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继发于突变或不良微环境的mTOR信号通路失调会导致癌症和伤口愈合不良。

Dysregulation of the mTOR pathway secondary to mutations or a hostile microenvironment contributes to cancer and poor wound healing.

作者信息

Clark Richard A F, Pavlis Michelle

机构信息

Department of Biomedical Engineering, Stony Brook University, Stony Brook, New York 11794-8165, USA.

出版信息

J Invest Dermatol. 2009 Mar;129(3):529-31. doi: 10.1038/jid.2008.441.

DOI:10.1038/jid.2008.441
PMID:19209152
Abstract

Either heredity mutations or adverse microenvironment conditions may result in dysregulation of the mammalian target of the rapamycin (mTOR) pathway. The former lead to clinical syndromes such as tuberous sclerosis, Peutz-Jeghers syndrome, and Cowden's disease, which are characterized by hamartomatous growth or cancer. The latter can be associated with poor wound healing as described by Goren et al. (2009, this issue).

摘要

遗传性突变或不良微环境条件均可能导致哺乳动物雷帕霉素靶蛋白（mTOR）信号通路失调。前者会引发结节性硬化症、黑斑息肉综合征和考登病等临床综合征，其特征为错构瘤性生长或癌症。后者可能如戈伦等人（2009年，本期）所述，与伤口愈合不良有关。

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