Dysregulation of the mTOR pathway secondary to mutations or a hostile microenvironment contributes to cancer and poor wound healing
- PMID: 19209152
- DOI: 10.1038/jid.2008.441
Dysregulation of the mTOR pathway secondary to mutations or a hostile microenvironment contributes to cancer and poor wound healing
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).
Comment on
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Akt1 controls insulin-driven VEGF biosynthesis from keratinocytes: implications for normal and diabetes-impaired skin repair in mice.J Invest Dermatol. 2009 Mar;129(3):752-64. doi: 10.1038/jid.2008.230. Epub 2008 Jul 31. J Invest Dermatol. 2009. PMID: 18668138
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