Microdissection-based analysis of mature ovarian teratoma

Citation
Ao. Vortmeyer et al., Microdissection-based analysis of mature ovarian teratoma, AM J PATH, 154(4), 1999, pp. 987-991
Citations number
17
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
AMERICAN JOURNAL OF PATHOLOGY
ISSN journal
00029440 → ACNP
Volume
154
Issue
4
Year of publication
1999
Pages
987 - 991
Database
ISI
SICI code
0002-9440(199904)154:4<987:MAOMOT>2.0.ZU;2-4
Abstract
The genotypic features of mature ovarian teratomas (MOTs) are controversial . Early studies detected a homozygous genotype in MOTs suggesting that thes e tumors are composed of germ cells that have undergone meiosis I. Other st udies, however, revealed a heterozygous genotype in a substantial proportio n of MOTs suggesting an origin either from premeiotic germ cells or from a somatic cell line. In view of the complex morphology of MOTs and to increas e the sensitivity of teratoma genotyping, we applied tissue microdissection before genetic analysis of teratomatous tissue. This approach allowed sele ctive analysis of different heterotopic tissue elements as well as the lymp hoid tissues within MOTs the origin of which is unknown. After DNA extracti on, the tissue samples were polymerase chain reaction amplified using a ran dom panel of highly informative genetic markers for different chromosomes t o evaluate heterozygosity versus homozygosity, In all seven cases that were analyzed, heterotopic tissues consistently revealed a homozygous genotype with several markers; in two cases, heterozygosity was detected with a sing le marker, indicating a meiotic recombination event. Lymphoid aggregates wi thin MOTs were heterozygous and derived from host tissue rather than from t eratomatous growth. However, well differentiated thymic tissue was consiste ntly homozygous, suggesting lymphoid differentiation capability of MOTs, We conclude that potential pitfalls in genotyping of teratomas including meio tic recombination and host cell participation can be avoided by a microdiss ection-based approach in combination with a panel of genetic markers.