Levy Andy, Lightman Stafford
University Research Centre for Neuroendocrinology, Bristol University, Jenner Yard, Bristol BS2 8HW, UK.
Front Neuroendocrinol. 2003 Apr;24(2):94-127. doi: 10.1016/s0091-3022(03)00012-8.
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.
大多数垂体腺瘤在营养方面是稳定的，多年来大小变化相对较小。相对较小比例的垂体腺瘤行为更具侵袭性，通过不适当的激素分泌或对周围结构的不良影响而引起临床关注。伴有转移扩散的真正恶性行为非常罕见。接受手术的垂体腺瘤主要起源于单克隆，大约一半为非整倍体，这表明在其发育过程中的某个时间点存在持续的基因不稳定或经历一段基因不稳定时期。很少与肿瘤形成的经典机制相关，但一般认为，与正常垂体相比，大多数垂体腺瘤在分子组成上存在数量上的差异，即便不是质量上的差异。尽管垂体腺瘤很常见且活检材料容易获取，但目前大多数垂体腺瘤的确切分子发病机制仍不清楚。本综述总结了当前的观点。
