Astrinidis Research Lab
  • Home
  • What is TSC and LAM?
    • TSC and LAM
    • Rapamycin treatment
  • Research
    • Background
    • Current projects
    • Funding
    • Publications
  • Positions
  • About
    • Lab members
    • Collaborators
    • Contact
    • Disclaimer

Funding

Ongoing Grant Support

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
  • 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).

Next topic: Publications
Go back to Research overview, Background on our research, or Current projects
© 2007-2016 Aristotelis Astrinidis, and the Astrinidis Lab | Disclaimer
Current projects | Lab Members | Contact
Proudly powered by Weebly