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首页> 外文期刊>Frontiers in neuroendocrinology >Molecular defects in the pathogenesis of pituitary tumours.
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Molecular defects in the pathogenesis of pituitary tumours.

机译:垂体肿瘤发病机理中的分子缺陷。

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摘要

The majority of pituitary adenomas are trophically stable and change relatively little in size over many years. A comparatively small proportion behave more aggressively and come to clinical attention through inappropriate hormone secretion or adverse effects on surrounding structures. True malignant behaviour with metastatic spread is very atypical. Pituitary adenomas that come to surgery are predominantly monoclonal in origin and roughly half are aneuploid, indicating either ongoing genetic instability or transition through a period of genetic instability at some time during their development. Few are associated with the classical mechanisms of tumour formation but it is generally believed that the majority harbour quantitative if not qualitative differences in molecular composition compared to the normal pituitary. Despite their prevalence and the ready availability of biopsy material, at the present time, the precise molecular pathogenesis of the majority of pituitary adenomas remains unclear. Thisreview summarizes current thinking.
机译:大多数垂体腺瘤在营养上是稳定的,并且在多年内大小变化相对较小。相对较小的比例表现出更强的攻击性,并由于不适当的激素分泌或对周围结构的不利影响而引起临床关注。具有转移性扩散的真正恶性行为是非常典型的。垂体腺瘤的起源主要是单克隆的,大约一半是非整倍体的,说明其发展过程中持续的遗传不稳定或遗传不稳定时期的过渡。很少有与肿瘤形成的经典机制相关联的,但是通常认为,与正常垂体相比,大多数在分子组成上具有定量的,即使不是定性的差异。尽管它们普遍存在并且容易获得活检材料,但是目前,大多数垂体腺瘤的确切分子发病机制仍不清楚。这篇综述总结了当前的想法。

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