Dysregulation of the mTOR Pathway Secondary to Mutations or a Hostile Microenvironment Contributes to Cancer and Poor Wound Healing

被引：17

作者：

Clark, Richard A. F. ^{[1
,2
,3
]}

Pavlis, Michelle ^{[4
]}

机构：

[1] SUNY Stony Brook, Dept Biomed Engn, Ctr Tissue Engn, Stony Brook, NY 11794 USA

[2] SUNY Stony Brook, Dept Dermatol, Stony Brook, NY 11794 USA

[3] SUNY Stony Brook, Dept Med, Stony Brook, NY 11794 USA

[4] Emory Univ, Sch Med, Atlanta, GA USA

来源：

JOURNAL OF INVESTIGATIVE DERMATOLOGY | 2009年 / 129卷 / 03期

关键词：

GENOTYPE-PHENOTYPE CORRELATIONS; PHOSPHOINOSITIDE; 3-KINASE; PROTEUS-SYNDROME; COWDEN-SYNDROME; PTEN; GROWTH; ACTIVATION; DISEASE; COMPLEX;

D O I：

10.1038/jid.2008.441

中图分类号：

R75 [皮肤病学与性病学];

学科分类号：

100206 ;

摘要：

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).

引用

页码：529 / 531

页数：3

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