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KMID : 0360319930250040556
Journal of Korean Cancer Research Association
1993 Volume.25 No. 4 p.556 ~ p.562
Genetic Classification of Hydatidiform Mole Using Restriction Fragment Length Polymorphisms(RELPs)
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Abstract
Genetically, hydatidiform mole(HM) can be classified into three major types, such as partial HM(PHM), homozygous complete HM(CHM) and heterozygous CHM. PHM is genetically triploid which is composed of one maternal and two paternal contributions
mostly.
The CHM is genetically androgenic, since it is arise by fertilization of empty egg by haploidy sperm. Homozygous CHM is originated by fertilization of one haploid sperm followed by duplication of its genome and heterozygous mole by two haploid
sperms.
It is well established that CHM is more likely to progress to trophoblastic tumor than PHM, and the heterozygous type among CHM has the highest malignant potential.
To classify HM genetically, restriction fragment length polymorphisms(RFLPs) identified with three locus specific minisatellite probes and Y chromosome specific probe have been examined in 19 mole tissues which were diagnosed as CHM
histologically.
@The results were as follows.
@EN 1) Two cases among them that were diagnosed as CHM by histologic diagnosis were finally identified as partial mole. This discrepancy seems to be occurred due to dependence that histologic diagnosis was made by the presence of fetal tissue.
2) There were 14 homozygous CHMs and they had only one paternal allele without maternal contribution.
3) Three heterozygous CHMs were identified. They showed two paternal alleles without maternal contribution and the presence of Y chromosome in 2 patients with 46, XY karyotype could be detected by Y chromosome specific probe.
4) The means of prognostic mole score were 3.0 in PHM, 5.6 in homozygous CHM and 8.3 in heterozygous CHM respectively. The heterozygous CHM had the highest prognostic mole score and two cases had received chemotherapy due to persistent
trophoblastic
disease.
In this study, we determined genetic types of HM that closely related with the progress of HM into trophoblastic disease. Prophylactic treatment for patients with heterozygous CHM should substantially decrease the morbidity associated with
postmolar
trophoblastic disease. Further characterization of genetic markers for persistent gestational trophoblastic disease meight clarify genetic basis of the disease.
KEYWORD
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