[Molecular biological analysis of the DNA in trophoblastic disease--with special reference to genetic information of hPL and hCG(alpha, beta)].
Genomic DNAs extracted from normal placenta, while blood cells, hydatidiform mole and choriocarcinoma were examined to see if they had the same coding structure for hPL, hCG alpha and hCG beta using each of the complementary DNAs. The restriction analysis of these genomic DNAs showed the same pattern even for the DNA of choriocarcinoma that transcribed no hPL mRNA but a relatively high level of hCG(alpha,beta)mRNA. We considered that during trophoblastic malignant transformation, neither the gene deletion for hPL nor the gene amplification for hCG occurred. Moreover, the genomic DNA sequence in hCG alpha gene has polymorphic restriction sites designated as R+/- and H+/-. Using these polymorphisms, we confirmed the hypothesis that a hydatidiform mole develops from an androgenetic origin. We also observed that it is possible that a hydatidiform mole having R- and H+ homozygous DNA may develop into a choriocarcinoma. These observation suggested that some intervening sequence between these polymorphic sites is related to the tumorigenesis of choriocarcinoma.
D006063:Chorionic Gonadotropin / Q000235:genetics*; D003001:Cloning, Molecular; D004273:DNA, Neoplasm / Q000235:genetics*; D005260:Female; D006801:Humans; D006824:Hybridization, Genetic; D011110:Polymorphism, Genetic; D011247:Pregnancy; D011388:Prolactin / Q000235:genetics*; D012333:RNA, Messenger; D014328:Trophoblastic Neoplasms / Q000209:etiology / Q000235:genetics*; D014594:Uterine Neoplasms / Q000209:etiology / Q000235:genetics*
D006063:Chorionic Gonadotropin; D004273:DNA, Neoplasm; D012333:RNA, Messenger; D011388:Prolactin