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甲状腺髓样癌或嗜铬细胞瘤的肿瘤发生并不需要p53基因失活。

Inactivation of the p53 gene is not required for tumorigenesis of medullary thyroid carcinoma or pheochromocytoma.

作者信息

Yana I, Nakamura T, Shin E, Karakawa K, Kurahashi H, Kurita Y, Kobayashi T, Mori T, Nishisho I, Takai S

机构信息

Department of Medical Genetics, Osaka University Medical School.

出版信息

Jpn J Cancer Res. 1992 Nov;83(11):1113-6. doi: 10.1111/j.1349-7006.1992.tb02730.x.

Abstract

A polymerase chain reaction (PCR)-mediated RNase protection analysis was performed to detect subtle genetic alterations of p53 in medullary thyroid carcinoma (MTC) and pheochromocytoma. None of the 30 pheochromocytomas showed abnormal RNase protection patterns. Only one of 32 MTCs showed an abnormal pattern, and subsequent DNA sequencing of the PCR product revealed that it had a G to C transversion in codon 49 that resulted in a change from aspartic acid to histidine. However, this was a sporadic MTC with no specific clinicopathological characteristics. On the basis of a previous report that genes on chromosome 17p were not deleted in MTCs and were relatively infrequently deleted in pheochromocytomas, our results suggest that the p53 gene is not involved in tumorigenesis of MTC or pheochromocytoma.

摘要

采用聚合酶链反应(PCR)介导的核糖核酸酶保护分析来检测甲状腺髓样癌(MTC)和嗜铬细胞瘤中p53基因的细微遗传改变。30例嗜铬细胞瘤均未显示异常的核糖核酸酶保护模式。32例MTC中仅1例显示异常模式,随后对PCR产物进行DNA测序发现,其密码子49处发生了G到C的颠换,导致天冬氨酸变为组氨酸。然而,这是一例散发的MTC,无特异性临床病理特征。基于之前的一份报告,即17号染色体短臂上的基因在MTC中未缺失,在嗜铬细胞瘤中相对较少缺失,我们的结果表明,p53基因不参与MTC或嗜铬细胞瘤的肿瘤发生。

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