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N‐ myc oncogene expression in histopathologically unrelated bilateral pediatric renal tumors
Author(s) -
Nisen Perry D.,
Rich Mark A.,
Gloster Elizabeth,
Valderrama Elsa,
Saric Olga,
Shende Ashok,
Lanzkowsky Philip,
Alt Frederick W.
Publication year - 1988
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19880501)61:9<1821::aid-cncr2820610917>3.0.co;2-t
Subject(s) - neuroblastoma , synaptophysin , pathology , wilms' tumor , medicine , kidney , enolase , renal tumor , oncogene , immunohistochemistry , in situ hybridization , cancer research , cell culture , nephrectomy , cancer , biology , gene , gene expression , cell cycle , biochemistry , genetics
Renal tumors of childhood occasionally exhibit histopathologic and clinical features that preclude accurate diagnosis. Molecular and cell culture techniques may be helpful in better characterizing these cases. This approach was used to examine unusual bilateral renal tumors from a young boy. The left kidney tumor was an undifferentiated neoplasm with light microscopic features suggestive of both Wilms' tumor and neuroblastoma, and the right kidney tumor was identified as multilocular cystic nephroma (MLCN). In vitro tissue culture of tumor cells and hybridization experiments with an N‐ myc oncogene DNA probe contributed to a revised diagnosis of intrarenal neuroblastoma of the left kidney. A cell line established from the left tumor exhibited neurite outgrowth and was positive for neuron‐specific enolase and synaptophysin. N‐ myc was greater than ten‐fold amplified in chromosomal DNA from the left kidney tumor. Measurement of N‐ myc RNA expression enabled distinction between benign and malignant tumor tissue. The detection of N‐ myc gene amplification predicted a poor prognosis which was confirmed by the patient's subsequent clinical course.