Chudek J, Ritz E, Kovacs G
Department of Urology, Ruprecht-Karls-University, Heidelberg, Germany.
Clin Cancer Res. 1998 Jan;4(1):211-4.
The molecular pathway of autonomous growth of the parathyroid glands in uremic patients is poorly understood. We have analyzed 71 parathyroid lesions from 24 patients with refractory hyperparathyroidism for allelic loss at chromosomes 1, 3, 6, 9, 11, 12, 13, 15, and 17 and at the X chromosome. Microsatellite analysis was performed using 24 highly polymorphic markers. Deletions at chromosomes 1, 3, 6, 11, 12, and 13 and at the X chromosome were detected in only 10 of 67 nodules (15%). No allelic loss of the p16 and p53 tumor suppressor genes or the extracellular calcium receptor gene was found. The X-chromosome inactivation assay revealed a monoclonal pattern in 58% of hyperplastic nodules in females. Our results indicate monoclonal growth in the majority of hyperplastic nodules and suggest that some of these lesions might be considered precursors for adenoma development.
尿毒症患者甲状旁腺自主生长的分子途径目前尚不清楚。我们分析了24例难治性甲状旁腺功能亢进患者的71个甲状旁腺病变，检测其1、3、6、9、11、12、13、15、17号染色体及X染色体上的等位基因缺失情况。使用24个高度多态性标记进行微卫星分析。在67个结节中，仅10个（15%）检测到1、3、6、11、12、13号染色体及X染色体上的缺失。未发现p16和p53肿瘤抑制基因或细胞外钙受体基因的等位基因缺失。X染色体失活分析显示，女性增生性结节中58%呈单克隆模式。我们的结果表明，大多数增生性结节呈单克隆生长，提示其中一些病变可能被视为腺瘤发生的前体。
