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Department of Pediatrics, Division of Hematology-Oncology, Schneider Children's Hospital of Long Island-Jewish Medical Center, New Hyde Park, New York 11042, and School of Medicine, State University of New York at Stony Brook, Stony Brook, New York 11794 [P. D. N., S. V. C.]; Department of Biochemistry and Molecular Biophysics, and Institute for Cancer Research, Columbia University College of Physicians and Surgeons, New York, New York 10032 [K. A. Z., F. W. A.]; and Department of Pediatrics, Division of Genetics, Mt. Sinai School of Medicine, New York, New York 10029 [F. G.]
Activation of myc-family oncogenes has been implicated in the genesis of a variety of neoplasms. In addition, these genes exhibit specific patterns of expression during murine development. We now report that N- and c-myc are differentially expressed in normal developing human renal tissues and in Wilms' tumor, a neoplasm which derives from primitive kidney cells. Twelve of 13 Wilms' tumors tested exhibited greatly enhanced levels of expression which occurred in the absence of gene amplification. We also detected N-myc expression in other primitive neoplasms including medulloblastoma and hepatoblastoma. Our observations suggest that N-myc expression is not limited to neuroectodermal tumors as was previously thought, but is a marker for several neoplasms that derive from primitive cell precursors. Finally, high level expression of N-myc was associated with markedly diminished levels of c-myc, suggesting that enhanced expression of N-myc gene might lead to down-regulation of c-myc.
1 This work was supported by the Rosalind and Sol Chaikin Institute for Childhood Cancer Research of the Schneider Children's Hospital and by NIH grants 2-POI CA23767-06 and CA 42335, American Cancer Society Grant CD-269, and a Searle Scholars Award to F. A. F. A. is an Irma T. Hirschl Career Scientist and Malinckrodt Scholar.
2 To whom requests for reprints should be addressed.
Received 5/27/86. Revised 8/14/86. Accepted 8/15/86.
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