The functional analysis of the putative choriocarcinoma suppressor gene, HTF12 in choriocarcinoma.

HTF12基因位于人类第7条染色体7q11.2，有3个cdna，剪接变体。我检查了绒毛膜癌中从纯合缺失到恶性转化的干预。我检查了是否有一个独特的序列要表达，但没有发现针对启动子的特异性序列。由于很难在绒毛膜癌的提取组织中进行表达分析，因此我确定了在正常绒毛中的表达位点。原位杂交证实滋养细胞转变为合胞滋养细胞，HTF12表达。未分化为合胞滋养细胞的滋养细胞未被识别。据此估计HTF12基因是影响联合化的基因。此外，在绒毛细胞中加入可使HTF12在滋养细胞中更深入地进行联合化的化学物质福斯克林（forskolin），可明显促进其联合化，增强其在滋养细胞中的表达。因此，有人建议福斯克林对HTF12起作用。在已知的痣中，HTF12区域的缺失至今未被发现，并且HTF12的表达并未消失。HTF12不作用于绒毛向磨牙水肿转化的水平，提示HTF12参与了致癌水平的转化。此外，所有痣均为68例，其中绒毛中有154例为包囊性痣，其中包囊性痣为包囊性痣，部分痣为显微镜下痣。然而，通过多态性分析，我们发现有120例是雄激素性的，这一结果让我们预见到，通过基因诊断的诊断将被未来的宏观诊断所打破。除了所有痣外，有必要重新检查一例外壳癌变。目前还没有广泛的多态性分析资料，但通过多态性分析，日本人的多态性分布至今仍得到证实。少

The HTF12 gene is in the 7th human chromosome at 7q11.2, and has three cDNAs, splice variants.I examined intervention from this region being homozygous deletion to malignant transformation in choriocarcinoma. I reviewed whether there was an unique sequence to express, but nothing specific for promoter was not found. Because expression analysis in an extractive tissues of choriocarcinoma was difficulty, I confirmed the expression locus about expression in a normal villus. The trophoblastic cell which changed into syncitiotrophoblast, and expression of HTF12 was recognized by in situ hybridization. The trophoblastic cell which did not change into syncitiotrophoblast was not recognized. On this account that a HTF12 gene was the gene which affected syncitionization was estimated. Furthermore, the syncitionyzation was promoted obviously, and expression of HTF12 in a trophoblastic cell was enhanced when having added forskolin which was the syncitionyzation chemical material which let you cha … More nge into it in a villus cell. On this account it was suggested that forskolin acted over HTF12. Deficiency of HTF12 region was not recognized till now in a provided mole, and expression of HTF12 did not disappear. HTF12 did not act on the level that a villus turned molar edematization into, and that participated in transformation by a cancer-causing level was suggested. In addition, all moles were 68 examples macroscopically, and, among villus 154 examples that a cyst changed into it as for the hydatidiform mole, as for the part mole, a microscopical mole was had elsewhere. However, by analysis with polymorphism, it was recognized that 120 examples were androgenesis, and it was it with the consequence which let you foresee that a diagnosis by gene diagnosis was broken for the future, macroscopic diagnosis. Necessity to reexamine a case of canceration of shell besides all moles was confirmed till now. There were not data of wide polymorphism analysis, but distribution of polymorphism of a Japanese was confirmed to a Japanese till now by polymorphism analysis. Less