Noguchi S, Motomura K, Inaji H, Imaoka S, Koyama H
Department of Surgery, Center for Adult Diseases, Osaka, Japan.
Cancer Lett. 1994 Apr 1;78(1-3):93-7. doi: 10.1016/0304-3835(94)90036-1.
Clonality of parathyroid adenomas and normal parathyroid glands was analyzed by a method based on restriction fragment length polymorphism of the X-chromosome-linked phosphoglycerokinase (PGK) gene and on random inactivation of the gene by methylation. Through the introduction of the polymerase chain reaction to this method, clonal analysis could be performed on small DNA samples prepared from cryostat sections of these specimens. Every normal parathyroid gland was found to be polyclonal while every parathyroid adenoma was found to be monoclonal. When DNA samples obtained from four widely separated sites of an adenoma were independently analyzed, each sample was found to be monoclonal and, in addition, the same allele of PGK gene was inactivated. These results suggest that parathyroid adenoma, which has a single cell origin, is a true neoplasm and that its pathogenesis is probably different from that of parathyroid hyperplasia which is polyclonal in origin.
采用基于X染色体连锁磷酸甘油激酶(PGK)基因限制性片段长度多态性及该基因通过甲基化随机失活的方法,分析甲状旁腺腺瘤和正常甲状旁腺的克隆性。通过将聚合酶链反应引入该方法,可对从这些标本的冷冻切片制备的小DNA样本进行克隆分析。发现每个正常甲状旁腺都是多克隆的,而每个甲状旁腺腺瘤都是单克隆的。当对从腺瘤四个相距较远部位获得的DNA样本进行独立分析时,每个样本均为单克隆,此外,PGK基因的相同等位基因被失活。这些结果表明,起源于单个细胞的甲状旁腺腺瘤是一种真正的肿瘤,其发病机制可能与起源于多克隆的甲状旁腺增生不同。