chromosomal translocations. The principal experimental model for studying these translocations is the T(12;15), the hallmark mutation of BALB/c mouse plasmacytomas (PCT). The T(12;15) translocation is the direct counterpart of the human MYC-activating t(8;14)(q24;q32) translocation most commonly found in human Burkitt lymphoma (BL), thus highly relevant to human cancer. Because the T(12;15) is the only translocation in mice that occurs with high incidence, spontaneity, and cell-type specificity (B and plasma cells), it affords a unique model for exploring the fundamental outstanding questions on the mechanisms, genetics, and biological consequences of chromosomal translocations in experimental and human neoplasia. Currently, his research is focusing on three specific aims, all centered around Myc, T(12;15), and its human homologue, t(8;14). The first aim is a gene-targeting program to mimic different states of T(12;15)/t(8;14) in genetically engineered mice. The second aim is to develop genetic methods for detecting T(12;15) in individual mouse B and plasma cells as well as refining the detection of t(8;14) for epidemiological studies. The third aim involves Myc transgenics as a platform for improved mouse models of human plasma cell tumors, such as plasmacytoma and multiple myeloma. All three aims rely on genetically engineered mice that were generated in Janz' own laboratory. In the Gallery section of this website, he has attempted to illustrate and describe in more detail how we will use the new mouse strains to study mechanisms of neoplastic development in B and plasma cells, learn about tumor biology, and assess new intervention approaches for the benefit of human patients. In the Selected Links section of this website, additional information on research efforts sponsored by the federal government, the state of Iowa, and private foundations can be found. |