Benign ovarian teratomas. An analysis of their cellular origin.

Abstract

To determine the cellular origin of benign ovarian teratomas with a 46,XX chromosome constitution, DNA markers recognizing restriction fragment length polymorphisms (RFLPs) were hybridized to DNA from six teratomas and their hosts. DNA markers heterozygous in the host were completely heterozygous in two of the teratomas. The remaining four showed a mixture of homozygosity and heterozygosity. These results suggests that most of the analyzed benign ovarian teratomas arose from germ cells after the first meiotic division by failure of meiosis II. Teratomas heterozygous for all tested markers may arise from failure of meiosis I. In addition, 21 cases were karyotyped and analyzed for centromeric chromosome markers to study the mechanism by which they were generated. Three of these tumors were homozygous when the host was heterozygous and therefore resulted from a failure of meiosis II or duplication of a mature ovum. Three cases were heterozygous for the centromeric chromosomal marker like the host and therefore probably originate from a premeiotic cell or a cell in which meiosis I has failed. One ovarian teratoma had an aberrant karyotype 47,XX,+8.

• Authors: N Dahl, K H Gustavson, C Rune, I Gustavsson, U Pettersson
• Journal: Cancer genetics and cytogenetics (Cancer Genet Cytogenet) Vol. 46 Issue 1 Pg. 115-23 (May 1990) ISSN: 0165-4608 [Print] United States
• PMID: 1970513 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• DNA, Neoplasm

Topics

• Alleles
• Chromosome Aberrations
• Chromosome Banding
• Chromosome Disorders
• DNA, Neoplasm (genetics)
• Dermoid Cyst (genetics, pathology)
• Female
• Humans
• Karyotyping
• Lymphocytes (analysis)
• Ovarian Neoplasms (genetics, pathology)
• Polymorphism, Restriction Fragment Length