[Chromosome instability observed in cells from monospermic, homozygous moles].
The present study was undertaken to disclose the mechanism which concerned to the propensity to malignancy of complete moles. For this purpose, the incidence of chromosomal aberrations and sister chromatid exchanges(SCE) after the administration of 0-30 ng/ml mitomycin C(MMC) were compared among cells cultured from molar and normal villi, and peripheral blood. Abnormally high induction of chromosomal aberrations and SCE was observed in molar cells without MMC treatment when compared with those of the remaining two cells. Then, higher susceptible responses to the low concentration of MMC were also noticeable in molar cells rather than two kinds of cells. As a result, it was assumed that chromosome instability possibly played an important role for choriocarcinogenesis of molar cells. Homozygosity of paternally derived genes may be responsible for this chromosome fragility. Six chromosomal bands (1q 21, 2p 24, 2p 13, 7q 31, 8q 22, 13q 33) were preferentially involved in the formation of chromosomal aberrations occurred spontaneously in molar cells. Four of these six bands were identical with the break points necessary for the production of the marker chromosomes in various tumors described previously, though one band was consistent with the N-myc oncogene locus. Thus, the possible association between chromosome rearrangements occurred in those six bands and the choriocarcinogenesis was assumed, though further accumulation of cytogenetic and molecular data was absolutely necessary.
Hoshi
S
S
Department of Obstetrics and Gynecology, Hokkaido University School of Medicine, Sapporo, Japan.
D002869:Chromosome Aberrations; D002873:Chromosome Fragility; D005260:Female; D005306:Fertilization; D006801:Humans; D006828:Hydatidiform Mole / Q000235:genetics*; D011247:Pregnancy; D012854:Sister Chromatid Exchange; D014407:Tumor Cells, Cultured; D014594:Uterine Neoplasms / Q000235:genetics*