Alterations of the AKT Pathway in Sporadic Human Tumors, Inherited Susceptibility to Cancer, and Overgrowth Syndromes.

3区 医学 Q2 Medicine
Craig W Menges, Dalal Hassan, Mitchell Cheung, Alfonso Bellacosa, Joseph R Testa
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引用次数: 0

Abstract

The AKT kinases are critical signaling molecules that regulate cellular physiology upon the activation of tyrosine kinase receptors and phosphatidylinositol 3-kinases (PI3K). AKT kinases govern many cellular processes considered hallmarks of cancer, including cell proliferation and survival, cell size, tumor invasion, metastasis, and angiogenesis. AKT signaling is regulated by multiple tumor suppressors and oncogenic proteins whose loss or activation, respectively, leads to dysregulation of this pathway, thereby contributing to oncogenesis. Herein, we review the enormous body of literature documenting how the AKT pathway becomes hyperactivated in sporadic human tumors and various hereditary cancer syndromes. We also discuss the role of activating mutations of AKT pathway genes in various chimeric overgrowth disorders, including Proteus syndrome, hypoglycemia with hypertrophy, CLOVES and SOLAMEN syndromes, and hemimegalencephaly.

散发性人类肿瘤、遗传性癌症易感性和过度生长综合征中 AKT 通路的改变
AKT 激酶是一种重要的信号分子,在激活酪氨酸激酶受体和磷脂酰肌醇 3- 激酶(PI3K)后可调节细胞生理机能。AKT 激酶控制着许多被认为是癌症标志的细胞过程,包括细胞增殖和存活、细胞大小、肿瘤侵袭、转移和血管生成。AKT 信号转导受多种肿瘤抑制蛋白和致癌蛋白的调控,它们的缺失或激活分别导致该通路失调,从而导致肿瘤发生。在此,我们回顾了大量文献,这些文献记录了 AKT 通路是如何在散发性人类肿瘤和各种遗传性癌症综合征中被过度激活的。我们还讨论了 AKT 通路基因的活化突变在各种嵌合型生长过快疾病中的作用,包括 Proteus 综合征、低血糖伴肥大症、CLOVES 和 SOLAMEN 综合征以及巨脑症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
5.60
自引率
0.00%
发文量
26
审稿时长
>12 weeks
期刊介绍: The review series Current Topics in Microbiology and Immunology provides a synthesis of the latest research findings in the areas of molecular immunology, bacteriology and virology. Each timely volume contains a wealth of information on the featured subject. This review series is designed to provide access to up-to-date, often previously unpublished information.
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