甲状腺肿瘤中磷脂酰肌醇3激酶途径的失调。
Dysregulation of the phosphatidylinositol 3-kinase pathway in thyroid neoplasia.
作者信息
Paes John E, Ringel Matthew D
机构信息
Division of Endocrinology, The Ohio State University Medical Center, The Ohio State University, 1581 Dodd Drive, 4th Floor, McCampbell Hall, Columbus, OH 43210, USA.
出版信息
Endocrinol Metab Clin North Am. 2008 Jun;37(2):375-87, viii-ix. doi: 10.1016/j.ecl.2008.01.001.
Abstract
The phosphatidylinositol 3-kinase (PI3K) signaling pathway is an important regulator of many cellular events, including apoptosis, proliferation, and motility. Enhanced activation of this pathway can occur through several mechanisms, such as inactivation of its negative regulator, phosphatase and tensin homolog deleted on chromosome ten (PTEN), and activating mutations and gene amplification of the gene encoding the catalytic subunit of PI3K (PIK3CA). These genetic abnormalities have been particularly associated with follicular thyroid neoplasia and anaplastic thyroid cancer, suggesting an important role for PI3K signaling in these disorders. In this article, the role of PI3K pathway activation in thyroid cancer is discussed, with a focus on recent advances.
摘要
磷脂酰肌醇3-激酶（PI3K）信号通路是许多细胞事件的重要调节因子，包括细胞凋亡、增殖和运动。该通路的增强激活可通过多种机制发生，例如其负调节因子第10号染色体上缺失的磷酸酶和张力蛋白同源物（PTEN）的失活，以及编码PI3K催化亚基的基因（PIK3CA）的激活突变和基因扩增。这些基因异常尤其与滤泡性甲状腺肿瘤和间变性甲状腺癌相关，提示PI3K信号在这些疾病中起重要作用。本文讨论了PI3K通路激活在甲状腺癌中的作用，并重点介绍了近期的进展。
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