Faculty Research 1990 - 1999

Multigenic and imprinting control of ovarian granulosa cell tumorigenesis in mice.

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Alleles, Animal, Crosses, Genetic, Disease Susceptibility, Female, Genetic Markers, Genotype, Granulosa Cell Tumor/*genetics, Logistic Models, Mice, Ovarian Neoplasms, Species Specificity

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Cancer Res 1998 Aug 15;58(16):3694-9


CA62434/CA/NCI, GM20919/GM/NIGMS, CA34196/CA/NCI


Spontaneous juvenile ovarian granulosa cell (GC) tumors that occur in young girls are similar to GC carcinomas that develop in SWR-derived inbred mice. We analyzed female offspring from a series of matings among SWR and SJL inbred mice for chromosomal loci underlying tumor susceptibility. Intercross F2 female mice were produced by reciprocal matings of (SWR x SJL)F1 and (SJL x SWR)F1 parents. Tumorigenesis in these F2 mice as well as in SWXJ recombinant inbred and congenic strains of mice derived from SWR and SJL showed significant (P < 0.001) association with Gct1, a dominant susceptibility locus on chromosome (CHR) 4 and with Gct2 on CHR 12. Suggestive (P < 0.01) association was found with Gct3 on CHR 15. A fourth susceptibility locus, Gct4 on CHR X, was demonstrated with a strong parent-of-origin effect associated with the paternal genotype. Imprinting and complex interactions among these four loci combine to establish the probability for GC tumorigenesis in this mouse model.

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