Dysregulation of the mTOR pathway secondary to mutations or a hostile microenvironment contributes to cancer and poor wound healing.
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).
Clark
Richard A F
RA
Department of Biomedical Engineering, Stony Brook University, Stony Brook, New York 11794-8165, USA. richard.clark@sunysb.edu
Pavlis
Michelle
M
D000818:Animals; D015972:Gene Expression Regulation, Neoplastic; D006222:Hamartoma / Q000235:genetics; D006223:Hamartoma Syndrome, Multiple / Q000235:genetics; D006801:Humans; D051379:Mice; D009154:Mutation; D009389:Neovascularization, Pathologic; D010580:Peutz-Jeghers Syndrome / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D011494:Protein Kinases / Q000096:biosynthesis* / Q000235:genetics*; D058570:TOR Serine-Threonine Kinases; D014402:Tuberous Sclerosis / Q000378:metabolism; D000077004:Tuberous Sclerosis Complex 1 Protein; D000077005:Tuberous Sclerosis Complex 2 Protein; D025521:Tumor Suppressor Proteins / Q000378:metabolism; D014945:Wound Healing
D019869:Phosphatidylinositol 3-Kinases; D011494:Protein Kinases; D058570:TOR Serine-Threonine Kinases; D000077004:Tuberous Sclerosis Complex 1 Protein; D000077005:Tuberous Sclerosis Complex 2 Protein; D025521:Tumor Suppressor Proteins; C546842:MTOR protein, human; C546843:mTOR protein, mouse