Grossman Ashley B
Department of Endocrinology, Centre for Endocrinology, St Bartholomew's Hospital, West Smithfield, London EC1A 7BE, UK.
Pituitary. 2009;12(3):265-70. doi: 10.1007/s11102-008-0158-7.
Oncogenes and tumor suppressor genes involved in most common cancers are not involved in the great majority of pituitary adenomas. Similarly, there is little evidence to suggest that the mutations involved in genetic syndromes associated with pituitary tumors (such as the gsp, MEN1, PKAR1A or AIP mutations) are common in sporadic tumors. A novel pituitary tumor transforming gene (PTTG, securin) has been identified which is over-expressed in most tumors--but it is unclear as to its causal role in oncogenesis. Cell signaling abnormalities have been identified in pituitary tumors but their genetic basis is unknown. However, both the Akt pathway and the MAPK pathway are over-expressed in many pituitary tumors, which results in the inhibition of cell cycle inhibitors. These pathways share a common root in the tyrosine kinase receptor, and a change to these receptors or their relationship to membrane matrix-related proteins may be an early event in tumorigenesis.
大多数常见癌症所涉及的癌基因和肿瘤抑制基因在绝大多数垂体腺瘤中并不涉及。同样，几乎没有证据表明与垂体肿瘤相关的遗传综合征（如gsp、MEN1、PKAR1A或AIP突变）中涉及的突变在散发性肿瘤中很常见。已鉴定出一种新型垂体肿瘤转化基因（PTTG，分离酶），其在大多数肿瘤中过度表达，但尚不清楚其在肿瘤发生中的因果作用。垂体肿瘤中已发现细胞信号异常，但其遗传基础尚不清楚。然而，Akt通路和MAPK通路在许多垂体肿瘤中均过度表达，这导致细胞周期抑制剂受到抑制。这些通路在酪氨酸激酶受体中有共同的根源，这些受体或它们与膜基质相关蛋白的关系发生改变可能是肿瘤发生的早期事件。
