Funding
Ongoing Grant Support
Evaluation of PLK1 inhibitors in a pre-clinical LAM animal model
Evaluation of PLK1 inhibitors in a pre-clinical LAM animal model
- Funded by the University of Pennsylvania Orphan Disease Center (2015) / Million Dollar Bike Ride 2014
- We demonstrated that PLK1 inhibitors can decrease the survival and induce cell death of TSC1 and TSC2 negative cells
- This project will evaluate the efficacy of PLK1 inhibitors, alone or in combination with rapamycin, in a LAM mouse model to inhibit tumor growth and lung metastases, and prevent tumor regrowth and lung metastases after discontinuation of treatment.
- PI: Astrinidis, co-PIs: Magdalena Karbowniczek (TTUHSC), Jane J. Yu (University of Cincinnati College of Medicine)
Completed Grant Support
Screen of FDA-approved drugs as a therapeutic approach for Tuberous Sclerosis Complex
Role of the PLK1-Hamartin interaction in the pathogenesis of Tuberous Sclerosis Complex
Role of the hamartin-Plk1 interaction in the pathogenesis of pulmonary lymphangioleio-myomatosis
Screen of FDA-approved drugs as a therapeutic approach for Tuberous Sclerosis Complex
- Funded by the Tuberous Sclerosis Alliance (2010-2012).
- Current treatments for TSC are mostly symptomatic. Rapamycin provides significant imrpovement of quality of life, however it is not clear that rapamycin will be sufficient to provide a permament cure for TSC.
- Our goal is to identify new drugs that could be used as therapeutics for TSC. We are currently screening a library of FDA-approved drugs for their potential to inhibit the growth of TSC-related cells. After the initial screens, a number of targets will be further validated, interactions with other drugs will be investigated, and their effects on cell death and mTOR signaling will be studied.
- Future studies in TSC animal models will be required to test the efficacy of these drugs.
- PI: Astrinidis
Role of the PLK1-Hamartin interaction in the pathogenesis of Tuberous Sclerosis Complex
- Funded by the Department of Defense (2009-2012).
- We demonstrated that TSC1 interacts with the mitotic kinase PLK1. Furthermore, this interaction seems to render the TSC1/TSC2 complex inactive.
- This project focuses in three areas: (a) to investigate the mechanism of PLK1-dependent mTOR signaling, (b) to study the role of PLK1, TSC1/TSC2, and mTOR in mitotic progression, and (c) to determine whether PLK1 can be use as a therapeutic target for TSC.
- PI: Astrinidis
Role of the hamartin-Plk1 interaction in the pathogenesis of pulmonary lymphangioleio-myomatosis
- Funded by The LAM Foundation (2006-2009).
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