分泌生长激素的人垂体肿瘤分子生物学研究进展。

E F Adams, M Buchfelder, A Hüttner, S Moreth, R Fahlbusch
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引用次数: 3

摘要

DNA技术的应用使我们对gh分泌垂体肿瘤病因学的理解取得了重大进展。x染色体失活和RFLP分析表明,gh分泌肿瘤起源于单克隆,因此是单个细胞内体细胞突变的结果。利用聚合酶链反应和序列分析,在30-40%的肿瘤中发现了这种突变。这就是所谓的gsp突变,其中g蛋白的α s亚基基因转化为致癌基因,其表达导致构成腺苷环化酶活性,从而过量产生cAMP。在我们自己的研究中,我们证明生长激素基因启动子区域的缺陷不太可能被证明是肢端肥大症中生长激素分泌过多的原因。相反,我们已经证明生长激素基因在肿瘤来源的DNA中是低甲基化的,这可能至少部分地解释了生长激素基因异常表达的原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Recent advances in the molecular biology of growth-hormone secreting human pituitary tumours.

The application of DNA technology has led to significant progress in our understanding of the aetiology of GH-secreting pituitary tumours. X-chromosome inactivation and RFLP analysis has revealed that GH-secreting tumours are monoclonal in origin and thus arise as a consequence of a somatic mutation within a single cell. Using PCR and sequence analysis, such a mutation has been identified in 30-40% of tumours. This is the so-called gsp mutation in which the gene for the alpha s subunit of the Gs protein is converted to an oncogene the expression of which results in constitutive adenyl cyclase activity and thus excessive cAMP production. In our own studies, we demonstrate that it is unlikely that a defect within the promoter region of the GH gene will prove to be a cause of excessive GH secretion in acromegaly. In contrast, we have shown that the GH gene is hypomethylated in tumour derived DNA and this may account, at least in part, for abnormal GH gene expression.

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