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J Biomol Tech. 2007 February; 18(1): 55.
PMCID: PMC2292056

P158-M Expression of c-kit, p-mTOR and p-NFKappaB in Angiolymphoid Hyperplasia with Eosinophilia: Potential for Therapy with Imitanib Mesylate, Rapamycin and Bortezomib


We report a case of a 54-year-old white female with a seven year history of angiolymphoid hyperplasia with eosinophilia. (Figures 11,, 22)) A proteomic evaluation of the tumor was performed with the intention of identifying targets for therapy. The tissue had high expressions of the following: platelet derived growth factor-alpha(PDGFR-α), platelet derived growth factor-beta (PDGFR-β), c-kit (CD 117), angiotensin converting enzyme, p-mTOR (SER 2448) and p-NF-κB p-p65.

The signal transducers PDGFR-α and PDGFR-β are expressed in the cytoplasm of numerous mast cells. c-kit, another signal transducer, is expressed in the plasmalemmal compartment (cell membrane) by an appreciable number of mast cells. The transactivator, ACE, is expressed in the plasmalemmal compartment of the lesional endothelial cells. The downstream effector, p-mTOR is expressed in the nuclear, cytoplasmic and plasmalemmal compartments of the lesional endothelial cells. And, an antiapoptotic/tumorigenic factor, NF-κB p-p65 is expressed in the nuclear and cytoplasmic compartments of endothelial growth cells.

Imitanib mesylate (Gleevec) targets c-kit, PDGFR-α and PDGFR-β. ACE inhibitors, such as enalapril, target angiotensin converting enzyme. Sirolimis (Rapamycin) antagonizes p-mTOR whichinhibits mast cells and lymphocytes via reduced IL-5 and vascular endothelial growth factor (VEGF). Bortezomib (Velcade) blocks the activation of NF-κB which interrupts VEGF production and endothelial cell stimulation.

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