Further evidence for post ‐meiotic origin of teratomas in the human female*

Linder, David H.; Power, Judith

doi:10.1111/j.1469-1809.1970.tb00216.x

Cited by 82 publications

(37 citation statements)

References 35 publications

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“…Other workers have recorded a consistency in the difference between teratoma and host, which took the form of uniformly homozygous centromeres and homozygosity or heterozygosity at enzyme loci in the tumors of patients heterozygous for these markers (4)(5)(6). This is most reasonably explained by supposing that the tumors had completed a normal meiosis I but that the sister chromatids had failed to separate during meiosis II; such tumors would be expected to be uniformly homozygous unless crossing-over had occurred during meiosis I.…”

Section: Discussionmentioning

confidence: 99%

“…For example, in a woman who is heterozygous for one or more genetic markers, the teratoma is sometimes found to be homozygous at these loci, a phenomenon originally referred to as gene loss (3). Gene loss is not associated with a detectable reduction in gene dosage (4), indicating that hemizygosity or exclusive expression of one allele is not a likely basis for this phenomenon. The most extreme cases of homozygosity in tumors arising in a heterozygous host concerned structural polymorphisms at the centromeres of chromosomes.…”

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confidence: 96%

“…These results were explained (4,6) by postulating that the tumors contain all the chromosomal material segregated into one of the products of the first meiotic cleavage of oogenesis. Thus, the heterozygosity of enzyme markers is a consequence of chromatid exchange (crossing-over) that occurs during meiosis I prior to the first cleavage, but the failure ofsister chromatids to separate as they would in a normal second meiotic division results in homozygous centromeres.…”

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Diverse origins of multiple ovarian teratomas in a single individual.

Carritt¹,

Parrington²,

Welch³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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Centromereheteromorphisms andenzyme 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 ofthese 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 ofmeiosis 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.Benign ovarian teratomas, or dermoid cysts, are relatively common nonmalignant gonadal tumors that have some rather unusual properties (see ref. 1 for review). The most striking of these is the presence of a restricted range of differentiated tissues and structures, fully developed teeth and hair being frequently found within the cyst. Apart from these developmental curiosities, ovarian teratomas are unusual in that, although diploid (2), they frequently differ genetically from their hosts. For example, in a woman who is heterozygous for one or more genetic markers, the teratoma is sometimes found to be homozygous at these loci, a phenomenon originally referred to as gene loss (3). Gene loss is not associated with a detectable reduction in gene dosage (4), indicating that hemizygosity or exclusive expression of one allele is not a likely basis for this phenomenon. The most extreme cases of homozygosity in tumors arising in a heterozygous host concerned structural polymorphisms at the centromeres of chromosomes. In a survey of 42 chromosome heteromorphisms in 12 hosts, the teratomas were found to be uniformly homomorphic at the centromeres, although enzyme markers that were heterozygous in the hosts were either homozygous or heterozygous in the tumors (5).These results were explained (4, 6) by postulating that the tumors contain all the chromosomal material segregated into one of the products of the first meiotic cleavage of oogenesis. Thus, the heterozygosity of enzyme markers is a consequence of chromatid exchange (crossing-over) that occurs during meiosis I prior to the first cleavage, but the failure ofsister chromatids to separate as they would in a normal second meiotic division results in h...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 96%

mentioning

confidence: 99%

See 1 more Smart Citation

Diverse origins of multiple ovarian teratomas in a single individual.

Carritt¹,

Parrington²,

Welch³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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“…Earlier studies showed that teratoma cells are homozygous for enzyme markers that are heterozygous in host cells (19), suggesting that teratomas arise from a single germ cell during the meiotic process. Later studies showed that distal loci of chromosome arms from benign ovarian teratomas are heterozygous for genetic recombination during the long prophase of meiosis I, whereas centromeric markers are homozygous, suggesting that teratomas might originate from a germ cell that had completed the first meiotic division but failed the second (20,21).…”

Section: Discussionmentioning

confidence: 99%

Thyrotoxic adenoma followed by atypical hyperthyroidism due to struma ovarii: clinical and genetic studies

Ciccarelli

Valdes-Socin

Parma

et al. 2004

European Journal of Endocrinology

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Objective: Atypical forms of hyperthyroidism represent a diagnostic challenge for clinicians. Struma ovarii is an ovarian teratoma and constitutes a rare cause of ectopic thyroidal hormonal production. We describe a case of struma ovarii that combined two different sources of hyperthyroidism in the same patient and report genetic studies in order to contribute a better understanding of the autonomy and tumorigenesis of the struma ovarii. Case report: A 73-year-old nulliparous woman presented a thyroid toxic adenoma that was successfully treated with 10 mCi radioiodine. Unexpectedly, a new onset of hyperthyroidism prompted us to look for a second etiology. A whole-body scan with 123 I detected a pelvic hyperfixation suggesting struma ovarii, and a thyroid differentiated left ovarian teratoma 3 cm in size was surgically removed. We screened for mutations of thyroid-stimulating hormone receptor and Gs-a protein genes, as these mutations are common in thyroid adenomas. We did not identify any mutations. Androgen receptor study demonstrated a monoclonal status. Comparative genomic hybridization did not reveal any chromosomal abnormality. However, loss of heterozygosity analysis showed several structural abnormalities, compared with the majority of benign ovarian teratomas, which show a normal karyotype. Conclusions: This is the first well-documented report of thyrotoxic struma ovarii revealed after treatment of a single thyroid toxic adenoma. We have shown in this case that struma ovarii originates from a single germ cell, and, albeit benign, this tumor presents several chromosomal abnormalities. Struma ovarii-induced hyperthyroidism is likely to be mediated by mechanisms different from those of the classical thyroid toxic adenoma.

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“…4,5 In analogy to the homozygous postmeiotic germ cell, teratomas proved to be genetically homozygous in heterozygous hosts. [6][7][8] Subsequent studies, however, failed to consistently detect homozygous genetic composition of teratomas. Instead, heterozygous centromeric markers and other chromosomal heteromorphisms were reported in a subset of tumors.…”

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confidence: 99%