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ACTH非依赖性Cushing综合征的分子生物学研究进展 被引量:1

Research advance in molecular biochemistry of ACTH-independent Cushing syndrome
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摘要 促肾上腺皮质激素(ACTH)非依赖性Cushing综合征包括肾上腺皮质腺瘤、肾上腺皮质癌和肾上腺皮质结节样增生,其发病机制主要与基因突变(GNAS1、PRKAR1A和PDE11A)、异位受体表达、WNT通路异常激活及抑癌基因杂合丢失等诸多因素相关,该文就上述发病机制作一综述。 Adrenocorticotropic hormone(ACTH)-independent Cushing syndrome includes adrenocortical adenoma,adrenocortical carcinoma and adrenocortical nodular hyperplasia,the pathogenesis of which is related to genetic mutations(GNAS1,PRKAR1A and PDE11A),expression of aberrant hormone receptors,dysfunction of WNT pathway and loss of heterozygosity of tumor suppressor gene.The pathogenesis mentioned above is introduced in this article.
出处 《上海交通大学学报(医学版)》 CAS CSCD 北大核心 2010年第5期508-510,共3页 Journal of Shanghai Jiao tong University:Medical Science
基金 国家自然科学基金(30771018)~~
关键词 促肾上腺皮质激素非依赖性Cushing综合征 GNAS1基因 PRKAR1A基因 PDE11A基因 异位受体 WNT通路 adrenocorticotropic hormone-independent Cushing syndrome GNAS1gene PRKAR1A gene PDE11A gene aberrant hormone receptors WNT pathway
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参考文献19

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