Abstract：
:Hereditary renal carcinoma (RC) in the rat, originally reported by Eker in 1954, is an example of a Mendelian dominant predisposition to a specific cancer in an experimental animal. We previously reported that ionizing radiation induces additional tumors in a linear dose-response relationship, suggesting that in heterozygotes two events (one inherited, one somatic) are necessary to produce tumors. Recently, the predisposing gene has been mapped to rat chromosome 10. This study was designed to examine loss of heterozygosity (LOH) at chromosome 10 in the RCs developed from hybrid F1 rats carrying Eker mutation. In spontaneous RCs, 6 of 10 (60%) showed loss of the wild-type allele covering over 30 cM, consistent with two-hit hypothesis. Individual tumors have different patterns of LOH even from the same kidney, showing independent clonal origins of RCs. In contrast, none of N-ethyl-N-nitrosourea-induced RCs had allelic loss (0 of 9 = 0%, P < 0.01). Thus, the nature of the second event differs between spontaneous and chemically induced tumors in the Eker rat. These results suggest that chemically induced tumors in experimental animals involve intragenic mutations and so do not cause LOH of syntenic markers. Interestingly, 1 of 5 spontaneous pituitary tumors that developed in the Eker rat showed LOH for chromosome 10 markers.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Kubo Y,Mitani H,Hino Osubject
Has Abstractpub_date
1994-05-15 00:00:00pages
2633-5issue
10eissn
0008-5472issn
1538-7445journal_volume
54pub_type
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