Wednesday, August 02, 2006
Treating rhinophyma with tamoxifen?
An interesting laboratory study that speculates on the possible treatment of rhyinophyma (red, bulbous nose of rosacea, often with excess tissue) with the "breast cancer" drug, tamoxifen (also rarely used to treat retroperitoneal fibrosis).
A number of studies appear to have suggested that fibrosis (caused by overexpression of the fibrogenic protein TGF-beta 2?) is implicated in the development and progression of advanced rhinophyma.
Down-regulating causes of fibrosis with tamoxifen: a possible cellular/molecular approach to treat rhinophyma.
Ann Plast Surg. 2006 Mar;56(3):301-5.
Payne WG, Ko F, Anspaugh S, Wheeler CK, Wright TE, Robson MC.
Institute for Tissue Regeneration, Repair, and Rehabilitation, Department of Veterans Administration Medical Center, Bay Pines, FL, USA.
Fibrosis and proliferative scarring are prominent features of the severe forms of rhinophyma. Up-regulation of growth and fibroblast kinetics are hallmarks of fibrosis. Persistent overexpression or dysregulated activation of the fibrogenic isoforms of transforming growth factor beta (TGF-beta) is associated with the increased fibroblast function leading to fibrotic conditions such as rhinophyma. Tamoxifen, a synthetic nonsteroidal antiestrogen, can neutralize or down-regulate TGF-beta. Fibroblast-populated collagen lattices (FPCLs) were constructed from fibroblasts cultured from rhinophyma or normal nasal skin. One-half of each set of FPCLs was treated with Tamoxifen. Lattice contraction was serially measured over 5 days, and the supernatants of the cultures were analyzed for TGF-beta-2 by immunoassay. Tamoxifen significantly decreased fibroblast activity by decreasing contraction of the treated lattices.
A number of studies appear to have suggested that fibrosis (caused by overexpression of the fibrogenic protein TGF-beta 2?) is implicated in the development and progression of advanced rhinophyma.
Down-regulating causes of fibrosis with tamoxifen: a possible cellular/molecular approach to treat rhinophyma.
Ann Plast Surg. 2006 Mar;56(3):301-5.
Payne WG, Ko F, Anspaugh S, Wheeler CK, Wright TE, Robson MC.
Institute for Tissue Regeneration, Repair, and Rehabilitation, Department of Veterans Administration Medical Center, Bay Pines, FL, USA.
Fibrosis and proliferative scarring are prominent features of the severe forms of rhinophyma. Up-regulation of growth and fibroblast kinetics are hallmarks of fibrosis. Persistent overexpression or dysregulated activation of the fibrogenic isoforms of transforming growth factor beta (TGF-beta) is associated with the increased fibroblast function leading to fibrotic conditions such as rhinophyma. Tamoxifen, a synthetic nonsteroidal antiestrogen, can neutralize or down-regulate TGF-beta. Fibroblast-populated collagen lattices (FPCLs) were constructed from fibroblasts cultured from rhinophyma or normal nasal skin. One-half of each set of FPCLs was treated with Tamoxifen. Lattice contraction was serially measured over 5 days, and the supernatants of the cultures were analyzed for TGF-beta-2 by immunoassay. Tamoxifen significantly decreased fibroblast activity by decreasing contraction of the treated lattices.
