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垂体肿瘤的肿瘤发生与诱变

Oncogenesis and mutagenesis of pituitary tumors.

作者信息

Sonabend Adam M, Musleh Wael, Lesniak Maciej S

机构信息

The University of Chicago, Division of Neurosurgery, 5841 S. Maryland Avenue, MC 3026, Chicago, IL 60637, USA.

出版信息

Expert Rev Anticancer Ther. 2006 Sep;6 Suppl 9:S3-14. doi: 10.1586/14737140.6.9s.S3.

Abstract

Although pituitary tumors may be present in up to 10% of the population, the pathophysiology of these lesions is not well characterized. Pituitary tumors are composed of monoclonal cell populations with disrupted control of replication pathways. The oncogenes and tumor suppressor genes that are common in other malignancies (i.e. jun, fos, myc, and p53) are rarely involved in the development of these tumors. However, oncogenes, such as gsp, can be present in up to 40% of hormonally active adenomas. The process of pituitary oncogenesis further appears to involve oncogenes such as cyclin E, cyclin D1, and the pituitary tumor transforming gene (PTTG). Finally, the cAMP signaling cascade plays a significant role in generation of both benign and malignant pituitary tumors. In this review, the biology of pituitary adenomas is explored with a special emphasis on potential targets for the development of targeted therapeutics.

摘要

尽管垂体瘤在高达10%的人群中可能存在,但其病理生理学尚未得到充分表征。垂体瘤由复制途径控制紊乱的单克隆细胞群组成。在其他恶性肿瘤中常见的癌基因和肿瘤抑制基因(如jun、fos、myc和p53)很少参与这些肿瘤的发生。然而,诸如gsp等癌基因在高达40%的激素活性腺瘤中可能存在。垂体肿瘤发生过程似乎还涉及细胞周期蛋白E、细胞周期蛋白D1和垂体肿瘤转化基因(PTTG)等癌基因。最后,cAMP信号级联在良性和恶性垂体瘤的发生中都起着重要作用。在本综述中,探讨了垂体腺瘤的生物学特性,特别强调了靶向治疗开发的潜在靶点。

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