Acta obstetricia et gynecologica Scandinavica · 1994
Genetic origin analysis of hydatidiform mole and non-molar abortion using the polymerase chain reaction method.
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Fujita N, Tamura S, Shimizu N, Nozawa S
Аннотация
OBJECTIVES: The study attempts to determine the genetic origin of hydatidiform mole and non-molar abortion using the polymerase chain reaction (PCR) method, and reevaluates this method as a possible diagnostic tool for hydatidiform mole.
MATERIAL AND METHODS: A total of 71 cases which consists of 21 complete hydatidiform moles, three partial hydatidiform moles, and 47 non-molar abortions were investigated. The genetic origin was analyzed by the PCR method applied to the variable number of tandem repeat regions of the Apolipoprotein B gene, the human type-II collagen gene, and the probe YNZ22. Chromosomal analysis was also performed.
RESULTS: Genetic origin was determined in 58 out of 71 cases (83.1%). All of the complete hydatidiform moles were androgenic, having only paternal alleles. On the other hand, all the partial hydatidiform moles and non-molar abortions revealed clear biparental contribution. Besides triploid partial hydatidiform moles, one non-molar abortion showed two paternal and one maternal complements.
CONCLUSIONS: Our results were compatible with the classical theory of androgenic origin of complete hydatidiform mole; only complete hydatidiform mole is caused by androgenesis. We also found no complete hydatidiform mole of biparental origin. In conclusion, this PCR method brings a new aspect of genetic origin in the diagnosis of trophoblastic disease. It would be interesting to explore how morphologic subgrouping and genetic origin relate to the prognosis of trophoblastic disease.
MATERIAL AND METHODS: A total of 71 cases which consists of 21 complete hydatidiform moles, three partial hydatidiform moles, and 47 non-molar abortions were investigated. The genetic origin was analyzed by the PCR method applied to the variable number of tandem repeat regions of the Apolipoprotein B gene, the human type-II collagen gene, and the probe YNZ22. Chromosomal analysis was also performed.
RESULTS: Genetic origin was determined in 58 out of 71 cases (83.1%). All of the complete hydatidiform moles were androgenic, having only paternal alleles. On the other hand, all the partial hydatidiform moles and non-molar abortions revealed clear biparental contribution. Besides triploid partial hydatidiform moles, one non-molar abortion showed two paternal and one maternal complements.
CONCLUSIONS: Our results were compatible with the classical theory of androgenic origin of complete hydatidiform mole; only complete hydatidiform mole is caused by androgenesis. We also found no complete hydatidiform mole of biparental origin. In conclusion, this PCR method brings a new aspect of genetic origin in the diagnosis of trophoblastic disease. It would be interesting to explore how morphologic subgrouping and genetic origin relate to the prognosis of trophoblastic disease.