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Human Cancer Biology |
1 Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke and 2 Urologic Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland; 3 Laboratoire de Pathologie and4 Service d'Urologie, Hôpital de Bicêtre, Le Kremlin-Bicêtre, France; 5 Laboratoire de Génétique Oncologique EPHE-UMR 8125,Villejuif, France; 6 Service de Néphrologie, Hôpital Necker, Paris, France; 7 Genetic Laboratory, Hôpital Édouard Herriot, Lyon, France; and 8 Van Andel Research Institute, Grand Rapids, Michigan
Requests for reprints: Zhengping Zhuang, Molecular Pathogenesis Unit, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH, Building 10, Room 5D37, 10 Center Drive, Bethesda, MD 20892. Phone: 301-435-8445; Fax 301-480-1839.
Von Hippel-Lindau (VHL) disease is characterized by multiple tumors in specific target organs. The tumors at different sites share distinct morphologic and genetic characteristics but their cell of origin is unknown. We show that VHL disease–associated renal clear cell carcinomas (RCC) consistently coexpress erythropoietin (Epo) and Epo receptor (EpoR). In addition, coexpression of Epo and EpoR is detected in many renal cysts, providing further evidence that renal cysts are potential precursors for RCC. In conjunction with VHL gene deficiency, coexpression of Epo and EpoR in renal cysts and tumors may reflect a developmental arrest in immature mesenchymal cells. Such arrest may lead to autocrine stimulation, cell proliferation, and renal tumor development, similar to tumorigenesis of VHL disease–associated hemangioblastomas.
Key Words: Von Hippel-Lindau disease • renal cell carcinoma • renal cyst • Epo • EpoR • immunohistochemistry • RT-PCR • Western blot
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