Identification of a Chromosome Carrying a Putative Tumor Suppressor gene in Human Choriocarcinoma by Microcell-Mediated Chromosome Transfer.

完全性葡萄胎的起源主要有两种机制：a）空卵被一个单倍体精子受精，然后重复; B）这样一个卵被两个单倍体精子受精。人们普遍认为，在所有形式的妊娠中，与绒毛膜癌相关的风险是迄今为止最高的。痣的隐性突变的纯合表达被认为与这种恶性倾向有关。几种肿瘤抑制基因的改变以及癌基因的激活被认为是绒毛膜癌发生所必需的。在痣中显示的遗传特征表明，前者的改变是特别重要的，以探讨多步骤的恶性肿瘤的转换。因此，来自正常细胞的单个染色体通过微细胞融合被引入绒毛膜癌细胞。在微细胞杂交瘤的致瘤性的评价表明，染色体#7携带绒毛膜癌的推定的肿瘤抑制基因。基因印记或隐性突变可能是造成这种基因失活的原因。能够与痣的高恶性倾向相对应。现在，可以产生对正常#7染色体特异的cDNA表达自由度。用正常绒毛和CCI绒毛膜癌的mRNA探针进行集落杂交，再结合自杀选择克隆，将能克隆到绒毛膜癌的抑癌基因。

There are two main mechanisms of origin for complete hydatidiform mole ; a) fertilization of an empty egg by a haploid sperm followed by duplication and b) fertilization of such an egg by two haploid spermatozoa. It is widely accepted that of all forms of pregnancy that had to choriocarcinoma the risk associated with moles is by far the highest. Homozygous expression of a recessive mutation of moles has been assumed to associate with this propensity to malignancies.Alterations of several tumor suppressor genes together with activation of oncogenes are assumed to be necessary for choriocarcinogenesis. Genetic characteristics shown in the moles suggest that the former alterations are especially important to explore the multistep conversions to malignancies. Thus, individual chromosomes derived from normal cells were introduced into choriocarcinoma cells via microcell fusion. Evaluation of tumorigenicity in microcell hybrids suggested that chromosome #7 carried a putative tumor suppressor gene for choriocarcinoma. The gene imprinting or recessive mutation mmy be responsible for the inactivation of such a gene. Being able to correspond with the high propensity to malignancy of moles. Now, the cDNA expression liberaties specific to the normal #7 chromosome could be produced. Colony hybridization using mRNA probes obtained from normal villi and CCI choriarcinoma in addition to suicide selection cloning the revertant will be able to clone the tumor suppressor genes of choriocarcinoma.