Diverse origins of multiple ovarian teratomas in a single individual.

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RESUMO

Centromere heteromorphisms and enzyme markers were examined in cells cultured from seven benign ovarian teratomas arising in a single patient. Three of the teratomas were homozygous for all eight enzyme and centromere markers found to be heterozygous in the host. The other four tumors were heterozygous at the centromeres of chromosomes 1, 16, 17, and 18, as in the patient, but were homozygous for at least one of the enzyme markers. The linkage phases of the heterozygous enzyme markers phosphogluconate dehydrogenase and phosphoglucomutase 1 and the chromosome 1 centromere heteromorphism were established for the patient and for three of the heterozygous teratomas by analysis of Chinese hamster-human somatic cell hybrids. The linkage phase of these markers in homozygous and heterozygous tumors was in every case different from that in the host. The finding of heterozygous centromeres in ovarian teratomas excludes suppression of meiosis II as a mechanism for their origin, and we suggest rather that they arise by failure of meiosis I. The linkage phases in the fully homozygous tumors are most readily derived from that in the patient, we suggest, by endoreduplication of a haploid gamete. The varied origin of ovarian teratomas has important implications for the suitability of such material for centromere-based gene mapping.

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