Friedman E, Bale A E, Marx S J, Norton J A, Arnold A, Tu T, Aurbach G D, Spiegel A M
Molecular Pathophysiology Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
J Clin Endocrinol Metab. 1990 Aug;71(2):293-7. doi: 10.1210/jcem-71-2-293.
We analyzed genomic DNA from 43 sporadic benign parathyroid adenomas for rearrangements of the PTH gene, and for point mutations of the H-ras (codons 12, 13, and 61), N-ras (codons 12, 13, and 61), and K-ras (codons 12 and 13) genes. One of 43 parathyroid adenomas showed a chromosome 11 rearrangement involving both the PTH gene on the short arm of chromosome 11 (at band p15) and a locus on the long arm (11q13). This rearrangement was indistinguishable from one that was previously described in a parathyroid adenoma by Arnold et al., indicating that this may be an important contributor to tumorigenesis in a small subset of patients with parathyroid adenoma. H-ras, K-ras, and N-ras oncogene activation by point mutation at codons 12, 13, or 61, known to occur in many tumors, could not be detected in any parathyroid adenoma.
我们分析了43例散发性良性甲状旁腺腺瘤的基因组DNA，以检测甲状旁腺激素（PTH）基因的重排，以及H-ras基因（密码子12、13和61）、N-ras基因（密码子12、13和61）和K-ras基因（密码子12和13）的点突变。43例甲状旁腺腺瘤中有1例显示11号染色体重排，涉及11号染色体短臂（p15带）上的PTH基因和长臂（11q13）上的一个位点。这种重排与Arnold等人之前在甲状旁腺腺瘤中描述的重排无法区分，这表明这可能是一小部分甲状旁腺腺瘤患者肿瘤发生的重要因素。在任何甲状旁腺腺瘤中均未检测到已知在许多肿瘤中发生的密码子12、13或61处的点突变导致的H-ras、K-ras和N-ras癌基因激活。
