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. This review summarizes current thinking.

中文翻译：

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垂体瘤发病机制中的分子缺陷

大多数垂体腺瘤营养稳定，多年来大小变化相对较小。相对较小的比例表现得更积极，并通过不适当的激素分泌或对周围结构的不利影响引起临床注意。具有转移扩散的真正恶性行为是非常不典型的。进行手术的垂体腺瘤主要是单克隆起源的，大约一半是非整倍体，这表明在其发展过程中的某个时间，要么是持续的遗传不稳定性，要么是通过一段遗传不稳定性过渡。很少与肿瘤形成的经典机制相关，但通常认为，与正常垂体相比，大多数分子组成在分子组成上存在数量上的差异（如果不是质量上的差异）。尽管它们的流行和活检材料的现成可用，但目前，大多数垂体腺瘤的确切分子发病机制仍不清楚。这篇评论总结了当前的想法。